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Sample records for arsenite induced oxidative

  1. Arsenite treatment induces oxidative stress, upregulates antioxidant system, and causes phytochelatin synthesis in rice seedlings.

    Science.gov (United States)

    Mishra, Shruti; Jha, A B; Dubey, R S

    2011-07-01

    The effects of arsenite treatment on generation of reactive oxygen species, induction of oxidative stress, response of antioxidative system, and synthesis of phytochelatins were investigated in two indica rice (Oryza sativa L.) cvs. Malviya-36 and Pant-12 grown in sand cultures for a period of 5-20 days. Arsenite (As(2)O(3); 25 and 50 μM) treatment resulted in increased formation of superoxide anion (O (2) (.-) ), elevated levels of H(2)O(2) and thiobarbituric acid reactive substances, showing enhanced lipid peroxidation. An enhanced level of ascorbate (AA) and glutathione (GSH) was observed irrespective of the variation in the level of dehydroascorbate (DHA) and oxidized glutathione (GSSG) which in turn influenced redox ratios AA/DHA and GSH/GSSG. With progressive arsenite treatment, synthesis of total acid soluble thiols and phytochelatins (PC) increased in the seedlings. Among antioxidative enzymes, the activities of superoxide dismutase (EC 1.15.1.1), catalase (EC 1.11.1.6), total ascorbate peroxidase (APX, EC 1.11.1.11), chloroplastic ascorbate peroxidase, guaiacol peroxidase (EC 1.11.1.7), monodehydroascorbate reductase (EC 1.6.5.4), and glutathione reductase (EC 1.6.4.2) increased in arsenite treated seedlings, while dehyroascorbate reductase (EC 1.8.5.1) activity declined initially during 5-10 days and increased thereafter. Results suggest that arsenite treatment causes oxidative stress in rice seedlings, increases the levels of many enzymatic and non-enzymatic antioxidants, and induces synthesis of thiols and PCs, which may serve as important components in mitigating arsenite-induced oxidative damage.

  2. Arsenite induced oxidative damage in mouse liver is associated with increased cytokeratin 18 expression

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    Gonsebatt, M.E. [UNAM, Ciudad Universitaria, Dept. Medicina Genomica y Toxicologia Ambiental, Instituto de Investigaciones Biomedicas, Mexico (Mexico); Razo, L.M. del; Sanchez-Pena, L.C. [Seccion de Toxicologia, CINVESTAV, Mexico (Mexico); Cerbon, M.A. [Facultad de Quimica, UNAM, Departamento de Biologia, Mexico (Mexico); Zuniga, O.; Ramirez, P. [Facultad de Estudios Superiores Cuautitlan, UNAM, Laboratorio de Toxicologia Celular, Coordinacion General de Estudios de Posgrado e Investigacion, Cuautitlan Izcalli, Estado de Mexico (Mexico)

    2007-09-15

    Cytokeratins (CK) constitute a family of cytoskeletal intermediate filament proteins that are typically expressed in epithelial cells. An abnormal structure and function are effects that are clearly related to liver diseases as non-alcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. We have previously observed that sodium arsenite (SA) induced the synthesis of CK18 protein and promotes a dose-related disruption of cytoplasmic CK18 filaments in a human hepatic cell line. Both abnormal gene expression and disturbance of structural organization are toxic effects that are likely to cause liver disease by interfering with normal hepatocyte function. To investigate if a disruption in the CK18 expression pattern is associated with arsenite liver damage, we investigated CK18 mRNA and protein levels in liver slices treated with low levels of SA. Organotypic cultures were incubated with 0.01, 1 and 10 {mu}M of SA in the absence and presence of N-acetyl cysteine (NAC). Cell viability and inorganic arsenic metabolism were determined. Increased expression of CK18 was observed after exposure to SA. The addition of NAC impeded the oxidative effects of SA exposure, decreasing the production of thiobarbituric acid-reactive substances and significantly diminishing the up regulation of CK18 mRNA and protein. Liver arsenic levels correlated with increased levels of mRNA. Mice treated with intragastric single doses of 2.5 and 5 mg/kg of SA showed an increased expression of CK18. Results suggest that CK18 expression may be a sensible early biomarker of oxidative stress and damage induced by arsenite in vitro and in vivo. Then, during SA exposure, altered CK expression may compromise liver function. (orig.)

  3. Auxin and its transport play a role in plant tolerance to arsenite-induced oxidative stress in Arabidopsis thaliana.

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    Krishnamurthy, Aparna; Rathinasabapathi, Bala

    2013-10-01

    The role of auxin in plant development is well known; however, its possible function in root response to abiotic stress is poorly understood. In this study, we demonstrate a novel role of auxin transport in plant tolerance to oxidative stress caused by arsenite. Plant response to arsenite [As(III)] was evaluated by measuring root growth and markers for stress on seedlings treated with control or As(III)-containing medium. Auxin transporter mutants aux1, pin1 and pin2 were significantly more sensitive to As(III) than the wild type (WT). Auxin transport inhibitors significantly reduced plant tolerance to As(III) in the WT, while exogenous supply of indole-3-acetic acid improved As(III) tolerance of aux1 and not that of WT. Uptake assays using H(3) -IAA showed As(III) affected auxin transport in WT roots. As(III) increased the levels of H2 O2 in WT but not in aux1, suggesting a positive role for auxin transport through AUX1 on plant tolerance to As(III) stress via reactive oxygen species (ROS)-mediated signalling. Compared to the WT, the mutant aux1 was significantly more sensitive to high-temperature stress and salinity, also suggesting auxin transport influences a common element shared by plant tolerance to arsenite, salinity and high-temperature stress.

  4. [6]-Gingerol isolated from ginger attenuates sodium arsenite induced oxidative stress and plays a corrective role in improving insulin signaling in mice.

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    Chakraborty, Debrup; Mukherjee, Avinaba; Sikdar, Sourav; Paul, Avijit; Ghosh, Samrat; Khuda-Bukhsh, Anisur Rahman

    2012-04-05

    Arsenic toxicity induces type 2 diabetes via stress mediated pathway. In this study, we attempt to reveal how sodium arsenite (iAs) could induce stress mediated impaired insulin signaling in mice and if an isolated active fraction of ginger, [6]-gingerol could attenuate the iAs intoxicated hyperglycemic condition of mice and bring about improvement in their impaired insulin signaling. [6]-Gingerol treatment reduced elevated blood glucose level and oxidative stress by enhancing activity of super oxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and GSH. [6]-Gingerol also helped in increasing plasma insulin level, brought down after iAs exposure. iAs treatment to primary cell culture of β-cells and hepatocytes in vitro produced cyto-degenerative effect and accumulated reactive oxygen species (ROS) in pancreatic β-cells and hepatocytes of mice. [6]-Gingerol appeared to inhibit/intervene iAs induced cyto-degeneration of pancreatic β-cells and hepatocytes, helped in scavenging the free radicals. The over-expression of TNFα and IL6 in iAs intoxicated mice was down-regulated by [6]-gingerol treatment. iAs intoxication reduced expression levels of GLUT4, IRS-1, IRS-2, PI3K, AKT, PPARγ signaling molecules; [6]-gingerol mediated its action through enhancing the expressions of these signaling molecules, both at protein and mRNA levels. Thus, our results suggest that [6]-gingerol possesses an anti-hyperglycemic property and can improve impaired insulin signaling in arsenic intoxicated mice.

  5. N-acetylcysteine and meso-2,3-dimercaptosuccinic acid alleviate oxidative stress and hepatic dysfunction induced by sodium arsenite in male rats

    Science.gov (United States)

    Abu El-Saad, Ahmed M; Al-Kahtani, Mohammed A; Abdel-Moneim, Ashraf M

    2016-01-01

    Environmental exposure to arsenic represents a serious challenge to humans and other animals. The aim of the present study was to test the protective effect of antioxidant N-acetylcysteine (NAC) either individually or in combination with a chelating agent, meso-2,3-dimercaptosuccinic acid (DMSA), against sodium arsenite oral toxicity in male rats. Five groups were used: control; arsenic group (orally administrated in a concentration of 2 mg/kg body weight [b.w.]); the other three groups were orally administrated sodium arsenite in a concentration of 2 mg/kg b.w. followed by either NAC (10 mg/kg b.w., intraperitoneally [i.p.]), DMSA (50 mg/kg b.w., i.p.) or NAC plus DMSA. Arsenic toxicity caused significant rise in serum aspartate aminotransferase, alanine aminotransferase and total bilirubin, and a significant decrease in total protein (TP) and albumin levels after 3 weeks of experimental period. In addition, arsenic-treated rats showed significantly higher arsenic content in liver and significant rise in hepatic malondialdehyde level. By contrast, sharp decreases in glutathione content and catalase and glutathione reductase activities were discernible. NAC and/or DMSA counteracted most of these physiologic and biochemical defects. NAC monotherapy was more effective than DMSA in increasing TP, while DMSA was more effective in decreasing alanine aminotransferase. The combined treatment was superior over monotherapies in recovery of TP and glutathione. Biochemical data were well supported by histopathological and ultrastructural findings. In conclusion, the combination therapy of NAC and DMSA may be an ideal choice against oxidative insult induced by arsenic poisoning.

  6. Photoinduced Oxidation of Arsenite to Arsenate on Ferrihydrite

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    N Bhandari; R Reeder; D Strongin

    2011-12-31

    The photochemistry of an aqueous suspension of the iron oxyhydroxide, ferrihydrite, in the presence of arsenite has been investigated using attenuated total reflection Fourier transform infrared spectroscopy (ATR-FTIR), X-ray absorption near edge structure (XANES), and solution phase analysis. Both ATR-FTIR and XANES show that the exposure of ferrihydrite to arsenite in the dark leads to no change in the As oxidation state, but the exposure of this arsenite-bearing surface, which is in contact with pH 5 water, to light leads to the conversion of the majority of the adsorbed arsenite to the As(V) bearing species, arsenate. Analysis of the solution phase shows that ferrous iron is released into solution during the oxidation of arsenite. The photochemical reaction, however, shows the characteristics of a self-terminating reaction in that there is a significant suppression of this redox chemistry before 10% of the total iron making up the ferrihydrite partitions into solution as ferrous iron. The self-terminating behavior exhibited by this photochemical arsenite/ferrihydrite system is likely due to the passivation of the ferrihydrite surface by the strongly bound arsenate product.

  7. The defensive effect of benfotiamine in sodium arsenite-induced experimental vascular endothelial dysfunction.

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    Verma, Sanjali; Reddy, Krishna; Balakumar, Pitchai

    2010-10-01

    The present study has been designed to investigate the effect of benfotiamine, a thiamine derivative, in sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Sodium arsenite (1.5 mg(-1) kg(-1) day(-1) i.p., 2 weeks) was administered in rats to produce VED. The development of VED was assessed by employing isolated aortic ring preparation and estimating the serum and aortic concentrations of nitrite/nitrate. Further, the integrity of vascular endothelium in thoracic aorta was assessed by scanning electron microscopy. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide anion generation. The administration of sodium arsenite markedly produced VED by attenuating acetylcholine-induced endothelium-dependent relaxation, decreasing serum and aortic concentrations of nitrite/nitrate, and impairing the integrity of vascular endothelium. Further, sodium arsenite produced oxidative stress by increasing serum TBARS and aortic superoxide generation. The treatment with benfotiamine (25, 50, and 100 mg(-1) kg(-1) day(-1) p.o.) or atorvastatin (30 mg(-1) kg(-1) day(-1) p.o., a standard agent) prevented sodium arsenite-induced VED and oxidative stress. However, the beneficial effects of benfotiamine in preventing the sodium arsenite-induced VED were attenuated by co-administration with N-omega-nitro-L: -arginine methyl ester (L: -NAME) (25 mg(-1) kg(-1) day(-1), i.p.), an inhibitor of NOS. Thus, it may be concluded that benfotiamine reduces oxidative stress and activates endothelial nitric oxide synthase to enhance the generation and bioavailability of NO and subsequently improves the integrity of vascular endothelium to prevent sodium arsenite-induced experimental VED.

  8. N-acetylcysteine and meso-2,3 dimercaptosuccinic acid alleviate oxidative stress and hepatic dysfunction induced by sodium arsenite in male rats

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    Abu El-Saad AM

    2016-10-01

    ultrastructural findings. In conclusion, the combination therapy of NAC and DMSA may be an ideal choice against oxidative insult induced by arsenic poisoning. Keywords: arsenic, N-acetylcysteine, meso-2,3-dimercaptosuccinic acid, liver pathology, oxidative imbalance

  9. Antioxidant Potential of Spirulina platensis Mitigates Oxidative Stress and Reprotoxicity Induced by Sodium Arsenite in Male Rats

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    Samir A. E. Bashandy

    2016-01-01

    Full Text Available The present study aimed to examine the protective role of Spirulina platensis (S. platensis against arsenic-induced testicular oxidative damage in rats. Arsenic (in the form of NaAsO2 at a dose of 6.3 mg/kg body weight for 8 weeks caused a significant accumulation of arsenic in testicular tissues as well as a decrease in the levels of testicular superoxide dismutase (SOD, catalase (CAT, reduced glutathione, and zinc. Moreover, it significantly decreased plasma testosterone, luteinizing hormone (LH, triiodothyronine (T3, and thyroxine (T4 levels and reduced sperm motility and sperm count. Arsenic (AS led to a significant increase in testicular malondialdehyde (MDA, tumour necrosis factor alpha (TNF-α, nitric oxide (NO, and sperm abnormalities. S. platensis at a dose of 300 mg/kg was found to attenuate As-induced oxidative stress, testicular damage, and sperm abnormalities by its potent antioxidant activity. S. platensis may represent a potential therapeutic option to protect the testicular tissue from arsenic intoxication.

  10. Effect of rosiglitazone in sodium arsenite-induced experimental vascular endothelial dysfunction.

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    Kaur, Tajpreet; Goel, Rajesh Kumar; Balakumar, Pitchai

    2010-04-01

    The present study has been designed to investigate the effect of rosiglitazone, a peroxisome proliferator activated receptor gamma agonist in sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. The rats were administered sodium arsenite (1.5 mg/kg/day, i.p., 2 weeks) to induce VED. The development of VED was assessed by employing isolated aortic ring preparation and estimating serum nitrite/nitrate concentration. Further, the integrity of the aortic endothelium was assessed histologically using haematoxylin-eosin staining. Moreover, the oxidative stress was assessed by estimating serum thiobarbituric acid reactive substances, aortic reactive oxygen species and reduced form of glutathione. The administration of sodium arsenite produced VED by impairing acetylcholine-induced endothelium dependent relaxation, diminishing the integrity of vascular endothelium and decreasing the serum nitrite/nitrate concentration. In addition, sodium arsenite was noted to produce oxidative stress as it increased serum thiobarbituric acid reactive substances and aortic reactive oxygen species and consequently decreased glutathione. Treatment with rosiglitazone (3 mg/kg/day, p.o., 2 weeks and 5 mg/kg/day, p.o., 2 weeks) significantly prevented sodium arsenite-induced VED by enhancing acetylcholine-induced endothelium dependent relaxation, improving the integrity of vascular endothelium, increasing the nitrite/nitrate concentration and decreasing the oxidative stress. However, the vascular protective effect of rosiglitazone was markedly abolished by co-administration of nitric oxide synthase inhibitor, N-Omega-Nitro-L-Arginine Methyl Ester (L-NAME) (25 mg/kg/day, i.p., 2 weeks). Thus, it may be concluded that rosiglitazone reduces oxidative stress, activates eNOS and enhances the generation of nitric oxide to prevent sodium arsenite-induced VED in rats.

  11. The genetic basis of anoxygenic photosynthetic arsenite oxidation

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    Hernandez-Maldonado, Jamie; Sanchez-Sedillo, Benjamin; Stoneburner, Brendon; Boren, Alison; Miller, Laurence G.; McCann, Shelley; Rosen, Michael R.; Oremland, Ronald S.; Saltikov, Chad W.

    2017-01-01

    “Photoarsenotrophy”, the use of arsenite as an electron donor for anoxygenic photosynthesis, is thought to be an ancient form of phototrophy along with the photosynthetic oxidation of Fe(II), H2S, H2, and NO2-. Photoarsenotrophy was recently identified from Paoha Island's (Mono Lake, CA) arsenic-rich hot springs. The genomes of several photoarsenotrophs revealed a gene cluster, arxB2AB1CD, where arxA is predicted to encode for the sole arsenite oxidase. The role of arxA in photosynthetic arsenite oxidation was confirmed by disrupting the gene in a representative photoarsenotrophic bacterium, resulting in the loss of light-dependent arsenite oxidation. In situ evidence of active photoarsenotrophic microbes was supported by arxA mRNA detection for the first time, in red-pigmented microbial mats within the hot springs of Paoha Island. This work expands on the genetics for photosynthesis coupled to new electron donors and elaborates on known mechanisms for arsenic metabolism, thereby highlighting the complexities of arsenic biogeochemical cycling.

  12. Arsenite Oxidation and Arsenite Resistance by Bacillus sp. PNKP-S2

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    Pranee Pattanapipitpaisal

    2015-01-01

    Full Text Available Arsenic causes human health problems after accumulate in the body for 10-15 years and arsenite [As(III] is generally regarded as being more mobile and toxic than other oxidation states. In this study, two-hundred and three bacterial strains were isolated from groundwater and soil samples collecting in Ubon Ratchathani Province, Thailand. All strains were screened for arsenic tolerant efficiency at 1-10 mM of sodium arsenite. Eighteen selected strains which had the highest resistance to 10 mM of As(III were further studied for their As(III-oxidizing activity and growth in enrichment and growth medium (EG medium supplemented with 0.58 mM of As(III. It was found that strain PNKP-S2 was able to grow in the medium with As(III as a sole energy source and had 89.11% As(III removal within 48 h. The PCR-based 16S rDNA sequencing analysis revealed that the strain PNKP-S2 was closed relative to Bacillus sp. This is the first report on Bacillus sp. chemolithoautotrophic As(III-oxidizer and this strain could be a potential candidate for application in arsenic remediation of contaminated water.

  13. Anaerobic oxidation of arsenite in Mono Lake water and by a facultative, arsenite-oxidizing chemoautotroph, strain MLHE-1

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    Oremland, R.S.; Hoeft, S.E.; Santini, J.M.; Bano, N.; Hollibaugh, R.A.; Hollibaugh, J.T.

    2002-01-01

    Arsenite [As(III)]-enriched anoxic bottom water from Mono Lake, California, produced arsenate [As(V)] during incubation with either nitrate or nitrite. No such oxidation occurred in killed controls or in live samples incubated without added nitrate or nitrite. A small amount of biological As(III) oxidation was observed in samples amended with Fe(III) chelated with nitrolotriacetic acid, although some chemical oxidation was also evident in killed controls. A pure culture, strain MLHE-1, that was capable of growth with As(III) as its electron donor and nitrate as its electron acceptor was isolated in a defined mineral salts medium. Cells were also able to grow in nitrate-mineral salts medium by using H2 or sulfide as their electron donor in lieu of As(III). Arsenite-grown cells demonstrated dark 14CO2 fixation, and PCR was used to indicate the presence of a gene encoding ribulose-1,5-biphosphate carboxylase/oxygenase. Strain MLHE-1 is a facultative chemoautotroph, able to grow with these inorganic electron donors and nitrate as its electron acceptor, but heterotrophic growth on acetate was also observed under both aerobic and anaerobic (nitrate) conditions. Phylogenetic analysis of its 16S ribosomal DNA sequence placed strain MLHE-1 within the haloalkaliphilic Ectothiorhodospira of the ??-Proteobacteria. Arsenite oxidation has never been reported for any members of this subgroup of the Proteobacteria.

  14. The novel role of fenofibrate in preventing nicotine- and sodium arsenite-induced vascular endothelial dysfunction in the rat.

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    Kaur, Jagdeep; Reddy, Krishna; Balakumar, Pitchai

    2010-09-01

    The present study investigated the effect of fenofibrate, an agonist of PPAR-alpha, in nicotine- and sodium arsenite-induced vascular endothelial dysfunction (VED) in rats. Nicotine (2 mg/kg/day, i.p., 4 weeks) and sodium arsenite (1.5 mg/kg/day, i.p., 2 weeks) were administered to produce VED in rats. The scanning electron microscopy study in thoracic aorta revealed that administration of nicotine or sodium arsenite impaired the integrity of vascular endothelium. Further, administration of nicotine or sodium arsenite significantly decreased serum and aortic concentrations of nitrite/nitrate and subsequently reduced acetylcholine-induced endothelium-dependent relaxation. Moreover, nicotine or sodium arsenite produced oxidative stress by increasing serum thiobarbituric acid reactive substances (TBARS) and aortic superoxide generation. However, treatment with fenofibrate (30 mg/kg/day, p.o.) or atorvastatin (30 mg/kg/day p.o., a standard agent) significantly prevented nicotine- and sodium arsenite-induced VED and oxidative stress by improving the integrity of vascular endothelium, increasing the concentrations of serum and aortic nitrite/nitrate, enhancing the acetylcholine-induced endothelium-dependent relaxation and decreasing serum TBARS and aortic superoxide anion generation. Conversely, co-administration of L-NAME (25 mg/kg/day, i.p.), an inhibitor of nitric oxide synthase, markedly attenuated these vascular protective effects of fenofibrate. The administration of nicotine or sodium arsenite altered the lipid profile by increasing serum cholesterol and triglycerides and consequently decreasing high-density lipoprotein levels, which were significantly prevented by treatment with fenofibrate or atorvastatin. It may be concluded that fenofibrate improves the integrity and function of vascular endothelium, and the vascular protecting potential of fenofibrate in preventing the development of nicotine- and sodium arsenite-induced VED may be attributed to its

  15. Bioaccumulation and oxidative stress in Daphnia magna exposed to arsenite and arsenate.

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    Fan, Wenhong; Ren, Jinqian; Li, Xiaomin; Wei, Chaoyang; Xue, Feng; Zhang, Nan

    2015-11-01

    Arsenic pollution and its toxicity to aquatic organisms have attracted worldwide attention. The bioavailability and toxicity of arsenic are highly related to its speciation. The present study investigated the differences in bioaccumulation and oxidative stress responses in an aquatic organism, Daphnia magna, induced by 2 inorganic arsenic species (As(III) and As(V)). The bioaccumulation of arsenic, Na(+) /K(+) -adenosine triphosphatase (ATPase) activity, reactive oxygen species (ROS) content, total superoxide dismutase (SOD) activity, total antioxidative capability, and malondialdehyde content in D. magna were determined after exposure to 500 µg/L of arsenite and arsenate for 48 h. The results showed that the oxidative stress and antioxidative process in D. magna exposed to arsenite and arsenate could be divided into 3 phases, which were antioxidative response, oxidation inhibition, and antioxidative recovery. In addition, differences in bioaccumulation, Na(+) /K(+) -ATPase activity, and total SOD activity were also found in D. magna exposed to As(III) and As(V). These differences might have been the result of the high affinity of As(III) with sulfhydryl groups in enzymes and the structural similarity of As(V) to phosphate. Therefore, arsenate could be taken up by organisms through phosphate transporters, could substitute for phosphate in biochemical reactions, and could lead to a change in the bioaccumulation of arsenic and activity of enzymes. These characteristics were the possible reasons for the different toxicity mechanisms in the oxidative stress process of arsenite and arsenate.

  16. Hepatoprotective Role of Hydrangea macrophylla against Sodium Arsenite-Induced Mitochondrial-Dependent Oxidative Stress via the Inhibition of MAPK/Caspase-3 Pathways

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    Md Rashedunnabi Akanda

    2017-07-01

    Full Text Available Sodium arsenite (NaAsO2 has been recognized as a worldwide health concern. Hydrangea macrophylla (HM is used as traditional Chinese medicine possessing antioxidant activities. The study was performed to investigate the therapeutic role and underlying molecular mechanism of HM on NaAsO2-induced toxicity in human liver cancer (HepG2 cells and liver in mice. The hepatoprotective role of HM in HepG2 cells was assessed by using 3-(4,5-dimethylthiazol-2-Yl-2,5-diphenyltetrazolium bromide (MTT, reactive oxygen species (ROS, and lactate dehydrogenase (LDH assays. Histopathology, lipid peroxidation, serum biochemistry, quantitative real-time polymerase chain reaction (qPCR and Western blot analyses were performed to determine the protective role of HM against NaAsO2 intoxication in liver tissue. In this study, we found that co-treatment with HM significantly attenuated the NaAsO2-induced cell viability loss, intracellular ROS, and LDH release in HepG2 cells in a dose-dependent manner. Hepatic histopathology, lipid peroxidation, and the serum biochemical parameters alanine aminotransferase (ALT and aspartate aminotransferase (AST were notably improved by HM. HM effectively downregulated the both gene and protein expression level of the mitogen-activated protein kinase (MAPK cascade. Moreover, HM well-regulated the Bcl-2-associated X protein (Bax/B-cell lymphoma-2 (Bcl-2 ratio, remarkably suppressed the release of cytochrome c, and blocked the expression of the post-apoptotic transcription factor caspase-3. Therefore, our study provides new insights into the hepatoprotective role of HM through its reduction in apoptosis, which likely involves in the modulation of MAPK/caspase-3 signaling pathways.

  17. The influence of environmental conditions on kinetics of arsenite oxidation by manganese-oxides

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    Fischel, Matthew H. H.; Fischel, Jason S.; Lafferty, Brandon J.; Sparks, Donald L.

    2015-01-01

    Background Manganese-oxides are one of the most important minerals in soil due to their widespread distribution and high reactivity. Despite their invaluable role in cycling many redox sensitive elements, numerous unknowns remain about the reactivity of different manganese-oxide minerals under varying conditions in natural systems. By altering temperature, pH, and concentration of arsenite we were able to determine how manganese-oxide reactivity changes with simulated environmental conditions...

  18. Involvement of HIF-2α-mediated inflammation in arsenite-induced transformation of human bronchial epithelial cells

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    Xu, Yuan; Zhao, Yue; Xu, Wenchao; Luo, Fei; Wang, Bairu; Li, Yuan; Pang, Ying; Liu, Qizhan, E-mail: drqzliu@hotmail.com

    2013-10-15

    Arsenic is a well established human carcinogen that causes diseases of the lung. Some studies have suggested a link between inflammation and lung cancer; however, it is unknown if arsenite-induced inflammation causally contributes to arsenite-caused malignant transformation of cells. In this study, we investigated the molecular mechanisms underlying inflammation during neoplastic transformation induced in human bronchial epithelial (HBE) cells by chronic exposure to arsenite. The results showed that, on acute or chronic exposure to arsenite, HBE cells over-expressed the pro-inflammatory cytokines, interleukin-6 (IL-6), interleukin-8 (IL-8), and interleukin-1β (IL-1β). The data also indicated that HIF-2α was involved in arsenite-induced inflammation. Moreover, IL-6 and IL-8 were essential for the malignant progression of arsenite-transformed HBE cells. Thus, these experiments show that HIF-2α mediates arsenite-induced inflammation and that such inflammation is involved in arsenite-induced malignant transformation of HBE cells. The results provide a link between the inflammatory response and the acquisition of a malignant transformed phenotype by cells chronically exposed to arsenite and thus establish a previously unknown mechanism for arsenite-induced carcinogenesis. - Highlights: • Arsenite induces inflammation. • Arsenite-induced the increases of IL-6 and IL-8 via HIF-2α. • Inflammation is involved in arsenite-induced carcinogenesis.

  19. Effect of arsenite-oxidizing bacterium B. laterosporus on arsenite toxicity and arsenic translocation in rice seedlings.

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    Yang, Gui-Di; Xie, Wan-Ying; Zhu, Xi; Huang, Yi; Yang, Xiao-Jun; Qiu, Zong-Qing; Lv, Zhen-Mao; Wang, Wen-Na; Lin, Wen-Xiong

    2015-10-01

    Arsenite [As (III)] oxidation can be accelerated by bacterial catalysis, but the effects of the accelerated oxidation on arsenic toxicity and translocation in rice plants are poorly understood. Herein we investigated how an arsenite-oxidizing bacterium, namely Brevibacillus laterosporus, influences As (III) toxicity and translocation in rice plants. Rice seedlings of four cultivars, namely Guangyou Ming 118 (GM), Teyou Hang II (TH), Shanyou 63 (SY) and Minghui 63 (MH), inoculated with or without the bacterium were grown hydroponically with As (III) to investigate its effects on arsenic toxicity and translocation in the plants. Percentages of As (III) oxidation in the solutions with the bacterium (100%) were all significantly higher than those without (30-72%). The addition of the bacterium significantly decreased As (III) concentrations in SY root, GM root and shoot, while increased the As (III) concentrations in the shoot of SY, MH and TH and in the root of MH. Furthermore, the As (III) concentrations in the root and shoot of SY were both the lowest among the treatments with the bacterium. On the other hand, its addition significantly alleviated the As (III) toxicity on four rice cultivars. Among the treatments amended with B. laterosporus, the bacterium showed the best remediation on SY seedlings, with respect to the subdued As (III) toxicity and decreased As (III) concentration in its roots. These results indicated that As (III) oxidation accelerated by B. laterosporus could be an effective method to alleviate As (III) toxicity on rice seedlings.

  20. Possible vasculoprotective role of linagliptin against sodium arsenite-induced vascular endothelial dysfunction.

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    Jyoti, Uma; Kansal, Sunil Kumar; Kumar, Puneet; Goyal, Sandeep

    2016-02-01

    Vascular endothelial dysfunction (VED) interrupts the integrity and function of endothelial lining through enhanced markers of oxidative stress and decrease endothelial nitric oxide synthase (eNOS) expression. The main aim of the present study has been designed to investigate the possible vasculoprotective role of linagliptin against sodium arsenite-induced VED. Sodium arsenite (1.5 mg/kg, i.p., 2 weeks) abrogated the acetylcholine-induced, endothelium-dependent vasorelaxation by depicting the decrease in serum nitrite/nitrate concentration, reduced glutathione level, and simultaneously enhance the thiobarbituric acid reactive substances (TBARS) level, superoxide level, and tumor necrosis factor-alpha. These elevated markers interrupt the integrity of endothelial lining of thoracic aorta which was assessed histologically. The study elicits dose dependent effect of linagliptin (1.5 mg/kg, i.p. and 3 mg/kg, i.p.) or atorvastatin (30 mg/kg, p.o.) treatment, improved the endothelium-dependent independent relaxation, improve the integrity of endothelium lining which was assessed histologically by enhancing the serum nitrite/nitrate level, reduced glutathione level and simultaneously decreasing the TBARS level, superoxide anion level and tumor necrosis factor-alpha (TNF-α) level. L-NAME (25 mg/kg, i.p.), eNOS inhibitor, abrogated the ameliorative potential of linagliptin. However, the ameliorative potential of linagliptin has been enhanced by l-arginine (200 mg/kg, i.p.) which elicits that ameliorative potential of linagliptin was through eNOS signaling cascade and it may be concluded that linagliptin 3 mg/kg, i.p. has more significantly activated the eNOS and decreased the oxidative markers than linagliptin 1.5 mg/kg, i.p. and prevented sodium arsenite-induced VED.

  1. Reduction of arsenite-enhanced ultraviolet radiation-induced DNA damage by supplemental zinc

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    Cooper, Karen L.; King, Brenee S.; Sandoval, Monica M.; Liu, Ke Jian; Hudson, Laurie G., E-mail: lhudson@salud.unm.edu

    2013-06-01

    Arsenic is a recognized human carcinogen and there is evidence that arsenic augments the carcinogenicity of DNA damaging agents such as ultraviolet radiation (UVR) thereby acting as a co-carcinogen. Inhibition of DNA repair is one proposed mechanism to account for the co-carcinogenic actions of arsenic. We and others find that arsenite interferes with the function of certain zinc finger DNA repair proteins. Furthermore, we reported that zinc reverses the effects of arsenite in cultured cells and a DNA repair target protein, poly (ADP-ribose) polymerase-1. In order to determine whether zinc ameliorates the effects of arsenite on UVR-induced DNA damage in human keratinocytes and in an in vivo model, normal human epidermal keratinocytes and SKH-1 hairless mice were exposed to arsenite, zinc or both before solar-simulated (ss) UVR exposure. Poly (ADP-ribose) polymerase activity, DNA damage and mutation frequencies at the Hprt locus were measured in each treatment group in normal human keratinocytes. DNA damage was assessed in vivo by immunohistochemical staining of skin sections isolated from SKH-1 hairless mice. Cell-based findings demonstrate that ssUVR-induced DNA damage and mutagenesis are enhanced by arsenite, and supplemental zinc partially reverses the arsenite effect. In vivo studies confirm that zinc supplementation decreases arsenite-enhanced DNA damage in response to ssUVR exposure. From these data we can conclude that zinc offsets the impact of arsenic on ssUVR-stimulated DNA damage in cells and in vivo suggesting that zinc supplementation may provide a strategy to improve DNA repair capacity in arsenic exposed human populations. - Highlights: • Low levels of arsenite enhance UV-induced DNA damage in human keratinocytes. • UV-initiated HPRT mutation frequency is enhanced by arsenite. • Zinc supplementation offsets DNA damage and mutation frequency enhanced by arsenite. • Zinc-dependent reduction of arsenite enhanced DNA damage is confirmed in vivo.

  2. Arsenite oxidation by three types of manganese oxides

    Institute of Scientific and Technical Information of China (English)

    2006-01-01

    Oxidation of As(Ⅲ) by three types of manganese oxides and the effects of pH, ion strength and tartaric acid on the oxidation were investigated by means of chemical analysis, equilibrium redox, X-ray diffraction (XRD) and transmission electron microscopy (TEM). Three synthesized Mn oxide minerals, birnessite, cryptomelane, and hausmarnite, which widely occur in soil and sediments, could actively oxidize As(Ⅲ) to As(Ⅴ). However, their ability in As(Ⅲ)-oxidation varied greatly depending on their structure, composition and surface properties. Tunnel structured cryptomelane exhibited the highest ability of As (Ⅲ) oxidation, followed by the layer structured birnessite and the lower oxide hausmannite. The maximum amount of As (Ⅴ) produced by the oxidation was in the order (mmol/kg) ofcryptomelane (824.2) > birnessite (480.4) > hausmannite (117.9). As pH increased from the very low value(pH 2.5), the amount of As(Ⅲ) oxidized by the tested Mn oxides was firstly decreased, then negatively peaked in pH 3.0-6.5,and eventually increased remarkably. Oxidation of As(Ⅲ) by the Mn oxides had a buffering effects on the pH variation in the solution.It is proposed that the oxidative reaction processes between As( Ⅲ ) and birnessite(or cryptomelane) are as follows: (1) at lower pH condition: (MnO2)x + H3AsO3 + 0.5H+=0.5H2AsO4- + 0.5HAsO42- +Mn2++ (MnO2)x-1 + H2O; (2) at higher pH condition: (MnO2)x +cryptomelane decreased and was negatively correlated with ion strength. However, ion strength had little influence on As (Ⅲ) oxidation by the hausmannite. The presence of tartaric acid promoted oxidation of As(Ⅲ) by birnessite. As for cryptomelane and hausmannite, the same effect was observed when the concentration of tartaric acid was below 4 mmol/L, otherwise the oxidized As(Ⅲ)decreased. These findings are of great significance in improving our understanding of As geochemical cycling and controlling As contamination.

  3. Arsenite-induced autophagy is associated with proteotoxicity in human lymphoblastoid cells

    Energy Technology Data Exchange (ETDEWEB)

    Bolt, Alicia M.; Zhao, Fei; Pacheco, Samantha; Klimecki, Walter T., E-mail: klimecki@pharmacy.arizona.edu

    2012-10-15

    Epidemiological studies of arsenic-exposed populations have provided evidence that arsenic exposure in humans is associated with immunosuppression. Previously, we have reported that arsenite-induced toxicity is associated with the induction of autophagy in human lymphoblastoid cell lines (LCL). Autophagy is a cellular process that functions in the degradation of damaged cellular components, including protein aggregates formed by misfolded or damaged proteins. Accumulation of misfolded or damaged proteins in the endoplasmic reticulum (ER) lumen causes ER stress and activates the unfolded protein response (UPR). In an effort to investigate the mechanism of autophagy induction by arsenite in the LCL model, we examined the potential contribution of ER stress and activation of the UPR. LCL exposed to sodium arsenite for 8-days induced expression of UPR-activated genes, including CHOP and GRP78, at the RNA and the protein level. Evidence for activation of the three arms of the UPR was observed. The arsenite-induced activation of the UPR was associated with an accumulation of protein aggregates containing p62 and LC3, proteins with established roles in the sequestration and autophagic clearance of protein aggregates. Taken together, these data provide evidence that arsenite-induced autophagy is associated with the generation of ER stress, activation of the UPR, and formation of protein aggregates that may be targeted to the lysosome for degradation. -- Highlights: ► Arsenite induces endoplasmic reticulum stress and the unfolded protein response. ► Arsenite induces the formation of protein aggregates that contain p62 and LC3-II. ► Time-course data suggests that arsenite-induced autophagy precedes ER stress.

  4. Aqueous and ethanolic leaf extracts of Ocimum basilicum (sweet basil) protect against sodium arsenite-induced hepatotoxicity in Wistar rats.

    Science.gov (United States)

    Gbadegesin, M A; Odunola, O A

    2010-11-25

    We evaluated the effects of aqueous and ethanolic leaf extracts of Ocimum basilicum (sweet basil) on sodium arsenite-induced hepatotoxicity in Wistar rats. We observed that treatment of the animals with the extracts before or just after sodium arsenite administration significantly (p basilicum before the administration of sodium arsenite resulted in the attenuation of the sodium arsenite-induced aspartate and alanine aminotransferase activities: ALT (from 282.6% to 167.7% and 157.8%), AST (from 325.1% to 173.5% and 164.2%) for the group administered sodium arsenite alone, the aqueous extracts plus sodium arsenite, and ethanolic extracts plus sodium arsenite respectively, expressed as percentage of the negative control. These findings support the presence of hepatoprotective activity in the O.basilicum extracts.

  5. Adsorption and oxidation of arsenite by iron minerals in the presence of microorganisms

    Science.gov (United States)

    Perelomov, Leonid; Corsini, Anna; Andreoni, Vincenza

    2010-05-01

    It is known the two most commonly occurring forms of As in the environment are anionic arsenate [AsO43-, As(V)] and arsenite [AsO33-, As(III)]. Arsenite has been found to be the more mobile and toxic species in soil environments (Tamaki and Frankenberger, 1992). Arsenic speciation and toxicity are functions of pH, redox potential, the presence and type of adsorbing surfaces, and microbial populations. Biotransformation of arsenic species (reduction or oxidation) is mainly enzymatic process, while biosorption is metabolism independent process that governed by physico-chemical interactions on the cell surface. Special ternary bio-mineral systems, consisting of iron minerals (synthetic goethite, and magnetite, which was prepared by oxidation from special commercial product - nano-iron), special strains of arsenite-oxidizing microorganisms (Ancylobacter dichlorometanicus) and arsenite solution, were constructed and processes of arsenic compounds adsorption and oxidation were studied. As control experiments without microorganisms or without minerals were carried out. For determination of arsenic species, adsorbed on the surface of the minerals, desorption experiments were carried out also. Desorption ability of several chemicals, used for arsenic extraction from soils, was tested. Magnetite and goethite, with very small size of particles, have high chemical affinity to arsenite at wide range of pH values, but at pH above 9 adsorption of arsenite decreased in comparison with pH below of the isoelectric points of the minerals. We carried out experiments at initial pH 7,2. Experiments on kinetics of adsorption showed that equilibrium time for adsorption is 2 hours. In the ternary bio-mineral systems consisting of fresh-prepared magnetite,the effect of arsenite-oxidizing microorganisms on the oxidation process was negligible in all cases, because magnetite demonstrated very high oxidation ability in comparison with bacteria. During 4 hours all arsenite, adsorbed on the

  6. Altered Hepatic Transport by Fetal Arsenite Exposure in Diet-Induced Fatty Liver Disease.

    Science.gov (United States)

    Ditzel, Eric J; Li, Hui; Foy, Caroline E; Perrera, Alec B; Parker, Patricia; Renquist, Benjamin J; Cherrington, Nathan J; Camenisch, Todd D

    2016-07-01

    Non-alcoholic fatty liver disease can result in changes to drug metabolism and disposition potentiating adverse drug reactions. Furthermore, arsenite exposure during development compounds the severity of diet-induced fatty liver disease. This study examines the effects of arsenite potentiated diet-induced fatty liver disease on hepatic transport in male mice. Changes were detected for Mrp2/3/4 hepatic transporter gene expression as well as for Oatp1a4/2b1/1b2. Plasma concentrations of Mrp and Oatp substrates were increased in arsenic exposure groups compared with diet-only controls. In addition, murine embryonic hepatocytes and adult primary hepatocytes show significantly altered transporter expression after exposure to arsenite alone: a previously unreported phenomenon. These data indicate that developmental exposure to arsenite leads to changes in hepatic transport which could increase the risk for ADRs during fatty liver disease.

  7. In Vitro Protective Potentials of Annona muricata Leaf Extracts Against Sodium Arsenite-induced Toxicity.

    Science.gov (United States)

    George, Vazhappilly Cijo; Kumar, Devanga Ragupathi Naveen; Suresh, Palamadai Krishnan; Kumar, Rangasamy Ashok

    2015-01-01

    Sodium arsenite (NaAsO2) is a metalloid which is present widely in the environment and its chronic exposure can contribute to the induction of oxidative stress, resulting in disturbances in various metabolic functions including liver cell death. Hence, there is a need to develop drugs from natural sources, which can reduce arsenic toxicity. While there have been reports regarding the antioxidant and protective potentials of Annona muricataleaf extracts, our study is the first ofits kind to extend these findings by specifically evaluating its ability to render protection against sodium arsenite (NaAsO2) induced toxicity (10 μM) in WRL-68 (human hepatic cells) and human erythrocytes by employing XTT and haemolysis inhibition assays respectively. The methanolic extract exhibited higher activity than the aqueous extract in both assays. The results showed a dose-dependent decrease in arsenic toxicity in both WRL-68 cells and erythrocytes, suggesting the protective nature of Annona muricatato mitigate arsenic toxicity. Hence the bioactive extracts can further be scrutinized for the identification and characterization of their principal contributors.

  8. Severe systemic toxicity and urinary bladder cytotoxicity and regenerative hyperplasia induced by arsenite in arsenic (+3 oxidation state) methyltransferase knockout mice. A preliminary report

    Science.gov (United States)

    Arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes reactions which convert inorganic arsenic to methylated metabolites. This study determined whether the As3mt null genotype in the mouse modifies cytotoxic and proliferative effects seen in urinary bladders of wild t...

  9. Functions and Unique Diversity of Genes and Microorganisms Involved in Arsenite Oxidation from the Tailings of a Realgar Mine.

    Science.gov (United States)

    Zeng, Xian-Chun; E, Guoji; Wang, Jianing; Wang, Nian; Chen, Xiaoming; Mu, Yao; Li, Hao; Yang, Ye; Liu, Yichen; Wang, Yanxin

    2016-12-15

    The tailings of the Shimen realgar mine have unique geochemical features. Arsenite oxidation is one of the major biogeochemical processes that occurs in the tailings. However, little is known about the functional and molecular aspects of the microbial community involved in arsenite oxidation. Here, we fully explored the functional and molecular features of the microbial communities from the tailings of the Shimen realgar mine. We collected six samples of tailings from sites A, B, C, D, E, and F. Microcosm assays indicated that all of the six sites contain both chemoautotrophic and heterotrophic arsenite-oxidizing microorganisms; their activities differed considerably from each other. The microbial arsenite-oxidizing activities show a positive correlation with soluble arsenic concentrations. The microbial communities of the six sites contain 40 phyla of bacteria and 2 phyla of archaea that show extremely high diversity. Soluble arsenic, sulfate, pH, and total organic carbon (TOC) are the key environmental factors that shape the microbial communities. We further identified 114 unique arsenite oxidase genes from the samples; all of them code for new or new-type arsenite oxidases. We also isolated 10 novel arsenite oxidizers from the samples, of which 4 are chemoautotrophic and 6 are heterotrophic. These data highlight the unique diversities of the arsenite-oxidizing microorganisms and their oxidase genes from the tailings of the Shimen realgar mine. To the best of our knowledge, this is the first report describing the functional and molecular features of microbial communities from the tailings of a realgar mine. This study focused on the functional and molecular characterizations of microbial communities from the tailings of the Shimen realgar mine. We fully explored, for the first time, the arsenite-oxidizing activities and the functional gene diversities of microorganisms from the tailings, as well as the correlation of the microbial activities/diversities with

  10. Absorption of Arsenite on Several Iron (Hydro-)Oxides and Impact from Pre-processing Methods

    Institute of Scientific and Technical Information of China (English)

    YE Ying; JI Shanshan; WU Daidai; LI Jun; ZHANG Weirui

    2006-01-01

    The absorption reactions of arsenite on Fe (hydro-)oxides are studied. The three absorbent types are Fe(OH)3 gel and two Fe (hydro-)oxides, in which the Fe(OH)3 gel was dried in a microwave oven under vacuum at 80℃. It is found that pH changes from 9.71 to 10.36 in 6 minutes after the Fe (OH)3 gel was mixed with NaAsO2 solution, as the arsenite replaces the OH- in goethite and Fe(OH)3.At the 40th minute after the start of the reaction, pH decreases, which is most probably because that the monodentate surface complex of absorbed arsenite has changed into mononuclear-bidentate complex and released proton. The decline in pH values indicates not the end of the absorption but a change in the reaction type. Temperature and dissolved gas has little effect on these two types of reactions. The total absorption of arsenite increases after the absorbent is irradiated with ultrasound, which also lead to difficulty in separating the solids from solution. The absorption capacity for arsenite of Fe(OH)3 gel dried in a microwave oven under vacuum is 53.18% and 17.22% respectively better than that of Fe (OH)3 gel and gel dried at 80℃. The possible reasons are that the water molecules in the gel vibrates with high frequency under the effect of microwave irradiation, thereby producing higher porosity and improved surface activity.

  11. The Arsenite Oxidation Potential of Native Microbial Communities from Arsenic-Rich Freshwaters.

    Science.gov (United States)

    Fazi, Stefano; Crognale, Simona; Casentini, Barbara; Amalfitano, Stefano; Lotti, Francesca; Rossetti, Simona

    2016-07-01

    Microorganisms play an important role in speciation and mobility of arsenic in the environment, by mediating redox transformations of both inorganic and organic species. Since arsenite [As(III)] is more toxic than arsenate [As(V)] to the biota, the microbial driven processes of As(V) reduction and As(III) oxidation may play a prominent role in mediating the environmental impact of arsenic contamination. However, little is known about the ecology and dynamics of As(III)-oxidizing populations within native microbial communities exposed to natural high levels of As. In this study, two techniques for single cell quantification (i.e., flow cytometry, CARD-FISH) were used to analyze the structure of aquatic microbial communities across a gradient of arsenic (As) contamination in different freshwater environments (i.e., groundwaters, surface and thermal waters). Moreover, we followed the structural evolution of these communities and their capacity to oxidize arsenite, when experimentally exposed to high As(III) concentrations in experimental microcosms. Betaproteobacteria and Deltaproteobacteria were the main groups retrieved in groundwaters and surface waters, while Beta and Gammaproteobacteria dominated the bacteria community in thermal waters. At the end of microcosm incubations, the communities were able to oxidize up to 95 % of arsenite, with an increase of Alphaproteobacteria in most of the experimental conditions. Finally, heterotrophic As(III)-oxidizing strains (one Alphaproteobacteria and two Gammaproteobacteria) were isolated from As rich waters. Our findings underlined that native microbial communities from different arsenic-contaminated freshwaters can efficiently perform arsenite oxidation, thus contributing to reduce the overall As toxicity to the aquatic biota.

  12. Arsenite oxidation by a poorly-crystalline manganese oxide. 3. Arsenic and manganese desorption.

    Science.gov (United States)

    Lafferty, Brandon J; Ginder-Vogel, Matthew; Sparks, Donald L

    2011-11-01

    Arsenic (As) mobility in the environment is greatly affected by its oxidation state and the degree to which it is sorbed on metal oxide surfaces. Manganese oxides (Mn oxides) have the ability to decrease overall As mobility both by oxidizing toxic arsenite (As(III)) to less toxic arsenate (As(V)), and by sorbing As. However, the effect of competing ions on the mobility of As sorbed on Mn-oxide surfaces is not well understood. In this study, desorption of As(V) and As(III) from a poorly crystalline phyllomanganate (δ-MnO(2)) by two environmentally significant ions is investigated using a stirred-flow technique and X-ray absorption spectroscopy (XAS). As(III) is not observed in solution after desorption under any conditions used in this study, agreeing with previous studies showing As sorbed on Mn-oxides exists only as As(V). However, some As(V) is desorbed from the δ-MnO(2) surface under all conditions studied, while neither desorptive used in this study completely removes As(V) from the δ-MnO(2) surface.

  13. Cultivable diversity of thermophilic arsenite/ferrous-oxidizing microorganisms in hot springs of Taiwan

    Science.gov (United States)

    Lu, G.; Lin, Y.; Chang, Y.; Wang, P.; Lin, L.

    2009-12-01

    Elevated levels of arsenic in groundwater and surface water bodies have posed a stringent threat to the deterioration of the water quality for drinking and agriculture purposes around the world. In particular, arsenic liberated from volcanic and sedimentary rocks at high temperatures would be immobilized through adsorption on iron oxide and/or crystallization of iron-bearing minerals downstream at low temperatures. Understanding how microbially-catalytic reactions are involved in the changes of the redox state of arsenic and iron along a flow path would provide important constraints on the arsenic mobility in natural occurrences. The aims of this study were to isolate and characterize thermophilic arsenite- and iron-oxidizing microbes that would facilitate to establish the linkages between microbial distribution and in situ Fe/As cycling processes. Four source waters (LH05, LH08, SYK and MT) from acid-sulfate springs (pH 2-3, 60-97oC) located in the Tatun volcanic area of northern Taiwan were collected and inoculated into media targeting on autotrophic ferrous iron (FC3), arsenite (AC3 ,ACC3, AC7, ACC7), arsenite-resistant hydrogen (AH23), arsenite-resistant hydrogen-sulfur (AH2S3), and arsenite-resistant sulfur oxidations(AS3), and heterotrophic arsenite oxidation(AH3, AH7) at pH 3, and 7 at temperatures of 50, 70 and 80oC. Samples from the Kuantzuling mud springs (KTL) in southwestern Taiwan known with elevated arsenic levels (0.4 ppm) were also collected, inoculated into the heterotrophic medium and incubated at 50, 60, 70 and 80oC. Isolates obtained from KTL were subject to test on the AH7 and ACC7. Two positive enrichments for iron oxidation at 50oC and 70oC were confirmed by the steadily decrease of ferrous iron and increase of precipitates over 4 transfers for samples from the SYK spring. Diverse morphological types of microbes were enriched in all types of arsenite-bearing media at 50oC except for AH23. At 70oC, positive enrichments were found in media

  14. The fate of arsenic adsorbed on iron oxides in the presence of arsenite-oxidizing bacteria.

    Science.gov (United States)

    Zhang, Zhennan; Yin, Naiyi; Du, Huili; Cai, Xiaolin; Cui, Yanshan

    2016-05-01

    Arsenic (As) is a redox-active metalloid whose toxicity and mobility in soil depend on its oxidation state. Arsenite [As(III)] can be oxidized by microbes and adsorbed by minerals in the soil. However, the combined effects of these abiotic and biotic processes are not well understood. In this study, the fate of arsenic in the presence of an isolated As(III)-oxidizing bacterium (Pseudomonas sp. HN-1, 10(9) colony-forming units (CFUs)·ml(-1)) and three iron oxides (goethite, hematite, and magnetite at 1.6 g L(-1)) was determined using batch experiments. The total As adsorption by iron oxides was lower with bacteria present and was higher with iron oxides alone. The total As adsorption decreased by 78.6%, 36.0% and 79.7% for goethite, hematite and magnetite, respectively, due to the presence of bacteria. As(III) adsorbed on iron oxides could also be oxidized by Pseudomonas sp. HN-1, but the oxidation rate (1.3 μmol h(-1)) was much slower than the rate in the aqueous phase (96.2 μmol h(-1)). Therefore, the results of other studies with minerals only might overestimate the adsorptive capacity of solids in natural systems; the presence of minerals might hinder As(III) oxidation by microbes. Under aerobic conditions, in the presence of iron oxides and As(III)-oxidizing bacteria, arsenic is adsorbed onto iron oxides within the adsorption capacity, and As(V) is the primary form in the solid and aqueous phases. Copyright © 2016 Elsevier Ltd. All rights reserved.

  15. An Oxidoreductase AioE is Responsible for Bacterial Arsenite Oxidation and Resistance

    Science.gov (United States)

    Wang, Qian; Han, Yushan; Shi, Kaixiang; Fan, Xia; Wang, Lu; Li, Mingshun; Wang, Gejiao

    2017-01-01

    Previously, we found that arsenite (AsIII) oxidation could improve the generation of ATP/NADH to support the growth of Agrobacterium tumefaciens GW4. In this study, we found that aioE is induced by AsIII and located in the arsenic island near the AsIII oxidase genes aioBA and co-transcripted with the arsenic resistant genes arsR1-arsC1-arsC2-acr3-1. AioE belongs to TrkA family corresponding the electron transport function with the generation of NADH and H+. An aioE in-frame deletion strain showed a null AsIII oxidation and a reduced AsIII resistance, while a cytC mutant only reduced AsIII oxidation efficiency. With AsIII, aioE was directly related to the increase of NADH, while cytC was essential for ATP generation. In addition, cyclic voltammetry analysis showed that the redox potential (ORP) of AioBA and AioE were +0.297 mV vs. NHE and +0.255 mV vs. NHE, respectively. The ORP gradient is AioBA > AioE > CytC (+0.217 ~ +0.251 mV vs. NHE), which infers that electron may transfer from AioBA to CytC via AioE. The results indicate that AioE may act as a novel AsIII oxidation electron transporter associated with NADH generation. Since AsIII oxidation contributes AsIII detoxification, the essential of AioE for AsIII resistance is also reasonable. PMID:28128323

  16. Deficiency of long isoforms of Nfe2l1 sensitizes MIN6 pancreatic β cells to arsenite-induced cytotoxicity.

    Science.gov (United States)

    Cui, Qi; Fu, Jingqi; Hu, Yuxin; Li, Yongfang; Yang, Bei; Li, Lu; Sun, Jing; Chen, Chengjie; Sun, Guifan; Xu, Yuanyuan; Zhang, Qiang; Pi, Jingbo

    2017-08-15

    Increasing evidence indicates that chronic inorganic arsenic exposure is associated with type 2 diabetes (T2D), a disease of growing prevalence. Pancreatic β-cells were targeted and damaged by oxidative stress induced by arsenite. We previously showed that nuclear factor erythroid 2 like 2 (Nfe2l2)-deficient pancreatic β-cells were vulnerable to cell damage induced by oxidative stressors including arsenite, due to a muted antioxidant response. Like nuclear factor erythroid 2 like 2 (NFE2L2), NFE2L1 also belongs to the cap 'n' collar (CNC) basic-region leucine zipper (bZIP) transcription factor family, and regulates antioxidant response element (ARE) related genes. Our prior work showed NFE2L1 regulates glucose-stimulated insulin secretion (GSIS) in pancreatic β-cells and isolated islets. In the current study, we demonstrated that MIN6 cells with a specific knockdown of long isoforms of Nfe2l1 (L-Nfe2l1) by lentiviral shRNA (Nfe2l1(L)-KD) were vulnerable to arsenite-induced apoptosis and cell damage. The expression levels of antioxidant genes, such as Gclc, Gclm and Ho-1, and intracellular reactive oxygen species (ROS) levels were not different in Scramble and Nfe2l1(L)-KD cells, while the expression of arsenic metabolism related-genes, such as Gsto1, Gstm1 and Nqo1, increased in Nfe2l1(L)-KD cells with or without arsenite treatment. The up-regulation of arsenic biotransformation genes was due to activated NFE2L2 in Nfe2l1(L)-KD MIN6 cells. Furthermore, the level of intracellular monomethylarsenic (MMA) was higher in Nfe2l1(L)-KD MIN6 cells than in Scramble cells. These results showed that deficiency of L-Nfe2l1 in pancreatic β-cells increased susceptibility to acute arsenite-induced cytotoxicity by promoting arsenic biotransformation and intracellular MMA levels. Copyright © 2017. Published by Elsevier Inc.

  17. Arsenite-oxidizing and arsenate-reducing bacteria associated with arsenic-rich groundwater in Taiwan

    Science.gov (United States)

    Liao, Vivian Hsiu-Chuan; Chu, Yu-Ju; Su, Yu-Chen; Hsiao, Sung-Yun; Wei, Chia-Cheng; Liu, Chen-Wuing; Liao, Chung-Min; Shen, Wei-Chiang; Chang, Fi-John

    2011-04-01

    Drinking highly arsenic-contaminated groundwater is a likely cause of blackfoot disease in Taiwan, but microorganisms that potentially control arsenic mobility in the subsurface remain unstudied. The objective of this study was to investigate the relevant arsenite-oxidizing and arsenate-reducing microbial community that exists in highly arsenic-contaminated groundwater in Taiwan. We cultured and identified arsenic-transforming bacteria, analyzed arsenic resistance and transformation, and determined the presence of genetic markers for arsenic transformation. In total, 11 arsenic-transforming bacterial strains with different colony morphologies and varying arsenic transformation abilities were isolated, including 10 facultative anaerobic arsenate-reducing bacteria and one strictly aerobic arsenite-oxidizing bacterium. All of the isolates exhibited high levels of arsenic resistance with minimum inhibitory concentrations of arsenic ranging from 2 to 200 mM. Strain AR-11 was able to rapidly oxidize arsenite to arsenate at concentrations relevant to environmental groundwater samples without the addition of any electron donors or acceptors. We provide evidence that arsenic-reduction activity may be conferred by the ars operon(s) that were not amplified by the designed primers currently in use. The 16S rRNA sequence analysis grouped the isolates into the following genera: Pseudomonas, Bacillus, Psychrobacter, Vibrio, Citrobacter, Enterobacter, and Bosea. Among these genera, we present the first report of the genus Psychrobacter being involved in arsenic reduction. Our results further support the hypothesis that bacteria capable of either oxidizing arsenite or reducing arsenate coexist and are ubiquitous in arsenic-contaminated groundwater.

  18. Diversity of arsenite oxidizing bacterial communities in arsenic-rich deltaic aquifers in West Bengal, India

    Directory of Open Access Journals (Sweden)

    Devanita eGhosh

    2014-11-01

    Full Text Available High arsenic (As concentration in groundwater has affected human health, particularly in South-East Asia putting millions of people at risk. Biogeochemical cycling of As carried out by different bacterial groups are suggested to control the As fluxes in aquifers. A functional diversity approach in link with As precipitation was adopted to study bacterial community structures and their variation within the As contaminated Bengal Delta Plain (BDP aquifers of India. Groundwater samples collected from two shallow aquifers in Karimpur II (West Bengal, India, during years 2010 and 2011, were investigated to trace the effects of inter-annual variability in precipitation on community structure and diversity of bacterial assemblages. The study focused on amplification, clone library generation and sequencing of the arsenite oxidase large sub-unit gene aioA and 16S rRNA marker, with respect to changes in elemental concentrations. New set of primers were designed to amplify the aioA gene as a phylogenetic marker to study taxonomically diverse arsenite oxidizing bacterial groups in these aquifers. Overall narrow distribution of bacterial communities based on aioA and 16S rRNA sequences observed was due to poor nutrient status and anoxic conditions in these As contaminated aquifers. Proteobacteria was the dominant phylum detected, within which Acidovorax, Hydrogenophaga, Albidiferax, Bosea and Polymorphum were the major arsenite oxidizing bacterial genera. The structure of bacterial assemblages including those of arsenite oxidizing bacteria were affected by an increase in major elemental concentrations (e.g., As, iron, sulfur, and silica within two sampling sessions, which was supported by PCA analysis. One of the significant findings of this study is detection of novel lineages of 16S rRNA-like bacterial sequences indicating presence of indigenous bacterial communities across both wells of BDP that can play important role in biogeochemical cycling of

  19. Photocatalytic oxidation and removal of arsenite by titanium dioxide supported on granular activated carbon.

    Science.gov (United States)

    Yao, Shu Hua; Jia, Yong Feng; Zhao, Shan Lin

    2012-01-01

    Arsenic contamination in drinking water is a worldwide concern. Photocatalysis can rapidly oxidize arsenite, i.e. As(III), to less labile arsenate, i.e. As(V), which then can be removed by adsorption on to various adsorbents. This study investigated the photocatalytic oxidation of arsenite in aqueous solution by granular activated carbon supporting a titanium dioxide photocatalyst (GAC-TiO2). The effects of photocatalyst dosage, solution pH values, initial concentration of As(III) and co-anions (SO4(2-), PO4(3-), SiO3(2-) and Cl-) on the oxidation of As(III) were studied. The photocatalytic oxidation of As(III) took place in minutes and followed first-order kinetics. The presence of phosphate and silicate significantly decreased As(III) oxidation, while the effect of sulphate, chloride was insignificant. The oxidation efficiency of As(III) was observed to increase with increasing pH. The results suggest that the supported photocatalyst developed in this study is an ideal candidate for pre-oxidation treatment of arsenic-contaminated water.

  20. Fenton Redox Chemistry: Arsenite Oxidation by Metallic Surfaces

    NARCIS (Netherlands)

    Borges Freitas, S.C.; Van Halem, D.; Badruzzaman, A.B.M.; Van der Meer, W.G.J.

    2014-01-01

    Pre-oxidation of As(III) is necessary in arsenic removal processes in order to increase its efficiency. Therefore, the Fenton Redox Chemistry is defined by catalytic activation of H2O2 and currently common used for its redox oxidative properties. In this study the effect of H2O2 production catalysed

  1. From the Cover: Arsenite Uncouples Mitochondrial Respiration and Induces a Warburg-like Effect in Caenorhabditis elegans.

    Science.gov (United States)

    Luz, Anthony L; Godebo, Tewodros R; Bhatt, Dhaval P; Ilkayeva, Olga R; Maurer, Laura L; Hirschey, Matthew D; Meyer, Joel N

    2016-08-01

    Millions of people worldwide are chronically exposed to arsenic through contaminated drinking water. Despite decades of research studying the carcinogenic potential of arsenic, the mechanisms by which arsenic causes cancer and other diseases remain poorly understood. Mitochondria appear to be an important target of arsenic toxicity. The trivalent arsenical, arsenite, can induce mitochondrial reactive oxygen species production, inhibit enzymes involved in energy metabolism, and induce aerobic glycolysis in vitro, suggesting that metabolic dysfunction may be important in arsenic-induced disease. Here, using the model organism Caenorhabditis elegans and a novel metabolic inhibition assay, we report an in vivo induction of aerobic glycolysis following arsenite exposure. Furthermore, arsenite exposure induced severe mitochondrial dysfunction, including altered pyruvate metabolism; reduced steady-state ATP levels, ATP-linked respiration and spare respiratory capacity; and increased proton leak. We also found evidence that induction of autophagy is an important protective response to arsenite exposure. Because these results demonstrate that mitochondria are an important in vivo target of arsenite toxicity, we hypothesized that deficiencies in mitochondrial electron transport chain genes, which cause mitochondrial disease in humans, would sensitize nematodes to arsenite. In agreement with this, nematodes deficient in electron transport chain complexes I, II, and III, but not ATP synthase, were sensitive to arsenite exposure, thus identifying a novel class of gene-environment interactions that warrant further investigation in the human populace.

  2. Sodium arsenite induces chromosome endoreduplication and inhibits protein phosphatase activity in human fibroblasts

    Energy Technology Data Exchange (ETDEWEB)

    Rong-Nan Huang; I-Ching Ho; Ling-Hui Yih [Institute of Biomedical Sciences, Taiwan (China)] [and others

    1995-08-01

    Arsenic, strongly associated with increased risks of human cancers, is a potent clastogen in a variety of mammalian cell systems. The effect of sodium arsenite (a trivalent arsenic compound) on chromatid separation was studied in human skin fibroblasts (HFW). Human fibroblasts were arrested in S phase by the aid of serum starvation and aphidicolin blocking and then these cells were allowed to synchronously progress into G2 phase. Treatment of the G2-enriched HFW cells with sodium arsenite (0-200 {mu}M) resulted in arrest of cells in the G2 phase, interference with mitotic division, inhibition of spindle assembly, and induction of chromosome endoreduplication in their second mitosis. Sodium arsenite treatment also inhibited the activities of serine/threonine protein phosphatases and enhanced phosphorylation levels of a small heat shock protein (HSP27). These results suggest that sodium arsenite may mimic okadaic acid to induce chromosome endoreduplication through its inhibitory effect on protein phosphatase activity. 61 refs., 6 figs., 2 tabs.

  3. Linking microbial oxidation of arsenic with detection and phylogenetic analysis of arsenite oxidase genes in diverse geothermal environments.

    Science.gov (United States)

    Hamamura, N; Macur, R E; Korf, S; Ackerman, G; Taylor, W P; Kozubal, M; Reysenbach, A-L; Inskeep, W P

    2009-02-01

    The identification and characterization of genes involved in the microbial oxidation of arsenite will contribute to our understanding of factors controlling As cycling in natural systems. Towards this goal, we recently characterized the widespread occurrence of aerobic arsenite oxidase genes (aroA-like) from pure-culture bacterial isolates, soils, sediments and geothermal mats, but were unable to detect these genes in all geothermal systems where we have observed microbial arsenite oxidation. Consequently, the objectives of the current study were to measure arsenite-oxidation rates in geochemically diverse thermal habitats in Yellowstone National Park (YNP) ranging in pH from 2.6 to 8, and to identify corresponding 16S rRNA and aroA genotypes associated with these arsenite-oxidizing environments. Geochemical analyses, including measurement of arsenite-oxidation rates within geothermal outflow channels, were combined with 16S rRNA gene and aroA functional gene analysis using newly designed primers to capture previously undescribed aroA-like arsenite oxidase gene diversity. The majority of bacterial 16S rRNA gene sequences found in acidic (pH 2.6-3.6) Fe-oxyhydroxide microbial mats were closely related to Hydrogenobaculum spp. (members of the bacterial order Aquificales), while the predominant sequences from near-neutral (pH 6.2-8) springs were affiliated with other Aquificales including Sulfurihydrogenibium spp., Thermocrinis spp. and Hydrogenobacter spp., as well as members of the Deinococci, Thermodesulfobacteria and beta-Proteobacteria. Modified primers designed around previously characterized and newly identified aroA-like genes successfully amplified new lineages of aroA-like genes associated with members of the Aquificales across all geothermal systems examined. The expression of Aquificales aroA-like genes was also confirmed in situ, and the resultant cDNA sequences were consistent with aroA genotypes identified in the same environments. The aroA sequences

  4. Protective effect of Juglans nigra on sodium arsenite-induced toxicity in rats

    Directory of Open Access Journals (Sweden)

    Solomon E Owumi

    2013-01-01

    Full Text Available Background: Consumption of arsenic contaminated water has been implicated in metalloid-induced carcinogenesis. Dietary intake of certain plant products with chemoprotective properties may protect against the onset of diseases and promote maintenance of health. Objectives: We investigated the outcome of black walnut Juglans nigra (JN consumption on sodium arsenite (SA-induced toxicity in rats. Materials and Methods: Wister albino rats were treated as follows: Control, SA only (positive control (2.5 mg/kg body weight, JN only (100 mg/kg weight, and JN+SA coadministered. After 5 weeks animals were sacrificed whole blood, femur, liver and testis harvested were assessed for hepatic transaminases and clastogenicity. Histology of the liver, sperm morphology and quality were also assessed. Data were analyzed (ANOVA and expressed as means ±SD. Results: SA treatment elevated hepatic transaminases level in serum (P < 0.05, induced histological changes in liver: fibroplasia and periportal hepatocytes infiltration by mononuclear cells. These changes were ameliorated by JN (P < 0.05 coadministration. SA induced micronuclei formation (P < 0.05. Again JN decreased (P < 0.05 micronuclei formation by 50%. Sperm count and motility decreased (P < 0.05 in all groups compared to control. Conclusion: JN showed no protection against arsenite effect on sperm quality. Hepatoprotective and anticlastogenic effects were apparent suggesting a chemopreventive potential active against arsenite genotoxicity and chromosomal instability which have implication for metalloid-induced carcinogenesis.

  5. The oxidative and adsorptive effectiveness of hydrous manganese dioxide for arsenite removal

    Institute of Scientific and Technical Information of China (English)

    Liu Ruiping; Yuan Baoling; Li Xing; Xia Shengji; Yang Yanling; Li Guibai

    2006-01-01

    This study focuses on the effectiveness of hydrous manganese dioxides (δMnO2) removing arsenite (As(Ⅲ)) from aqueous solution. Effects of such factors as permanganate oxidation, pH, humic acid and Ca2+ on As removal and possible mechanisms involved in have been investigated. Permanganate oxidation increases As removal to a certain extent; the higher pH results in the formation of more easily adsorbed As species, contributing to higher As removal; humic acid occupies adsorbing sites and decreases ζ potential of δMnO2, therefore inhibiting As removal; Ca2+ facilitates As adsorption on δMnO2, mainly through increasing ζ potential and decreasing repulsive forces between As and surface sites. δMnO2 exhibits oxidative and adsorptive potential for As(Ⅲ), and may be employed as adsorbents or filter coating for As removal in water treatment process.

  6. Sodium arsenite induced biochemical perturbations in rats: ameliorating effect of curcumin.

    Science.gov (United States)

    Yousef, Mokhtar I; El-Demerdash, Fatma M; Radwan, Fatma M E

    2008-11-01

    The present study was undertaken to evaluate the therapeutic efficacy of curcumin in terms of normalization of altered biochemical parameters following sodium arsenite treatment in rats. Animals were divided into four groups. The first group was used as control. While, groups 2, 3 and 4 were orally treated with curcumin (Cur, 15 mg/kg BW), sodium arsenite (Sa, 5 mg/kg BW) and sodium arsenite plus curcumin, respectively. Results showed that the activities of transaminases and phosphatases were significantly decreased in liver due to Sa administration, whereas increased in plasma. The activity of brain and plasma acetylcholinesterase (AChE) was decreased in rats treated with Sa. Also, Sa significantly decreased plasma total protein (TP), albumin (Alb) and high density lipoprotein-cholesterol (HDL-c), while increased glucose, urea, creatinine, bilirubin, total lipid (TL), cholesterol, triglyceride (TG) and low density lipoprotein-cholesterol (LDL-c). Curcumin alone decreased the levels of glucose, urea, creatinine, TL, cholesterol, TG and LDL-c. Curcumin reduced Sa-induced transaminases, phosphatases, glucose, urea, creatinine, bilirubin, TL, cholesterol and TG. Moreover, curcumin induced Sa-reduced liver transaminases and phosphatases, plasma and brain AChE, and the levels of TP and Alb. Experimental results, therefore suggested that curcumin protects arsenic induced biochemical alterations in rats.

  7. Removal of arsenite and arsenate using hydrous ferric oxide incorporated into naturally occurring porous diatomite.

    Science.gov (United States)

    Jang, Min; Min, Soo-Hong; Kim, Tak-Hyun; Park, Jae Kwang

    2006-03-01

    In this study, a simplified and effective method was tried to immobilize iron oxide onto a naturally occurring porous diatomite. Experimental resultsfor several physicochemical properties and arsenic edges revealed that iron oxide incorporated into diatomite was amorphous hydrous ferric oxide (HFO). Sorption trends of Fe (25%)-diatomite for both arsenite and arsenate were similar to those of HFO, reported by Dixit and Hering (Environ. Sci. Technol. 2003, 37, 4182-4189). The pH at which arsenite and arsenate are equally sorbed was 7.5, which corresponds to the value reported for HFO. Judging from the number of moles of iron incorporated into diatomite, the arsenic sorption capacities of Fe (25%)-diatomite were comparable to or higher than those of the reference HFO. Furthermore, the surface complexation modeling showed that the constants of [triple bond]SHAsO4- or [triple bond]SAsO4(2-) species for Fe (25%)-diatomite were larger than those reference values for HFO or goethite. Larger differences in constants of arsenate surface species might be attributed to aluminum hydroxyl ([triple bond]Al-OH) groups that can work better for arsenate removal. The pH-controlled differential column batch reactor (DCBR) and small-scale column tests demonstrated that Fe (25%)-diatomite had high sorption speeds and high sorption capacities compared to those of a conventional sorbent (AAFS-50) that is known to be the first preference for arsenic removal performance in Bangladesh. These results could be explained by the fact that Fe (25%)-diatomite contained well-dispersed HFO having a great affinity for arsenic species and well-developed macropores as shown by scanning electron microscopy (SEM) and pore size distribution (PSD) analyses.

  8. Fe/Ti co-pillared clay for enhanced arsenite removal and photo oxidation under UV irradiation

    Energy Technology Data Exchange (ETDEWEB)

    Li, Yuan [School of Chemical Engineering and Technology, Tianjin University, Tianjin 300072 (China); Guang Dong Electric Power Design Institute, China Energy Engineering Group Co. Ltd., Guangzhou 510663 (China); Cai, Xiaojiao [School of Chemical Engineering and Technology, Tianjin University, Tianjin 300072 (China); Guo, Jingwei [School of Chemical Engineering and Technology, Tianjin University, Tianjin 300072 (China); The 718th Research Institute of CSIC, Handan 056027 (China); Zhou, Shimin [School of Chemical Engineering and Technology, Tianjin University, Tianjin 300072 (China); Na, Ping, E-mail: naping@tju.edu.cn [School of Chemical Engineering and Technology, Tianjin University, Tianjin 300072 (China)

    2015-01-01

    Graphical abstract: - Highlights: • An iron and titanium co-pillared montmorillonite (Fe-Ti/MMT) was synthesized for arsenite removal. • Variety of characterization results indicated that Fe and Ti species were pillared in MMT. • A possible mechanism of arsenite adsorption/oxidation with UV light was established. • The participation of Fe component can promote the process of photocatalytic oxidation in Fe-Ti/MMT + As(III) system. • Fe-Ti/MMT can function as both photocatalyst and adsorbent for arsenite removal. - Abstract: A series of iron and titanium co-pillared montmorillonites (Fe-Ti/MMT) were prepared using hydrolysis of inserted titanium and different iron content in montmorillonite (MMT). The Fe-Ti/MMT were characterized by X-ray fluorescence, N{sub 2} adsorption and desorption, X-ray diffraction, scanning electron microscopy (SEM) and transmission electron microscopy (TEM), confirming the effective insertion of Fe species and TiO{sub 2} in the MMT. The Fe-Ti/MMT was used to remove arsenite (As(III)) from aqueous solutions under different conditions. The result of As(III) adsorption under UV irradiation showed that the photo activity can be enhanced by incorporating Fe and Ti in MMT. Fourier-transform infrared spectroscopy (FTIR) and X-ray photoelectron spectroscopy (XPS) analysis indicated that the hydroxyl groups bonded to metal oxide (M–OH) played an important role in the adsorption of As(III)

  9. Bacterial community succession during the enrichment of chemolithoautotrophic arsenite oxidizing bacteria at high arsenic concentrations

    Institute of Scientific and Technical Information of China (English)

    Nguyen Ai Le; Akiko Sato; Daisuke Inoue; Kazunari Sei; Satoshi Soda; Michihiko Ike

    2012-01-01

    To generate cost-effective technologies for the removal of arsenic from water,we developed an enrichment culture of chemolithoautotrophic arsenite oxidizing bacteria (CAOs) that could effectively oxidize widely ranging concentrations of As(Ⅲ) to As(Ⅴ).In addition,we attempted to elucidate the enrichment process and characterize the microbial composition of the enrichment culture.A CAOs enrichment culture capable of stably oxidizing As(Ⅲ) to As(Ⅴ) was successfully constructed through repeated batch cultivation for more than 700 days,during which time the initial As(Ⅲ) concentrations were increased in a stepwise manner from l to 10-12 mmol/L.As(Ⅲ) oxidation activity of the enrichment culture gradually improved,and 10-12 mmol/L As(Ⅲ) was almost completely oxidized within four days.Terminal restriction fragment length polymorphism analysis showed that the dominant bacteria in the enrichment culture varied drastically during the enrichment process depending on the As(Ⅲ) concentration.Isolation and characterization of bacteria in the enrichment culture revealed that the presence of multiple CAOs with various As(Ⅲ) oxidation abilities enabled the culture to adapt to a wide range of As(Ⅲ) concentrations.The CAOs enrichment culture constructed here may he useful for pretreatment of water from which arsenic is being removed.

  10. Flexible biological arsenite oxidation utilizing NOx and O2 as alternative electron acceptors.

    Science.gov (United States)

    Wang, Jie; Wan, Junfeng; Wu, Zihao; Li, Hongli; Li, Haisong; Dagot, Christophe; Wang, Yan

    2017-07-01

    The feasibility of flexible microbial arsenite (As(III)) oxidation coupled with the reduction of different electron acceptors was investigated. The results indicated the acclimated microorganisms could oxidize As(III) with oxygen, nitrate and nitrite as the alternative electron acceptors. A series of batch tests were conducted to measure the kinetic parameters of As(III) oxidation and to evaluate the effects of environmental conditions including pH and temperature on the activity of biological As(III) oxidation dependent on different electron acceptors. Kinetic results showed that oxygen-dependent As(III) oxidation had the highest oxidation rate (0.59 mg As g(-1) VSS min(-1)), followed by nitrate- (0.40 mg As g(-1) VSS min(-1)) and nitrite-dependent As(III) oxidation (0.32 mg As g(-1) VSS min(-1)). The kinetic data of aerobic As(III) oxidation were fitted well with the Monod kinetic model, while the Haldane substrate inhibition model was better applicable to describe the inhibition of anoxic As(III) oxidation. Both aerobic and anoxic As(III) oxidation performed the optimal activity at the near neutral pH. Besides, the optimal temperature for oxygen-, nitrate- and nitrite-dependent As(III) oxidation was 30 ± 1 °C, 40 ± 1 °C and 20 ± 1 °C, respectively. Copyright © 2017 Elsevier Ltd. All rights reserved.

  11. Arsenite Effects on Mitochondrial Bioenergetics in Human and Mouse Primary Hepatocytes Follow a Nonlinear Dose Response

    Directory of Open Access Journals (Sweden)

    Hemantkumar Chavan

    2017-01-01

    Full Text Available Arsenite is a known carcinogen and its exposure has been implicated in a variety of noncarcinogenic health concerns. Increased oxidative stress is thought to be the primary cause of arsenite toxicity and the toxic effect is thought to be linear with detrimental effects reported at all concentrations of arsenite. But the paradigm of linear dose response in arsenite toxicity is shifting. In the present study we demonstrate that arsenite effects on mitochondrial respiration in primary hepatocytes follow a nonlinear dose response. In vitro exposure of primary hepatocytes to an environmentally relevant, moderate level of arsenite results in increased oxidant production that appears to arise from changes in the expression and activity of respiratory Complex I of the mitochondrial proton circuit. In primary hepatocytes the excess oxidant production appears to elicit adaptive responses that promote resistance to oxidative stress and a propensity to increased proliferation. Taken together, these results suggest a nonlinear dose-response characteristic of arsenite with low-dose arsenite promoting adaptive responses in a process known as mitohormesis, with transient increase in ROS levels acting as transducers of arsenite-induced mitohormesis.

  12. Flexible bacterial strains that oxidize arsenite in anoxic or aerobic conditions and utilize hydrogen or acetate as alternative electron donors

    OpenAIRE

    Rodríguez-Freire, Lucía; Sun, Wenjie; Sierra-Alvarez, Reyes; Field, Jim A.

    2011-01-01

    Arsenic is a carcinogenic compound widely distributed in the groundwater around the world. The fate of arsenic in groundwater depends on the activity of microorganisms either by oxidizing arsenite (AsIII), or by reducing arsenate (AsV). Because of the higher toxicity and mobility of AsIII compared to AsV, microbial-catalyzed oxidation of AsIII to AsV can lower the environmental impact of arsenic. Although aerobic AsIII-oxidizing bacteria are well known, anoxic oxidation of AsIII with nitrate ...

  13. The accumulations of HIF-1α and HIF-2α by JNK and ERK are involved in biphasic effects induced by different levels of arsenite in human bronchial epithelial cells

    Energy Technology Data Exchange (ETDEWEB)

    Xu, Yuan; Li, Yuan [Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu (China); The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu (China); Li, Huiqiao [Qujing Center for Disease Control and Prevention, Qujing 655000, Yunnan (China); Pang, Ying; Zhao, Yue; Jiang, Rongrong; Shen, Lu [Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu (China); The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu (China); Zhou, Jianwei; Wang, Xinru [The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu (China); Liu, Qizhan, E-mail: drqzliu@hotmail.com [Institute of Toxicology, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu (China); The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University, Nanjing 210029, Jiangsu (China)

    2013-01-15

    The biphasic effects of arsenite, in which low levels of arsenite induce cell proliferation and high levels of arsenite induce DNA damage and apoptosis, apparently contribute to arsenite-induced carcinogenesis. However, the mechanisms underlying this phenomenon are not well understood. In this study, we investigated the effects of different levels of arsenite on cell proliferation, DNA damage and apoptosis as well as on signal transduction pathways in human bronchial epithelial (HBE) cells. Our results show that a low level of arsenite activates extracellular signal-regulated kinases (ERK), which probably mediate arsenite-inhibited degradation of ubiquitinated hypoxia-inducible factor-2α (HIF-2α) in HBE cells. ERK inhibition blocks cell proliferation induced by a low level of arsenite, in part via HIF-2α. In contrast, a high level of arsenite activates c-Jun N-terminal kinases (JNK), which provoke a response to suppress ubiquitinated HIF-1α degradation. Down-regulation of HIF-1α by inhibiting JNK, however, increases the DNA damage but decreases the apoptosis induced by a high level of arsenite. Thus, data in the present study suggest that the accumulations of HIF-1α and HIF-2α by JNK and ERK are involved in different levels of arsenite-induced biphasic effects, with low levels of arsenite inducing cell proliferation and high levels of arsenite inducing DNA damage and apoptosis in HBE cells. -- Highlights: ► Biphasic effects induced by different concentrations of arsenite. ► Different regulation of ERK or JNK signal pathway by arsenite. ► Different regulation of HIF1α or HIF 2α by arsenite.

  14. Acute Sodium Arsenite-Induced Hematological and Biochemical Changes in Wistar Rats: Protective Effects of Ethanol Extract of Ageratum conyzoides

    Science.gov (United States)

    Ola-Davies, Olufunke Eunice; Akinrinde, Akinleye Stephen

    2016-01-01

    Background: Ageratum conyzoides L. (Asteraceae) is an annual herbaceous plant used in folklore medicine for the treatment of a wide range of diseases. Objective: To investigate the protective effect of the ethanol leaf extract of A. conyzoides (EEAC) against hematological, serum biochemical and histological alterations induced by Sodium arsenite administration to Wistar rats. Materials and Methods: Twenty male Wistar rats were randomly assigned into four groups of five rats each. Group I received propylene glycol and Group II rats were given the (EEAC, 100 mg/kg b.w.) orally for 7 days. Group III were given a single oral dose of sodium arsenite (NaAsO2, 2.5 mg/kg b.w.). Animals in Group IV were pretreated with 100 mg/kg EEAC for 7 days followed by a single oral dose of sodium arsenite. Results: Arsenic exposure resulted in significant reductions (P produced significant reversal of the reduction in the erythrocytic indices (packed cell volume, red blood cell, and Hb) caused by sodium arseniteSodium arsenite-induced slight elevations in serum aspartate aminotransferase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP), correlating with the histopathological lesions observedAgeratum conyzoides produced only slight reductions in AST, ALT, and ALP compared to the sodium arsenite group, but significantly reduced the severity of histopathological lesions. Abbreviations Used: EEAC: Ethanol extract of Ageratum conyzoides; RBC: Red blood cell; WBC: White blood cell; Hb: Hemoglobin; ALT: Alanine transaminase; AST: Aspartate transaminase or Aspartate aminotransferase; ALP: Alkaline phosphatase; GGT: Gamma glutamyl transferase. PMID:27114688

  15. Sodium arsenite reduces severity of dextran sulfate sodium-induced ulcerative colitis in rats

    Institute of Scientific and Technical Information of China (English)

    Joshua J. MALAGO; Hortensia NONDOLI

    2008-01-01

    The histopathological features and the associated clinical findings of ulcerative colitis (UC) are due to persistent inflammatory response in the colon mucosa. Interventions that suppress this response benefit UC patients. We tested whether sodium arsenite (SA) benefits rats with dextran sulfate sodium (DSS)-colitis. The DSS-colitis was induced by 5% DSS in drinking water. SA (10 mg/kg; intraperitoneally) was given 8 h before DSS treatment and then every 48 h for 3 cycles of 7,14 or 21 d. At the end of each cycle rats were sacrificed and colon sections processed for histological examination. DSS induced diarrhea, loose stools, hemoccult positive stools, gross bleeding, loss of body weight, loss of epithelium, crypt damage, depletion of goblet cells and infiltration of inflammatory cells. The severity of these changes increased ir the order of Cycles 1,2 and 3. Treatment of rats with SA significantly reduced this severity and improved the weight gain.

  16. Stress-induced Start Codon Fidelity Regulates Arsenite-inducible Regulatory Particle-associated Protein (AIRAP) Translation*

    Science.gov (United States)

    Zach, Lolita; Braunstein, Ilana; Stanhill, Ariel

    2014-01-01

    Initial steps in protein synthesis are highly regulated processes as they define the reading frame of the translation machinery. Eukaryotic translation initiation is a process facilitated by numerous factors (eIFs), aimed to form a “scanning” mechanism toward the initiation codon. Translation initiation of the main open reading frame (ORF) in an mRNA transcript has been reported to be regulated by upstream open reading frames (uORFs) in a manner of re-initiation. This mode of regulation is governed by the phosphorylation status of eIF2α and controlled by cellular stresses. Another mode of translational initiation regulation is leaky scanning, and this regulatory process has not been extensively studied. We have identified arsenite-inducible regulatory particle-associated protein (AIRAP) transcript to be translationally induced during arsenite stress conditions. AIRAP transcript contains a single uORF in a poor-kozak context. AIRAP translation induction is governed by means of leaky scanning and not re-initiation. This induction of AIRAP is solely dependent on eIF1 and the uORF kozak context. We show that eIF1 is phosphorylated under specific conditions that induce protein misfolding and have biochemically characterized this site of phosphorylation. Our data indicate that leaky scanning like re-initiation is responsive to stress conditions and that leaky scanning can induce ORF translation by bypassing poor kozak context of a single uORF transcript. PMID:24898249

  17. Arsenite binding-induced zinc loss from PARP-1 is equivalent to zinc deficiency in reducing PARP-1 activity, leading to inhibition of DNA repair

    Energy Technology Data Exchange (ETDEWEB)

    Sun, Xi; Zhou, Xixi [Department of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico Health Sciences Center, Albuquerque, NM 87131 (United States); Du, Libo [Center for Molecular Science, Institute of Chemistry, Chinese Academy of Sciences, Beijing 100190 (China); Liu, Wenlan [Department of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico Health Sciences Center, Albuquerque, NM 87131 (United States); Liu, Yang [Center for Molecular Science, Institute of Chemistry, Chinese Academy of Sciences, Beijing 100190 (China); Hudson, Laurie G. [Department of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico Health Sciences Center, Albuquerque, NM 87131 (United States); Liu, Ke Jian, E-mail: kliu@salud.unm.edu [Department of Pharmaceutical Sciences, College of Pharmacy, University of New Mexico Health Sciences Center, Albuquerque, NM 87131 (United States)

    2014-01-15

    Inhibition of DNA repair is a recognized mechanism for arsenic enhancement of ultraviolet radiation-induced DNA damage and carcinogenesis. Poly(ADP-ribose) polymerase-1 (PARP-1), a zinc finger DNA repair protein, has been identified as a sensitive molecular target for arsenic. The zinc finger domains of PARP-1 protein function as a critical structure in DNA recognition and binding. Since cellular poly(ADP-ribosyl)ation capacity has been positively correlated with zinc status in cells, we hypothesize that arsenite binding-induced zinc loss from PARP-1 is equivalent to zinc deficiency in reducing PARP-1 activity, leading to inhibition of DNA repair. To test this hypothesis, we compared the effects of arsenite exposure with zinc deficiency, created by using the membrane-permeable zinc chelator TPEN, on 8-OHdG formation, PARP-1 activity and zinc binding to PARP-1 in HaCat cells. Our results show that arsenite exposure and zinc deficiency had similar effects on PARP-1 protein, whereas supplemental zinc reversed these effects. To investigate the molecular mechanism of zinc loss induced by arsenite, ICP-AES, near UV spectroscopy, fluorescence, and circular dichroism spectroscopy were utilized to examine arsenite binding and occupation of a peptide representing the first zinc finger of PARP-1. We found that arsenite binding as well as zinc loss altered the conformation of zinc finger structure which functionally leads to PARP-1 inhibition. These findings suggest that arsenite binding to PARP-1 protein created similar adverse biological effects as zinc deficiency, which establishes the molecular mechanism for zinc supplementation as a potentially effective treatment to reverse the detrimental outcomes of arsenic exposure. - Highlights: • Arsenite binding is equivalent to zinc deficiency in reducing PARP-1 function. • Zinc reverses arsenic inhibition of PARP-1 activity and enhancement of DNA damage. • Arsenite binding and zinc loss alter the conformation of zinc finger

  18. ATM/ATR-related checkpoint signals mediate arsenite-induced G{sub 2}/M arrest in primary aortic endothelial cells

    Energy Technology Data Exchange (ETDEWEB)

    Tsou, Tsui-Chun; Tsai, Feng-Yuan; Yeh, Szu-Ching; Chang, Louis W. [National Health Research Institutes, Division of Environmental Health and Occupational Medicine, Miaoli County (Taiwan)

    2006-12-15

    Epidemiological studies have demonstrated a high association of inorganic arsenic exposure with vascular disease. Our recent in vitro studies have linked this vascular damage to vascular endothelial dysfunction induced by arsenic exposure. However, cell-cycle arrest induced by arsenic and its involvement in vascular dysfunction remain to be clarified. In this study, we employed primary porcine aortic endothelial cells to investigate regulatory mechanisms of G{sub 2}/M phase arrest induced by arsenite. Our study revealed that lower concentrations of arsenite (1 and 3 {mu}M) increased cell proliferation, whereas higher concentrations of arsenite (10, 20, and 30 {mu}M) inhibited cell proliferation together with correlated increases in G{sub 2}/M phase arrest. We found that this arsenite-induced G{sub 2}/M phase arrest was accompanied by accumulation and/or phosphorylation of checkpoint-related molecules, including p53, Cdc25B, Cdc25C, and securin. Inhibition of activations of these checkpoint-related molecules by caffeine significantly attenuated the 30-{mu}M arsenite-induced G{sub 2}/M phase arrest by 93%. Our data suggest that the DNA damage responsive kinases ATM (ataxia-telangiectasia mutated) and ATR (ATM and Rad3-related) play critical roles in arsenite-induced G{sub 2}/M phase arrest in aortic endothelial cells possibly via regulation of checkpoint-related signaling molecules including p53, Cdc25B, Cdc25C, and securin. (orig.)

  19. Efficient removal of trace arsenite through oxidation and adsorption by magnetic nanoparticles modified with Fe-Mn binary oxide.

    Science.gov (United States)

    Shan, Chao; Tong, Meiping

    2013-06-15

    Magnetic nanoparticles (MNPs) modified simultaneously with amorphous Fe and Mn oxides (Mag-Fe-Mn) were synthesized to remove arsenite [As(III)] from water. Mag-Fe-Mn particles were fabricated through heterogeneous nucleation technique by employing the maghemite as the magnetic core and Fe-Mn binary oxide (FMBO) as the coating materials. Powder X-ray diffraction, X-ray photoelectron spectroscopy (XPS), Raman spectroscopy, and transmission electron microscopy were utilized to characterize the hybrid material. With a saturation magnetization of 23.2 emu/g, Mag-Fe-Mn particles with size of 20-50 nm could be easily separated from solutions with a simple magnetic process in short time (within 5 min). At pH 7.0, 200 μg/L of As(III) could be easily decreased to below 10 μg/L by Mag-Fe-Mn particles (0.1 g/L) within 20 min. As(III) could be effectively removed by Mag-Fe-Mn particles at initial pH range from 4 to 8 and the residual As was completely oxidized to less toxic arsenate [As(V)]. The co-occurring redox reactions between Mn oxide and As(III) was confirmed by XPS analysis. Chloride, sulfate, bicarbonate, and nitrate at common concentration range had negligible influence on As(III) removal, whereas, silicate and phosphate reduced the As(III) removal by competing with arsenic species for adsorption sites. As(III) removal was not obviously affected by natural organic matter (up to 8 mg/L as TOC). Mag-Fe-Mn could be regenerated with ternary solution of NaOH, NaCl, and NaClO. Throughout five consecutive cycles, the adsorption and desorption efficiencies maintained above 98% and 87%, respectively. Mag-Fe-Mn had a larger adsorption capacity for As(III) (47.76 mg/g) and could remove trace As(III) more thoroughly than MNPs modified solely with either Fe or Mn oxide due to the synergistic effect of the coating Fe and Mn oxides. This research extended the potential applicability of FMBO to a great extent and provided a convenient approach to efficiently remove trace As

  20. Fe-Mn binary oxide incorporated into diatomite as an adsorbent for arsenite removal: preparation and evaluation.

    Science.gov (United States)

    Chang, Fangfang; Qu, Jiuhui; Liu, Huijuan; Liu, Ruiping; Zhao, Xu

    2009-10-15

    Fe-Mn binary oxide incorporated into diatomite (FMBO-diatomite) was prepared by a simple coating method, and exhibited high oxidation and adsorption ability for arsenite [As(III)]. After being incorporated by Fe-Mn binary oxide, the surface area of diatomite increased 36%, and the pore volume increased five times. The pHzpc of FMBO-diatomite was determined to be 8.1. These characteristics are responsible for the increased As(III) adsorption efficiency. The adsorption equilibria of As(III) on FMBO-diatomite were described well by a Langmuir isotherm model due to the homogeneous distribution of Fe-Mn binary oxide on a diatomite surface. As(III) was oxidized into As(V), and then adsorbed by FMBO-diatomite. The oxidation and adsorption efficiencies for As(III) depended deeply on the pH of solution. When the pH was raised to 8.1, the As(III) adsorption efficiency of FMBO-diatomite was almost equal to the As(III) oxidation efficiency. Silicate and phosphate had negative effects on As(III) adsorption. Also the influence of silicate and phosphate with the pH variation was different.

  1. Efflux Transporters Regulate Arsenite Induced Genotoxicity in Double Negative and Double Positive T Cells.

    Science.gov (United States)

    Xu, Huan; Medina, Sebastian; Lauer, Fredine T; Douillet, Christelle; Jian Liu, Ke; Hudson, Laurie G; Stýblo, Miroslav; Aleksunes, Lauren M; Burchiel, Scott W

    2017-04-29

    Arsenite (As+3) exposure is known to cause immunotoxicity in human and animal models. Our previous studies demonstrated that As+3 at 50 to 500 nM concentrations induced both genotoxicity and non-genotoxicity in mouse thymus cells. Developing T cells at CD4-CD8- double negative (DN) stage, the first stage after early T cells are transported from bone marrow to thymus, were found to be more sensitive to As+3 toxicity than the T cells at CD4+CD8+ double positive (DP) stage in vitro. Induction of Mdr1 (Abcb1) and Mrp1 (Abcc1), two multidrug resistance transporters and exporters of As+3, was associated with the reversal of As+3-induced double strand breaks and DNA damage. In order to confirm that the thymus cell populations have different sensitivity to As+3in vivo, male C57BL/6J mice were exposed to 0, 100 and 500 ppb As+3 in drinking water for 30 d. A significant decrease in DN cell percentage was observed with exposure to 500 ppb As+3. Low to moderate concentrations of As+3 were shown to induce higher genotoxicity in sorted DN cells than DP cells in vitro. Calcein AM uptake and Mdr1/Mrp1 mRNA quantification results revealed that DN cells not only had limited As+3 exporter activity, but also lacked the ability to activate these exporters with As+3 treatments, resulting in a higher accumulation of intracellular As+3. Knockdown study of As+3 exporters in the DN thymic cell line, D1 using siRNA, demonstrated that Mdr1 and Mrp1 regulate intracellular As+3 accumulation and genotoxicity. Taken together, the results indicate that transporter regulation is an important mechanism for differential genotoxicity induced by As+3 in thymocytes at different developmental stages. © The Author 2017. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: journals.permissions@oup.com.

  2. Involvement of NO in sodium arsenite-induced yeast cell death%NO参与亚砷酸钠诱导酵母细胞死亡的调控

    Institute of Scientific and Technical Information of China (English)

    吴丽华; 仪慧兰; 张虎芳

    2012-01-01

    以模式生物酵母细胞为材料,研究亚砷酸钠胁迫对细胞死亡率和胞内NO水平的影响,以探讨NO在砷诱导细胞死亡中的作用.结果显示,浓度为1~7mmol·L^-1的亚砷酸钠可降低酵母细胞活性,诱导细胞死亡,随着处理浓度的升高和作用时间的延长,细胞死亡率增高;死细胞出现核固缩和核降解等凋亡特征;凋亡抑制剂Z-Asp-CH2-DCB(2"mol·L^-1)与3mmol·L^-1亚砷酸钠共同作用后,酵母细胞死亡率下降.在亚砷酸钠胁迫的过程中,酵母细胞内NO水平升高;一定浓度的NO清除剂c-PTIO(0.2mmol·L^-1)或NO生成抑制剂NaN3(1mmol·L^-1)均可降低亚砷酸钠引起的酵母细胞死亡率.结果表明,砷胁迫诱导的胞内NO升高是酵母细胞死亡的一个诱因,亚砷酸钠诱发的酵母细胞死亡中可能存在细胞凋亡过程.%Arsenic is a toxic metalloid widely distributed in the environment. Chronic exposure to arsenic is associated with increased risk of various diseases, such as neurotoxicity, birth defects and metabolic disorders. People exposed to high levels of arsenic are prone to skin, bladder, and lung cancer and occlusive vascular disease. However, the exact mechanisms of arsenic toxicity are not yet well understood. In this study, cytotoxie effects of sodium arsenite on yeast Saccharomyees cerevisiae were investigated with or without some antagonists. For arsenic treatments, yeast cells harvested from the early log phase were incubated in the fresh yeast extract peptone dextrose (YPD) media containing varying amounts of sodium arsenite. For other combination treatments, selected antagonists including broad caspase inhibitor Z-Asp-2,6-dichlorobenzoyloxymethylketone (Z-Asp-CH2-DCB), nitric oxide (NO) scavenger 2-( 4-carboxyphenyl)-4,4,5,5-teramethylimidazoline-l-oxyl-3-oxide ( c-PTIO ) and nitrate reductase inhibitor NaN3 were respectively added into YPD media in the presence of 3 mmol. L^-1 sodium arsenite. The results showed that

  3. Sodium arsenite-induced inhibition of cell proliferation is related to inhibition of IL-2 mRNA expression in mouse activated T cells

    Energy Technology Data Exchange (ETDEWEB)

    Conde, Patricia; Acosta-Saavedra, Leonor C.; Calderon-Aranda, Emma S. [Centro de Investigacion y de Estudios Avanzados, CINVESTAV, Seccion Toxicologia, P.O. Box 14-740, Mexico, D.F. (Mexico); Goytia-Acevedo, Raquel C. [Universidad Juarez del Estado de Durango, Facultad de Medicina, Gomez Palacio, Durango (Mexico)

    2007-04-15

    A proposed mechanism for the As-induced inhibition of cell proliferation is the inhibition of IL-2 secretion. However, the effects of arsenite on IL-2 mRNA expression or on the ERK pathway in activated-T cells have not yet been described. We examined the effect of arsenite on IL-2 mRNA expression, cell activation and proliferation in PHA-stimulated murine lymphocytes. Arsenite (1 and 10 {mu}M) decreased IL-2 mRNA expression, IL-2 secretion and cell proliferation. Arsenite (10 {mu}M) strongly inhibited ERK-phosphorylation. However, the partial inhibition (50%) of IL-2 mRNA produced by 1 {mu}M, consistent with the effects on IL-2 secretion and cell proliferation, could not be explained by the inhibition of ERK-phosphorylation, which was not affected at this concentration. The inhibition of IL-2 mRNA expression caused by 1 {mu}M could be associated to effects on pathways located downstream or parallel to ERK. Arsenite also decreased early activation (surface CD69{sup +} expression) in both CD4{sup +} and CD8{sup +}, and decreased total CD8{sup +} count without significantly affecting CD4{sup +}, supporting that the cellular immune response mediated by cytotoxic T cells is an arsenic target. Thus, our results suggest that arsenite decreases IL-2 mRNA levels and T-cell activation and proliferation. However, further studies on the effects of arsenite on IL-2 gene transcription and IL-2 mRNA stability are needed. (orig.)

  4. Continuous activation of Nrf2 and its target antioxidant enzymes leads to arsenite-induced malignant transformation of human bronchial epithelial cells.

    Science.gov (United States)

    Yang, Xu; Wang, Dapeng; Ma, Yuan; Xu, Xiguo; Zhu, Zhen; Wang, Xiaojuan; Deng, Hanyi; Li, Chunchun; Chen, Min; Tong, Jian; Yamanaka, Kenzo; An, Yan

    2015-12-01

    Long-term exposure to arsenite leads to human lung cancer, but the underlying mechanisms of carcinogenesis remain obscure. The transcription factor of nuclear factor-erythroid-2 p45-related factor (Nrf2)-mediated antioxidant response represents a critical cellular defense mechanism and protection against various diseases. Paradoxically, emerging data suggest that the constitutive activation of Nrf2 is associated with cancer development, progression and chemotherapy resistance. However, the role of Nrf2 in the occurrence of cancer induced by long-term arsenite exposure remains to be fully understood. By establishing transformed human bronchial epithelial (HBE) cells via chronic low-dose arsenite treatment, we showed that, in acquiring this malignant phenotype, continuous low level of ROS and sustained enhancement of Nrf2 and its target antioxidant enzyme levels were observed in the later-stage of arsenite-induced cell transformation. The downregulation of Keap1 level may be responsible for the over-activation of Nrf2 and its target enzymes. To validate these observations, Nrf2 was knocked down in arsenite-transformed HBE cells by SiRNA transfection, and the levels of Nrf2 and its target antioxidant enzymes, ROS, cell proliferation, migration, and colony formation were determined following these treatments. Results showed that blocked Nrf2 expression significantly reduced Nrf2 and its target antioxidant enzyme levels, restored ROS levels, and eventually suppressed cell proliferation, migration, and colony formation of the transformed cells. In summary, the results of the study strongly suggested that the continuous activation of Nrf2 and its target antioxidant enzymes led to the over-depletion of intracellular ROS levels, which contributed to arsenite-induced HBE cell transformation. Copyright © 2015 Elsevier Inc. All rights reserved.

  5. The molecular pathway of low concentration of sodium arsenite in inducing differentiation of liver cancer stem cells by down-regulating promyelocytic leukemia protein expression

    Directory of Open Access Journals (Sweden)

    Shi-long JIN

    2016-01-01

    Full Text Available Objective  To study the molecular pathway of low concentration of sodium arsenite in inducing differentiation of liver cancer stem cells. Methods  Western blotting analysis, immunofluorescence assay and quantitative PCR were used to examine the gene and protein expression of promyelocytic leukemia (PML, Oct4 and Sox2 in HCC tissue and cell lines, and the molecule pathway of low concentration of sodium arsenite inducing differentiation of liver cancer stem cells was confirmed by comparing the changes in the gene and protein expression of PML,Oct4 and Sox2 in HCC cells and biological function of LCSCs after the treatment with low concentration of sodium arsenite. Results  0.5μg/ml of sodium arsenite was shown to alter the biological characteristics of LCSCs in HuH7 and primary HCC cells, including the ability to form tumor spheres, resistance to pirarubicin (P<0.01, and the capability of forming tumors after allogeneic transplantation (P<0.05. Both HCC cells and tissues expressed the gene and protein of PML,Oct4 and Sox2, and 0.5μg/ml of sodium arsenite not only downregulated the gene and protein expression of Oct4 (P<0.05 and Sox2 in HCC cells (P<0.05, but also downregulated the protein expression of PML (P<0.05. In contrast, sodium arsenite did not inhibit the gene expression of PML in Hep3B, HepG2, SMCC-7721, HuH7 and primary HCC cells. Furthermore, through down-regulated PML protein expression with arsenite, the biological characteristics of HuH7 and primary HCC cells containing LCSCs was simultaneously altered, and the expression of stem gene Oct4 and Sox2 was downregulated (P<0.05, while HCC cells proliferation was inhibited as well. Conclusions  Both HCC tissues and cells can express the PML gene and PML protein. Low concentrations of sodium arsenite would directly bind to PML protein in HCC cells, resulting in degradation of the PML protein, followed by collapse of PML-NBs, inhibition of transcription of the proliferation

  6. Arsenite and ferrous iron oxidation linked to chemolithotrophic denitrification for the immobilization of arsenic in anoxic environments

    Science.gov (United States)

    Sun, W.; Sierra-Alvarez, R.; Milner, L.; Oremland, R.; Field, J.A.

    2009-01-01

    The objective of this study was to explore a bioremediation strategy based on injecting NO3- to support the anoxic oxidation of ferrous iron (Fe(II)) and arsenite (As(III)) in the subsurface as a means to immobilize As in the form of arsenate (As(V)) adsorbed onto biogenic ferric (Fe(III)) (hydr)oxides. Continuous flows and filled columns were used to simulate a natural anaerobic groundwater and sediment system with co-occurring As(III) and Fe(II) in the presence (column SF1) or absence (column SF2) of nitrate, respectively. During operation for 250 days, the average influent arsenic concentration of 567 ??g L-1 was reduced to 10.6 (??9.6) ??g L-1 in the effluent of column SF1. The cumulative removal of Fe(II) and As(III) in SF1 was 6.5 to 10-fold higher than that in SF2. Extraction and measurement of the mass of iron and arsenic immobilized on the sand packing of the columns were close to the iron and arsenic removed from the aqueous phase during column operation. The dominant speciation of the immobilized iron and arsenic was Fe(III) and As(V) in SF1, compared with Fe(II) and As(III) in SF2. The speciation was confirmed by X-ray diffraction (XRD) and X-ray photoelectron spectroscopy (XPS). The results indicate that microbial oxidation of As(III) and Fe(II) linked to denitrification resulted in the enhanced immobilization of aqueous arsenic in anaerobic environments by forming Fe(III) (hydr)oxide coated sands with adsorbed As(V). ?? 2009 American Chemical Society.

  7. Ribosomal protein S7 regulates arsenite-induced GADD45α expression by attenuating MDM2-mediated GADD45α ubiquitination and degradation.

    Science.gov (United States)

    Gao, Ming; Li, Xiaoguang; Dong, Wen; Jin, Rui; Ma, Hanghang; Yang, Pingxun; Hu, Meiru; Li, Yi; Hao, Yi; Yuan, Shengtao; Huang, Junjian; Song, Lun

    2013-05-01

    The stress-responding protein, GADD45α, plays important roles in cell cycle checkpoint, DNA repair and apoptosis. In our recent study, we demonstrate that GADD45α undergoes a dynamic ubiquitination and degradation in vivo, which process can be blocked by the cytotoxic reagent, arsenite, resulting in GADD45α accumulation to activate JNKs cell death pathway, thereby revealing a novel mechanism for the cellular GADD45α functional regulation. But the factors involved in GADD45α stability modulations are unidentified. Here, we demonstrated that MDM2 was an E3 ubiquitin ligase for GADD45α. One of MDM2-binding partner, ribosomal protein S7, interacted with and stabilized GADD45α through preventing the ubiquitination and degradation of GADD45α mediated by MDM2. This novel function of S7 is unrelated to p53 but seems to depend on S7/MDM2 interaction, for the S7 mutant lacking MDM2-binding ability lost its function to stabilize GADD45α. Further investigations indicated that arsenite treatment enhanced S7-MDM2 interaction, resulting in attenuation of MDM2-dependent GADD45α ubiquitination and degradation, thereby leading to GADD45α-dependent cell death pathway activation. Silencing S7 expression suppressed GADD45α-dependent cytotoxicity induced by arsenite. Our findings thus identify a novel function of S7 in control of GADD45α stabilization under both basal and stress conditions and its significance in mediating arsenite-induced cellular stress.

  8. Arsenite removal from aqueous solutions by γ-Fe2O3-TiO2 magnetic nanoparticles through simultaneous photocatalytic oxidation and adsorption.

    Science.gov (United States)

    Yu, Lian; Peng, Xianjia; Ni, Fan; Li, Jin; Wang, Dongsheng; Luan, Zhaokun

    2013-02-15

    A novel Fe-Ti binary oxide magnetic nanoparticles which combined the photocatalytic oxidation property of TiO(2) and the high adsorption capacity and magnetic property of γ-Fe(2)O(3) have been synthesized using a coprecipitation and simultaneous oxidation method. The as-prepared samples were characterized by powder XRD, TEM, TG-DTA, VSM and BET methods. Photocatalytic oxidation of arsenite, the effect of solution pH values and initial As(III) concentration on arsenite removal were investigated in laboratory experiments. Batch experimental results showed that under UV light, As(III) can be efficiently oxidized to As(V) by dissolved O(2) in γ-Fe(2)O(3)-TiO(2) nanoparticle suspensions at various pH values. At the same time, As(V) was effectively removed by adsorption onto the surface of nanoparticles. The maximum removal capability of the nano-material for arsenite was 33.03 mg/g at pH 7.0. Among all the common coexisting ions investigated, phosphate was the greatest competitor with arsenic for adsorptive sites on the nano-material. Regeneration studies verified that the γ-Fe(2)O(3)-TiO(2) nanoparticles, which underwent five successive adsorption-desorption processes, still retained comparable catalysis and adsorption performance, indicating the excellent stability of the nanoparticles. The excellent photocatalytic oxidation performance and high uptake capability of the magnetic nano-material make it potentially attractive material for the removal of As(III) from water.

  9. Molecular basis of arsenite (As+3-induced acute cytotoxicity in human cervical epithelial carcinoma cells

    Directory of Open Access Journals (Sweden)

    Muhammad Nauman Arshad

    2015-04-01

    Full Text Available Background: Rapid industrialization is discharging toxic heavy metals into the environment, disturbing human health in many ways and causing various neurologic, cardiovascular, and dermatologic abnormalities and certain types of cancer. The presence of arsenic in drinking water from different urban and rural areas of the major cities of Pakistan, for example, Lahore, Faisalabad, and Kasur, was found to be beyond the permissible limit of 10 parts per billion set by the World Health Organization. Therefore the present study was initiated to examine the effects of arsenite (As+3 on DNA biosynthesis and cell death. Methods: After performing cytotoxic assays on a human epithelial carcinoma cell line, expression analysis was done by quantitative polymerase chain reaction, western blotting, and flow cytometry. Results: We show that As+3 ions have a dose- and time-dependent cytotoxic effect through the activation of the caspase-dependent apoptotic pathway. In contrast to previous research, the present study was designed to explore the early cytotoxic effects produced in human cells during exposure to heavy dosage of As+3 (7.5 µg/ml. Even treatment for 1 h significantly increased the mRNA levels of p21 and p27 and caspases 3, 7, and 9. It was interesting that there was no change in the expression levels of p53, which plays an important role in G2/M phase cell cycle arrest. Conclusion: Our results indicate that sudden exposure of cells to arsenite (As+3 resulted in cytotoxicity and mitochondrial-mediated apoptosis resulting from up-regulation of caspases.

  10. Aqueous arsenite removal by simultaneous ultraviolet photocatalytic oxidation-coagulation of titanium sulfate.

    Science.gov (United States)

    Wang, Yuxia; Duan, Jinming; Li, Wei; Beecham, Simon; Mulcahy, Dennis

    2016-02-13

    This study explored the efficacy and efficiency of a simultaneous UV-catalyzed oxidation-coagulation process of titanium sulfate (UV/Ti(SO4)2) for efficient removal of As(III) from water. It revealed that, As(III) could be oxidized to As(V) during the UV catalyzed coagulation of Ti(SO4)2 with highly efficient As(III) removal in the pH range 4-6. The UV catalyzed oxidation-coagulation showed surprisingly effective oxidation of As(III) to As(V) within a short time. XPS indicated that 84.7% of arsenic on the coagulated precipitate was in the oxidized form of As(V) after the UV/Ti(SO4)2 treatment of As(III) aqueous solutions at pH 5. Arsenic remaining in solution at high pH was in the oxidized form As(V). Removal efficiencies of As(III) were investigated as a function of pH, Ti(SO4)2 dosage, initial As(III) concentration and irradiation energy. As(III) could almost completely be removed (>99%) by the photocatalytic oxidation-coagulation process with a moderate dose of Ti(SO4)2 in the pH range 4-6 at an initial arsenic concentration of 200 μg/L. The mechanisms of the photocatalytic coagulation oxidation of Ti(SO4)2 are similar to those of UV/crystalline TiO2 particles, involving the formation and reactions of the hydroxyl radical OH and superoxide HO2/O2(-).

  11. Silymarin protects plasma membrane and acrosome integrity in sperm treated with sodium arsenite

    Directory of Open Access Journals (Sweden)

    Farzaneh Eskandari

    2016-01-01

    Full Text Available Background: Exposure to arsenic is associated with impairment of male reproductive function by inducing oxidative stress. Silymarin with an antioxidant property scavenges free radicals. Objective: The aim of this study was to investigate if silymarin can prevent the adverse effects of sodium arsenite on ram sperm plasma membrane and acrosome integrity. Materials and Methods: Ram epidydimal spermatozoa were divided into five groups: spermatozoa at 0 hr, spermatozoa at 180 min (control, spermatozoa treated with silymarin (20 μM + sodium arsenite (10 μM for 180 min, spermatozoa treated with sodium arsenite (10 μM for 180 min and spermatozoa treated with silymarin (20 μM for 180 min. Double staining of Hoechst and propidium iodide was performed to evaluate sperm plasma membrane integrity, whereas comassie brilliant blue staining was used to assess acrosome integrity. Results: Plasma membrane (p< 0.001 and acrosome integrity (p< 0.05 of the spermatozoa were significantly reduced in sodium arsenite group compared to the control. In silymarin + sodium arsenite group, silymarin was able to significantly (p< 0.001 ameliorate the adverse effects of sodium arsenite on these sperm parameters compared to sodium arsenite group. The incubation of sperm for 180 min (control group showed a significant (p< 0.001 decrease in acrosome integrity compared to the spermatozoa at 0 hour. The application of silymarin alone for 180 min could also significantly (p< 0.05 increase sperm acrosome integrity compared to the control. Conclusion: Silymarin as a potent antioxidant could compensate the adverse effects of sodium arsenite on the ram sperm plasma membrane and acrosome integrity.

  12. Arsenic transformation and mobilization from minerals by the arsenite oxidizing strain WAO

    Science.gov (United States)

    Rhine, E.D.; Onesios, K.M.; Serfes, M.E.; Reinfelder, J.R.; Young, L.Y.

    2008-01-01

    Analysis of arsenic concentrations in New Jersey well water from the Newark Basin showed up to 15% of the wells exceed 10 ??g L-1, with a maximum of 215 ??g L-1. In some geologic settings in the basin, this mobile arsenic could be from the weathering of pyrite (FeS2) found in black shale that contains up to 4% arsenic by weight. We hypothesized that under oxic conditions at circumneutral pH, the microbially mediated oxidation of sulfide in the pyrite lattice would lead to the release of pyrite-bound arsenic. Moreover, the oxidation of aqueous As(III) to As(V) by aerobic microorganisms could further enhance arsenic mobilization from the solid phase. Enrichment cultures under aerobic, As(III)-oxidizing conditions were established under circumneutral pH with weathered black shale from the Newark Basin as the inoculum source. Strain WAO, an autotrophic inorganic-sulfur and As(III)-oxidizer, was isolated and phylogenetically and physiologically characterized. Arsenic mobilization studies from arsenopyrite (FeAsS) mineral, conducted with strain WAO at circumneutral pH, showed microbially enhanced mobilization of arsenic and complete oxidation of released arsenic and sulfur to stoichiometric amounts of arsenate and sulfate. In addition, WAO preferentially colonized pyrite on the surface of arsenic-bearing, black shale thick sections. These findings support the hypothesis that microorganisms can directly mobilize and transform arsenic bound in mineral form at circumneutral pH and suggest that the microbial mobilization of arsenic into groundwater may be important in other arsenic-impacted aquifers. ?? 2008 American Chemical Society.

  13. Organization and regulation of the arsenite oxidase operon of the moderately acidophilic and facultative chemoautotrophic Thiomonas arsenitoxydans.

    Science.gov (United States)

    Slyemi, Djamila; Moinier, Danielle; Talla, Emmanuel; Bonnefoy, Violaine

    2013-11-01

    Thiomonas arsenitoxydans is an acidophilic and facultatively autotrophic bacterium that can grow by oxidizing arsenite to arsenate. A comparative genomic analysis showed that the T. arsenitoxydans aioBA cluster encoding the two subunits of arsenite oxidase is distinct from the other clusters, with two specific genes encoding a cytochrome c and a metalloregulator belonging to the ArsR/SmtB family. These genes are cotranscribed with aioBA, suggesting that these cytochromes c are involved in arsenite oxidation and that this operon is controlled by the metalloregulator. The growth of T. arsenitoxydans in the presence of thiosulfate and arsenite, or arsenate, is biphasic. Real-time PCR experiments showed that the operon is transcribed during the second growth phase in the presence of arsenite or arsenate, whereas antimonite had no effect. These results suggest that the expression of the aioBA operon of T. arsenitoxydans is regulated by the electron donor present in the medium, i.e., is induced in the presence of arsenic but is repressed by more energetic substrates. Our data indicate that the genetic organization and regulation of the aioBA operon of T. arsenitoxydans differ from those of the other arsenite oxidizers.

  14. Arsenite oxidation-enhanced photocatalytic degradation of phenolic pollutants on platinized TiO2.

    Science.gov (United States)

    Kim, Jaesung; Kim, Jungwon

    2014-11-18

    The effect of As(III) on the photocatalytic degradation of phenolic pollutants such as 4-chlorophenol (4-CP) and bisphenol A (BPA) in a suspension of platinized TiO2 (Pt/TiO2) was investigated. In the presence of As(III), the photocatalytic degradation of 4-CP and BPA was significantly enhanced, and the simultaneous oxidation of As(III) to As(V) was also achieved. This positive effect of As(III) on the degradation of phenolic pollutants is attributed to the adsorption of As(V) (generated from As(III) oxidation) on the surface of Pt/TiO2, which facilitates the production of free OH radicals ((•)OHf) that are more reactive than surface-bound OH radicals ((•)OHs) toward phenolic pollutants. The generation of (•)OHf was indirectly verified by using coumarin as an OH radical trapper and comparing the yields of coumarin--OH adduct (i.e., 7-hydroxycoumarin) formed in the absence and presence of As(V). In repeated cycles of 4-CP degradation, the degradation efficiency of 4-CP gradually decreased in the absence of As(III), whereas it was mostly maintained in the presence of As(III), which was either initially present or repeatedly injected at the beginning of each cycle. The positive effect of As(III) on 4-CP degradation was observed over a wide range of As(III) concentrations (up to mM levels) with Pt/TiO2. However, a high concentration of As(III) (hundreds of μM) inhibited the degradation of 4-CP with bare TiO2. Therefore, Pt/TiO2 can be proposed as a practical photocatalyst for the simultaneous oxidation of phenolic pollutants and As(III) in industrial wastewaters.

  15. Protective effects of the dietary supplementation of turmeric (Curcuma longa L.) on sodium arsenite-induced biochemical perturbation in mice.

    Science.gov (United States)

    Karim, Md Rezaul; Haque, Abedul; Islam, Khairul; Ali, Nurshad; Salam, Kazi Abdus; Saud, Zahangir Alam; Hossain, Ekhtear; Fajol, Abul; Akhand, Anwarul Azim; Himeno, Seiichiro; Hossain, Khaled

    2010-12-01

    The present study was undertaken to evaluate the protective effect of turmeric powder on arsenic toxicity through mice model. Swiss albino male mice were divided into four groups. The first group was used as control, while groups 2, 3, and 4 were treated with turmeric powder (T, 50 mg/kg body weight/day), sodium arsenite (Sa, 10 mg/kg body weight/day) and turmeric plus Sa (T+Sa), respectively. Results showed that oral administration of Sa reduced the weight gain of the mice compared to the control group and food supplementation of turmeric prevented the reduction of weight gain. Turmeric abrogated the Sa-induced elevation of serum urea, glucose, triglyceride (TG) level and alanine aminotransferase (ALT) activity except the activity of alkaline phosphatase (ALP). Turmeric also prevented the Sa-induced perturbation of serum butyryl cholinesterase activity (BChE). Therefore, ameliorating effect of turmeric on Sa-treated mice suggested the future application of turmeric to reduce or to prevent arsenic toxicity in human.

  16. Arsenate uptake and arsenite simultaneous sorption and oxidation by Fe-Mn binary oxides: influence of Mn/Fe ratio, pH, Ca2+, and humic acid.

    Science.gov (United States)

    Zhang, Gaosheng; Liu, Huijuan; Qu, Jiuhui; Jefferson, William

    2012-01-15

    Arsenate retention, arsenite sorption and oxidation on the surfaces of Fe-Mn binary oxides may play an important role in the mobilization and transformation of arsenic, due to the common occurrence of these oxides in the environment. However, no sufficient information on the sorption behaviors of arsenic on Fe-Mn binary oxides is available. This study investigated the influences of Mn/Fe molar ratio, solution pH, coexisting calcium ions, and humic acids have on arsenic sorption by Fe-Mn binary oxides. To create Fe-Mn binary oxides, simultaneous oxidation and co-precipitation methods were employed. The Fe-Mn binary oxides exhibited a porous crystalline structure similar to 2-line ferrihydrite at Mn/Fe ratios 1:3 and below, whereas exhibited similar structures to δ-MnO(2) at higher ratios. The As(V) sorption maximum was observed at a Mn/Fe ratio of 1:6, but As(III) uptake maximum was at Mn/Fe ratio 1:3. However, As(III) adsorption capacity was much higher than that of As(V) at each Mn/Fe ratio. As(V) sorption was found to decrease with increasing pH, while As(III) sorption edge was different, depending on the content of MnO(2) in the binary oxides. The presence of Ca(2+) enhanced the As(V) uptake under alkaline pH, but did not significantly influence the As(III) sorption by 1:9 Fe-Mn binary oxide; whereas the presence of humic acid slightly reduced both As(V) and As(III) uptake. These results indicate that As(III) is more easily immobilized than As(V) in the environment, where Fe-Mn binary oxides are available as sorbents and they represent attractive adsorbents for both As(V) and As(III) removal from water and groundwater. Copyright © 2011 Elsevier Inc. All rights reserved.

  17. Life in an arsenic-containing gold mine: genome and physiology of the autotrophic arsenite-oxidizing bacterium rhizobium sp. NT-26.

    Science.gov (United States)

    Andres, Jérémy; Arsène-Ploetze, Florence; Barbe, Valérie; Brochier-Armanet, Céline; Cleiss-Arnold, Jessica; Coppée, Jean-Yves; Dillies, Marie-Agnès; Geist, Lucie; Joublin, Aurélie; Koechler, Sandrine; Lassalle, Florent; Marchal, Marie; Médigue, Claudine; Muller, Daniel; Nesme, Xavier; Plewniak, Frédéric; Proux, Caroline; Ramírez-Bahena, Martha Helena; Schenowitz, Chantal; Sismeiro, Odile; Vallenet, David; Santini, Joanne M; Bertin, Philippe N

    2013-01-01

    Arsenic is widespread in the environment and its presence is a result of natural or anthropogenic activities. Microbes have developed different mechanisms to deal with toxic compounds such as arsenic and this is to resist or metabolize the compound. Here, we present the first reference set of genomic, transcriptomic and proteomic data of an Alphaproteobacterium isolated from an arsenic-containing goldmine: Rhizobium sp. NT-26. Although phylogenetically related to the plant-associated bacteria, this organism has lost the major colonizing capabilities needed for symbiosis with legumes. In contrast, the genome of Rhizobium sp. NT-26 comprises a megaplasmid containing the various genes, which enable it to metabolize arsenite. Remarkably, although the genes required for arsenite oxidation and flagellar motility/biofilm formation are carried by the megaplasmid and the chromosome, respectively, a coordinate regulation of these two mechanisms was observed. Taken together, these processes illustrate the impact environmental pressure can have on the evolution of bacterial genomes, improving the fitness of bacterial strains by the acquisition of novel functions.

  18. Anabaena sp. mediated bio-oxidation of arsenite to arsenate in synthetic arsenic (III) solution: Process optimization by response surface methodology.

    Science.gov (United States)

    Jana, Animesh; Bhattacharya, Priyankari; Swarnakar, Snehasikta; Majumdar, Swachchha; Ghosh, Sourja

    2015-11-01

    Blue green algae Anabaena sp. was cultivated in synthetic arsenite solution to investigate its bio-oxidation potential for arsenic species. Response surface methodology (RSM) was employed based on a 3-level full factorial design considering four factors, viz. initial arsenic (III) concentration, algal dose, temperature and time. Bio-oxidation (%) of arsenic (III) was considered as response for the design. The study revealed that about 100% conversion of As (III) to As (V) was obtained for initial As (III) concentration of 2.5-7.5 mg/L at 30 °C for 72 h of exposure using 3 g/L of algal dose signifying a unique bio-oxidation potential of Anabaena sp. The dissolved CO2 (DCO2) and oxygen (DO) concentration in solution was monitored during the process and based on the data, a probable mechanism was proposed wherein algal cell acts like a catalytic membrane surface and expedites the bio-oxidation process. Bioaccumulation of arsenic, as well as, surface adsorption on algal cell was found considerably low. Lipid content of algal biomass grown in arsenite solution was found slightly lower than that of algae grown in synthetic media. Toxicity effects on algal cells due to arsenic exposure were evaluated in terms of comet assay and chlorophyll a content which indicated DNA damage to some extent along with very little decrease in chlorophyll a content. In summary, the present study explored the potential application of Anabaena sp. as an ecofriendly and sustainable option for detoxification of arsenic contaminated natural water with value-added product generation.

  19. Study of sodium arsenite induced biochemical changes on certain biomolecules of the freshwater catfish Clarias batrachus

    Directory of Open Access Journals (Sweden)

    Randhir Kumar

    2012-01-01

    Full Text Available Toxic impact of sublethal concentration (1 mg/L; 5% of 96h LC50 value of sodium arsenite (NaAsO2 on certain biomolecules (proteins, nucleic acids, lipids, and glycogen of five tissue components (muscles, liver, brain, skin, and gills of the freshwater catfish Clarias batrachus was analysed. The important toxic manifestations include marked decrease in the concentration of proteins (21.72-45.42% in muscles; 3.42-53.94% in liver; 15.39-45.42% in brain; 15.40-4.00% in skin and 11.35-64.13% in gills, DNA (0.55-22.95% in muscles; 8.33-14.06% in liver; 5.30-18.40% in brain; 13.57-52.80% in skin; and 12.38-31.01% in gills, RNA (42.68-76.16% in muscles; 10.68-39.75% in liver; 5.66-29.05% in brain; 7.72-27.93% in skin and 21.47-44.38% in gills and glycogen (24.00-51.72% in muscles; 49.11-72.45% in liver; 11.49-26.03% in brain; 26.13-38.05% in skin and 17.80-37.97% in gills. Excepting liver where the lipid content increases (15.82-24.13%, the fat content also showed depletion in their concentration (10.40-29.83% in muscles; 8.30-34.45% in brain; 8.94-31.47% in skin and 12.75-28.86% in gills, in the rest of the organ systems.Foi analisado o impacto tóxico da concentração subletal (1 mg/L; 5% do valor de LC50 de 96h do arsenito de sódio (NaAsO2 sobre certas biomoléculas (proteinas, ácidos nucleicos, lipídios e glicogênio de cinco tecidos (músculos, fígado, cérebro, pele e brânquias do bagre Clarias batrachus. As manifestações tóxicas importantes incluiram o decréscimo acentuado na concentração de proteinas (21,72-45,42% nos músculos; 3,42-53,94% no fígado; 15,39-45,42% no cérebro; 15,40-4,00% na pele e 11,35-64,13% nas brânquias, DNA (0,55-22,95% nos músculos; 8,33-14,06% no fígado; 5,30-18,40% no cérebro; 13,57-52,80% na pele e 12,38-31,01% nas brânquias, RNA (42,68-76,16% nos músculos; 10,68-39,75% no fígado; 5,66-29,05% no cérebro; 7,72-27,93% na pele e 21,47-44,38% nas brânquias e glicogênio (24,00-51,72% nos músculos; 49

  20. ArxA, a new clade of arsenite oxidase within the DMSO reductase family of molybdenum oxidoreductases

    Science.gov (United States)

    Zargar, Kamrun; Conrad, Alison; Bernick, David L.; Lowe, Todd M.; Stolc, Viktor; Hoeft, Shelley; Oremland, Ronald S.; Stolz, John; Saltikov, Chad W.

    2012-01-01

    Arsenotrophy, growth coupled to autotrophic arsenite oxidation or arsenate respiratory reduction, occurs only in the prokaryotic domain of life. The enzymes responsible for arsenotrophy belong to distinct clades within the DMSO reductase family of molybdenum-containing oxidoreductases: specifically arsenate respiratory reductase, ArrA, and arsenite oxidase, AioA (formerly referred to as AroA and AoxB). A new arsenite oxidase clade, ArxA, represented by the haloalkaliphilic bacterium Alkalilimnicola ehrlichii strain MLHE-1 was also identified in the photosynthetic purple sulfur bacterium Ectothiorhodospira sp. strain PHS-1. A draft genome sequence of PHS-1 was completed and an arx operon similar to MLHE-1 was identified. Gene expression studies showed that arxA was strongly induced with arsenite. Microbial ecology investigation led to the identification of additional arxA-like sequences in Mono Lake and Hot Creek sediments, both arsenic-rich environments in California. Phylogenetic analyses placed these sequences as distinct members of the ArxA clade of arsenite oxidases. ArxA-like sequences were also identified in metagenome sequences of several alkaline microbial mat environments of Yellowstone National Park hot springs. These results suggest that ArxA-type arsenite oxidases appear to be widely distributed in the environment presenting an opportunity for further investigations of the contribution of Arx-dependent arsenotrophy to the arsenic biogeochemical cycle.

  1. Oxidative DNA damage after acute exposure to arsenite and monomethylarsonous acid in biomethylation-deficient human cells.

    Science.gov (United States)

    Orihuela, Ruben; Kojima, Chikara; Tokar, Erik J; Person, Rachel J; Xu, Yuanyuan; Qu, Wei; Waalkes, Michael P

    2013-07-01

    The carcinogen inorganic arsenic (iAs) undergoes biomethylation (BMT) in some cells. The methylated metabolite, monomethylarsonous (MMA(3+)), may cause oxidative DNA damage (ODD). With chronic iAs exposure, BMT-competent cells show ODD while BMT-deficient do not. To further define these events, we studied ODD produced by acute iAs or MMA(3+) in the BMT-deficient human prostate cell line, RWPE-1. ODD, measured by the immuno-spin trapping method, was assessed after exposure to iAs or MMA(3+) alone, with the arsenic BMT inhibitor selenite or after glutathione (GSH) depletion. The expression of oxidative stress-related genes (HO-1, SOD-1, SOD-2, Nrf2 and Keap-1) was also assessed. Exposure to iAs at 24 h (0-20 µM), stimulated ODD only at levels above the LC50 of a 48 h exposure (17 µM). If iAs induced ODD, it also activated oxidative stress-related genes. Selenium did not alter iAs-induced ODD. MMA(3+) at 24 h (0-0.5 µM) caused ODD at levels below the LC50 of a 48 h exposure (1.5 µM), which were greatly increased by GSH depletion but not selenite. MMA(3+) induced ODD at levels not activating oxidant stress response genes. Overall, iAs induced ODD in BMT-deficient cells only at toxic levels. MMA(3+) caused ODD at non-toxic levels, independently of cellular BMT capacity and in a fashion not requiring further BMT.

  2. Alkalilimnicola ehrlichii sp. nov., a novel, arsenite-oxidizing haloalkaliphilic gammaproteobacterium capable of chemoautotrophic or heterotrophic growth with nitrate or oxygen as the electron acceptor

    Science.gov (United States)

    Hoeft, S.E.; Blum, J.S.; Stolz, J.F.; Tabita, F.R.; Witte, B.; King, G.M.; Santini, J.M.; Oremland, R.S.

    2007-01-01

    A facultative chemoautotrophic bacterium, strain MLHE-1T, was isolated from Mono Lake, an alkaline hypersaline soda lake in California, USA. Cells of strain MLHE-1T were Gram-negative, short motile rods that grew with inorganic electron donors (arsenite, hydrogen, sulfide or thiosulfate) coupled with the reduction of nitrate to nitrite. No aerobic growth was attained with arsenite or sulfide, but hydrogen sustained both aerobic and anaerobic growth. No growth occurred when nitrite or nitrous oxide was substituted for nitrate. Heterotrophic growth was observed under aerobic and anaerobic (nitrate) conditions. Cells of strain MLHE-1T could oxidize but not grow on CO, while CH4 neither supported growth nor was it oxidized. When grown chemoautotrophically, strain MLHE-1T assimilated inorganic carbon via the Calvin-Benson-Bassham reductive pentose phosphate pathway, with the activity of ribulose 1,5-bisphosphate carboxylase (RuBisCO) functioning optimally at 0.1 M NaCl and at pH 7.3. Strain MLHE-1T grew over broad ranges of pH (7.3-10.0; optimum, 9.3), salinity (115-190 g l-1; optimum 30 g l-1) and temperature (113-40 ??C; optimum, 30 ??C). Phylogenetic analysis of 16S rRNA gene sequences placed strain MLHE-1T in the class Gammaproteobacteria (family Ectothiorhodospiraceae) and most closely related to Alkalispirillum mobile (98.5%) and Alkalilimnicola halodurans (98.6%), although none of these three haloalkaliphilic micro-organisms were capable of photoautotrophic growth and only strain MLHE-1T was able to oxidize As(III). On the basis of physiological characteristics and DNA-DNA hybridization data, it is suggested that strain MLHE-1T represents a novel species within the genus Alkalilimnicola for which the name Alkalilimnicola ehrlichii is proposed. The type strain is MLHE-1T (=DSM 17681T =ATCC BAA-1101T). Aspects of the annotated full genome of Alkalilimnicola ehrlichii are discussed in the light of its physiology. ?? 2007 IUMS.

  3. Arsenite transport in plants.

    Science.gov (United States)

    Ali, Waqar; Isayenkov, Stanislav V; Zhao, Fang-Jie; Maathuis, Frans J M

    2009-07-01

    Arsenic is a metalloid which is toxic to living organisms. Natural occurrence of arsenic and human activities have led to widespread contamination in many areas of the world, exposing a large section of the human population to potential arsenic poisoning. Arsenic intake can occur through consumption of contaminated crops and it is therefore important to understand the mechanisms of transport, metabolism and tolerance that plants display in response to arsenic. Plants are mainly exposed to the inorganic forms of arsenic, arsenate and arsenite. Recently, significant progress has been made in the identification and characterisation of proteins responsible for movement of arsenite into and within plants. Aquaporins of the NIP (nodulin26-like intrinsic protein) subfamily were shown to transport arsenite in planta and in heterologous systems. In this review, we will evaluate the implications of these new findings and assess how this may help in developing safer and more tolerant crops.

  4. Quantitative transcriptome, proteome, and sulfur metabolite profiling of the Saccharomyces cerevisiae response to arsenite.

    Science.gov (United States)

    Thorsen, Michael; Lagniel, Gilles; Kristiansson, Erik; Junot, Christophe; Nerman, Olle; Labarre, Jean; Tamás, Markus J

    2007-06-19

    Arsenic is ubiquitously present in nature, and various mechanisms have evolved enabling cells to evade toxicity and acquire tolerance. Herein, we explored how Saccharomyces cerevisiae (budding yeast) respond to trivalent arsenic (arsenite) by quantitative transcriptome, proteome, and sulfur metabolite profiling. Arsenite exposure affected transcription of genes encoding functions related to protein biosynthesis, arsenic detoxification, oxidative stress defense, redox maintenance, and proteolytic activity. Importantly, we observed that nearly all components of the sulfate assimilation and glutathione biosynthesis pathways were induced at both gene and protein levels. Kinetic metabolic profiling evidenced a significant increase in the pools of sulfur metabolites as well as elevated cellular glutathione levels. Moreover, the flux in the sulfur assimilation pathway as well as the glutathione synthesis rate strongly increased with a concomitant reduction of sulfur incorporation into proteins. By combining comparative genomics and molecular analyses, we pinpointed transcription factors that mediate the core of the transcriptional response to arsenite. Taken together, our data reveal that arsenite-exposed cells channel a large part of assimilated sulfur into glutathione biosynthesis, and we provide evidence that the transcriptional regulators Yap1p and Met4p control this response in concert.

  5. Arsenite suppression of BMP signaling in human keratinocytes

    Energy Technology Data Exchange (ETDEWEB)

    Phillips, Marjorie A.; Qin, Qin [Department of Environmental Toxicology, University of California, Davis, CA 95616-8588 (United States); Hu, Qin; Zhao, Bin [State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085 (China); Rice, Robert H., E-mail: rhrice@ucdavis.edu [Department of Environmental Toxicology, University of California, Davis, CA 95616-8588 (United States)

    2013-06-15

    Arsenic, a human skin carcinogen, suppresses differentiation of cultured keratinocytes. Exploring the mechanism of this suppression revealed that BMP-6 greatly increased levels of mRNA for keratins 1 and 10, two of the earliest differentiation markers expressed, a process prevented by co-treatment with arsenite. BMP also stimulated, and arsenite suppressed, mRNA for FOXN1, an important transcription factor driving early keratinocyte differentiation. Keratin mRNAs increased slowly after BMP-6 addition, suggesting they are indirect transcriptional targets. Inhibition of Notch1 activation blocked BMP induction of keratins 1 and 10, while FOXN1 induction was largely unaffected. Supporting a requirement for Notch1 signaling in keratin induction, BMP increased levels of activated Notch1, which was blocked by arsenite. BMP also greatly decreased active ERK, while co-treatment with arsenite maintained active ERK. Inhibition of ERK signaling mimicked BMP by inducing keratin and FOXN1 mRNAs and by increasing active Notch1, effects blocked by arsenite. Of 6 dual-specificity phosphatases (DUSPs) targeting ERK, two were induced by BMP unless prevented by simultaneous exposure to arsenite and EGF. Knockdown of DUSP2 or DUSP14 using shRNAs greatly reduced FOXN1 and keratins 1 and 10 mRNA levels and their induction by BMP. Knockdown also decreased activated Notch1, keratin 1 and keratin 10 protein levels, both in the presence and absence of BMP. Thus, one of the earliest effects of BMP is induction of DUSPs, which increases FOXN1 transcription factor and activates Notch1, both required for keratin gene expression. Arsenite prevents this cascade by maintaining ERK signaling, at least in part by suppressing DUSP expression. - Highlights: • BMP induces FOXN1 transcription. • BMP induces DUSP2 and DUSP14, suppressing ERK activation. • Arsenite suppresses levels of phosphorylated Smad1/5 and FOXN1 and DUSP mRNA. • These actions rationalize arsenite suppression of keratinocyte

  6. Photosynthesis is induced in rice plants that associate with arbuscular mycorrhizal fungi and are grown under arsenate and arsenite stress.

    Science.gov (United States)

    de Andrade, Sara Adrian Lopez; Domingues, Adilson Pereira; Mazzafera, Paulo

    2015-09-01

    The metalloid arsenic (As) increases in agricultural soils because of anthropogenic activities and may have phytotoxic effects depending on the available concentrations. Plant performance can be improved by arbuscular mycorrhiza (AM) association under challenging conditions, such as those caused by excessive soil As levels. In this study, the influence of AM on CO2 assimilation, chlorophyll a fluorescence, SPAD-chlorophyll contents and plant growth was investigated in rice plants exposed to arsenate (AsV) or arsenite (AsIII) and inoculated or not with Rhizophagus irregularis. Under AsV and AsIII exposure, AM rice plants had greater biomass accumulation and relative chlorophyll content, increased water-use efficiency, higher carbon assimilation rate and higher stomatal conductance and transpiration rates than non-AM rice plants did. Chlorophyll a fluorescence analysis revealed significant differences in the response of AM-associated and -non-associated plants to As. Mycorrhization increased the maximum and actual quantum yields of photosystem II and the electron transport rate, maintaining higher values even under As exposure. Apart from the negative effects of AsV and AsIII on the photosynthetic rates and PSII efficiency in rice leaves, taken together, these results indicate that AM is able to sustain higher rice photosynthesis efficiency even under elevated As concentrations, especially when As is present as AsV.

  7. 三价砷氧化细菌Acidovorax sp.GW2中As(Ⅲ)氧化酶基因和调控序列的克隆鉴定%Isolation and identification of arsenite oxidase gene and regulatory sequences in an arsenite-oxidizing bacterium Acidovorax sp. GW2

    Institute of Scientific and Technical Information of China (English)

    赵凯; 黄银燕; 王倩; 王革娇

    2011-01-01

    Using reverse transcriptase PCR method and a bacterial fosmid library screening, an arsenite oxidase gene cluster were isolated from an arsenite-oxidizing bacterium Acidovorax sp. GW2. There are seven genes including aoxRSXABCD putatively encoding the transcriptional regulator AoxR of a two-component signal transduction system (68% identity), a periplasmic sensor histidine kinase AoxS (55 % identity), a periplasmic binding protein AoxX (55 % identity), arsenite oxidase AoxAB(74 % and 71% identity, respectively), nitroreductase AoxC (46 % identity) and cytochrome c AoxD (63 % identity) respectively. According to the reverse transcriptase PCR experiments,aoxR and aoxS encoding for a two-component system proteins are co-transcribed and located in opposite to structural genes aoxABCD.aoxX and aoxRS are not in the same operon. Functional analyses through gene knock-out of aoxS, aoxX and aoxD showed that aoxS and aoxX are the essential genes in arsenite oxidation of GW2, and the loss of aoxD did not show significant effects on arsenite oxidation.%通过反向PCR和细菌Fosmid文库筛选,克隆得到1株二三价砷[As(Ⅲ)]氧化细菌Acidovorax sp.GW2的As(Ⅲ)氧化酶Aox基因簇,包括aoxRSXABCD 7个基因,分别预测编码双组分信号传导系统转录调控子AoxR(同源性68%),周质感应组氨酸激酶AoxS(同源性55%),周质结合蛋白AoxX(同源性55%),砷氧化酶AoxAB(同源性分别为74%和71%),硝基还原酶AoxC(同源性46%),细胞色素C AoxD(同源性63%).反转录PCR结果显示,编码双组分系统的aoxRS基因共转录,而与之转录方向相反的结构基因aoxABCD处于同一操纵子中,aoxX基因和aoxRS基因不在同一操纵子中.通过对aoxS、aoxX、aoxD的基因敲除功能研究发现aoxS和aoxX基因为GW2三价砷氧化的必需基因,aoxD的功能丧失减慢了三价砷的氧化速率,但非关键基因.

  8. EMT and CSC-like properties mediated by the IKKβ/IκBα/RelA signal pathway via the transcriptional regulator, Snail, are involved in the arsenite-induced neoplastic transformation of human keratinocytes.

    Science.gov (United States)

    Jiang, Rongrong; Li, Yuan; Xu, Yuan; Zhou, Yun; Pang, Ying; Shen, Lu; Zhao, Yue; Zhang, Jianping; Zhou, Jianwei; Wang, Xinru; Liu, Qizhan

    2013-06-01

    Exposure of humans to inorganic arsenic can cause skin cancer. The epithelial-mesenchymal transition (EMT) and acquisition of cancer stem cell (CSC)-like properties are essential steps in the initiation of human skin cancers; however, the mechanisms of action remain obscure. We have found that, during the neoplastic transformation induced by a low concentration (1.0 μM) of arsenite in human keratinocyte HaCaT cells, the cells undergo an EMT and then acquire a malignant CSC-like phenotype. With longer times for transformation of HaCaT cells, there were increased activations of IκB kinase β (IKKβ), inhibitor nuclear factor-kappa B alpha (IκBα), and nuclear factor κB (NF-κB) RelA and increases in the level of Snail. Further, during the transformation of HaCaT cells, the activation of NF-κB RelA up-regulated Snail levels. Inhibition of NF-κB RelA blocked the arsenite-induced EMT, acquisition of a CSC-like phenotype, and neoplastic transformation. These observations show that EMT, along with acquisition of a CSC-like phenotype mediated by IKKβ/IκBα/RelA signal pathway via Snail, contributes to a low concentration of arsenite-induced tumorigenesis.

  9. Removal of Arsenite from Water by Ce-Al-Fe Trimetal Oxide Adsorbent: Kinetics, Isotherms, and Thermodynamics

    Directory of Open Access Journals (Sweden)

    Cuizhen Sun

    2016-01-01

    Full Text Available Ce-Al-Fe trimetal oxide adsorbent was prepared. The morphology characteristics of the new adsorbent were analysed by the transmission electron microscope (SEM method. The SEM results implied its ability in the adsorption of As (III. To verify the analyses, bench-scale experiments were performed for the removal of As (III from water. In the experiments of adsorption, As (III adsorption capacity of the trimetal oxide adsorbent was presented significantly higher than activated aluminium oxide and activated carbon. As (III adsorption kinetics resembled pseudo-second-order adsorption mode. When initial As (III concentration was 3, 8, and 10 mg·L−1, the maximum adsorption capacity achieved was 1.48, 3.73, and 5.12 mg·g−1, respectively. In addition, the experimental adsorption data were described well by the Freundlich adsorption isotherm model at 20, 30, and 40°C. The enthalpy change (ΔS, the standard free energy (ΔG, and entropy change (ΔH indicated that the nature of As (III adsorption was exothermic and spontaneous with increasing randomness on the interface of solid and liquid. And the adsorption mechanism can be interpreted as chemisorption with As (III multilayer coverage formation on the adsorbent surface.

  10. Adsorption of arsenite and selenite using an inorganic ion exchanger based on Fe–Mn hydrous oxide

    KAUST Repository

    Szlachta, Małgorzata

    2012-01-01

    The adsorption behaviour and mechanism of As(III) and Se(IV) oxyanion uptake using a mixed inorganic adsorbent were studied. The novel adsorbent, based on Fe(III)-Mn(III) hydrous oxides and manganese(II) carbonate, was synthesised using a hydrothermal precipitation approach in the presence of urea. The inorganic ion exchanger exhibited a high selectivity and adsorptive capacity towards As(III) (up to 47.6mg/g) and Se(IV) (up to 29.0mg/g), even at low equilibrium concentration. Although pH effects were typical for anionic species (i.e., the adsorption decreased upon pH increase), Se(IV) was more sensitive to pH changes than As(III). The rates of adsorption of both oxyanions were high. Fourier transform infrared (FTIR) and X-ray photoelectron spectroscopy (XPS) studies showed that the ion exchange adsorption of both anions took place via OH - groups, mainly from Fe(III) but also Mn(III) hydrous oxides. MnCO 3 did not contribute directly to As(III) and Se(IV) removal. A higher adsorptive capacity of the developed material towards As(III) was partly due to partial As(III) oxidation during adsorption. © 2011 Elsevier Inc.

  11. Efficient removal of arsenite through photocatalytic oxidation and adsorption by ZrO2-Fe3O4 magnetic nanoparticles

    Science.gov (United States)

    Sun, Tianyi; Zhao, Zhiwei; Liang, Zhijie; Liu, Jie; Shi, Wenxin; Cui, Fuyi

    2017-09-01

    Bifunctional ZrO2-Fe3O4 magnetic nanoparticles were synthesized and characterized, to remove As(III) through photocatalyic oxidation and adsorption. With a saturation magnetization of 27.39 emu/g, ZrO2-Fe3O4 nanoparticles with size of 10-30 nm could be easily separated from solutions with a simple magnetic process. Under UV light, As(III) could be completely oxidized to less toxic As(V) by ZrO2-Fe3O4 nanoparticles within 40 min in the photocatalytic reaction. Simultaneously, As(V) could be adsorbed onto the surface of nanoparticles with high efficiency. The adsorption of As(V) was well fitted by the pseudo-second-order model and the Freundlich isotherm model, respectively, and the maximum adsorption capacities of the nanoparticles was 133.48 mg/g at pH 7.0. As(III) could be effectively removed by ZrO2-Fe3O4 nanoparticles at initial pH range from 4 to 8. Among all the common coexisting ions investigated, except for chloride and sulfate, carbonate, silicate and phosphate decreased the As(III) removal by competing with arsenic species for adsorption sites. The synthesized magnetic ZrO2-Fe3O4 combined the photocatalytic oxidation property of ZrO2 and the high adsorption capacity of both ZrO2 and Fe3O4, which make it have significant potential applications in the As(III)-contaminated water treatment.

  12. Effects of arsenic on modification of promyelocytic leukemia (PML): PML responds to low levels of arsenite

    Energy Technology Data Exchange (ETDEWEB)

    Hirano, Seishiro, E-mail: seishiro@nies.go.jp [Research Center for Environmental Risk, National Institute for Environmental Studies (Japan); Graduate School of Pharmaceutical Sciences, Chiba University (Japan); Watanabe, Takayuki [Graduate School of Pharmaceutical Sciences, Chiba University (Japan); Kobayashi, Yayoi [Graduate School of Pharmaceutical Sciences, Chiba University (Japan); Center for Environmental Health Sciences, National Institute for Environmental Studies (Japan)

    2013-12-15

    Inorganic arsenite (iAs{sup 3+}) is a two-edged sword. iAs{sup 3+} is a well-known human carcinogen; nevertheless, it has been used as a therapeutic drug for acute promyelocytic leukemia (APL), which is caused by a fusion protein comprising retinoic acid receptor-α and promyelocytic leukemia (PML). PML, a nuclear transcription factor, has a RING finger domain with densely positioned cysteine residues. To examine PML-modulated cellular responses to iAs{sup 3+}, CHO-K1 and HEK293 cells were each used to establish cell lines that expressed ectopic human PML. Overexpression of PML increased susceptibility to iAs{sup 3+} in CHO-K1 cells, but not in HEK293 cells. Exposure of PML-transfected cells to iAs{sup 3+} caused PML to change from a soluble form to less soluble forms, and this modification of PML was observable even with just 0.1 μM iAs{sup 3+} (7.5 ppb). Western blot and immunofluorescent microscopic analyses revealed that the biochemical changes of PML were caused at least in part by conjugation with small ubiquitin-like modifier proteins (SUMOylation). A luciferase reporter gene was used to investigate whether modification of PML was caused by oxidative stress or activation of antioxidant response element (ARE) in CHO-K1 cells. Modification of PML protein occurred faster than activation of the ARE in response to iAs{sup 3+}, suggesting that PML was not modified as a consequence of oxidative stress-induced ARE activation. - Highlights: • PML was found in nuclear microspecles in response to arsenite. • Arsenite triggers SUMOylation of PML. • Arsenite modifies PML at as low as 0.1 μM. • Modification of PML is not caused by ARE activation.

  13. Possible mechanisms for arsenic-induced proliferative diseases

    Energy Technology Data Exchange (ETDEWEB)

    Wetterhahn, K.E.; Dudek, E.J.; Shumilla, J.A. [Dartmouth College and Medical School, Hanover, NH (United States)] [and others

    1996-12-31

    Possible mechanisms for cardiovascular diseases and cancers which have been observed on chronic exposure to arsenic have been investigated. We tested the hypothesis that nonlethal levels of arsenic are mitogenic, cause oxidative stress, increase nuclear translocation of trans-acting factors, and increase expression of genes involved in proliferation. Cultured porcine vascular (from aorta) endothelial cells were used as a model cell system to study the effects of arsenic on the target cells for cardiovascular diseases. Treatment of postconfluent cell cultures with nonovertly toxic concentrations of arsenite increased DNA synthesis, similar to the mitogenic response observed with hydrogen peroxide. Within 1 hour of adding noncytotoxic concentrations of arsenite, cellular levels of oxidants increased relative to control levels, indicating that arsenite promotes cellular oxidations. Arsenite treatment increased nuclear translocation of NF-{kappa}B, an oxidative stress-responsive transcription factor, in a manner similar to that observed with hydrogen peroxide. Pretreatment of intact cells with the antioxidants N-acetylcysteine and dimethylfumarate prevented the arsenite-induced increases in cellular oxidant formation and NF-KB translocation. Arsenite had little or no effect on binding of NF-KB to its DNA recognition sequence in vitro, indicating that it is unlikely that arsenite directly affects NF-KB. The steady-state mRNA levels of intracellular adhesion molecule and urokinase-like plasminogen activator, genes associated with the active endothelial phenotype in arteriosclerosis and cancer metastasis, were increased by nontoxic concentrations of arsenite. These data suggest that arsenite promotes proliferative diseases like heart disease and cancer by activating oxidant-sensitive endothelial cell signaling and gene expression. It is possible that antioxidant therapy would be useful in preventing arsenic-induced cardiovascular disease and cancer.

  14. One-step synthesis of sea urchin-like alpha-MnO2 using KIO4 as the oxidant and its oxidation of arsenite

    NARCIS (Netherlands)

    Wang, M.X.; Tan, W.F.; Feng, X.H.; Koopal, L.K.; Liu, M.M.; Liu, F.

    2012-01-01

    Among several types of manganese oxides alpha-MnO2 is the most active due to its good catalytic, adsorption and ion exchange properties. Sea urchin-like alpha-MnO2 particles were synthesized by a one-step chemistry route at room temperature using MnSO4 in combination with KIO4 as oxidant. The obtain

  15. Effects of arsenite and UVA-1 radiation on calcineurin signaling

    Energy Technology Data Exchange (ETDEWEB)

    Musson, Ruben E.A., E-mail: rm@ream.nl [Department of Clinical Chemistry, Leiden University Medical Center (Netherlands); Department of Toxicogenetics, Leiden University Medical Center (Netherlands); Mullenders, Leon H.F. [Department of Toxicogenetics, Leiden University Medical Center (Netherlands); Smit, Nico P.M. [Department of Clinical Chemistry, Leiden University Medical Center (Netherlands)

    2012-07-01

    Calcineurin is a Ca{sup 2+}-dependent serine/threonine phosphatase and the target of the immunosuppressive drugs cyclosporin and tacrolimus, which are used in transplant recipients to prevent rejection. Unfortunately, the therapeutic use of this drugs is complicated by a high incidence of skin malignancy, which has set off a number of studies into the role of calcineurin signaling in skin, particularly with respect to cell cycle control and DNA repair. Both UVA1 radiation and arsenic species are known to promote skin cancer development via production of reactive oxygen species. In light of the well-documented sensitivity of calcineurin to oxidative stress, we examined and compared the effects of UVA1 and arsenite on calcineurin signaling. In this paper, we show that physiologically relevant doses of UVA1 radiation and low micromolar concentrations of arsenite strongly inhibit calcineurin phosphatase activity in Jurkat and skin cells and decrease NFAT nuclear translocation in Jurkat cells. The effects on calcineurin signaling could be partly prevented by inhibition of NADPH oxidase in Jurkat cells or increased dismutation of superoxide in Jurkat and skin cells. In addition, both UVA1 and arsenite decreased NF-{kappa}B activity, although at lower concentrations, arsenite enhanced NF-{kappa}B activity. These data indicate that UVA1 and arsenite affect a signal transduction route of growingly acknowledged importance in skin and that calcineurin may serve as a potential link between ROS exposure and impaired tumor suppression.

  16. INDUCIBLE HEAT SHOCK PROTEIN (HSP70-1) PROTECTS MCF-7 CELLS FROM THE CYTOTOXIC AND GENOTOXIC EFFECTS OF ARSENITE

    Science.gov (United States)

    Heat shock proteins (HSPs) belong to the highly conserved family of stress proteins and are induced following exposure to arsenic. Elevated HSPs protect against cellular damage from heat but it is unclear wether HSP induction alters the damaging effects of environmental chemical ...

  17. INDUCIBLE HEAT SHOCK PROTEIN (HSP70-1) PROTECTS MCF-7 CELLS FROM THE CYTOTOXIC AND GENOTOXIC EFFECTS OF ARSENITE

    Science.gov (United States)

    Heat shock proteins (HSPs) belong to the highly conserved family of stress proteins and are induced following exposure to arsenic. Elevated HSPs protect against cellular damage from heat but it is unclear wether HSP induction alters the damaging effects of environmental chemical ...

  18. Regulation of apoptosis in human melanoma and neuroblastoma cells by statins, sodium arsenite and TRAIL: a role of combined treatment versus monotherapy

    Science.gov (United States)

    Ivanov, Vladimir N.; Hei, Tom K.

    2015-01-01

    Treatment of melanoma cells by sodium arsenite or statins (simvastatin and lovastatin) dramatically modified activities of the main cell signaling pathways resulting in the induction of heme oxygenase-1 (HO-1) and in a downregulation of cyclooxygenase-2 (COX-2) protein levels. Through heme degradation and the production of carbon monoxide and biliverdin, HO-1 plays a protective role in different scenario of oxidative stress followed by mitochondrial apoptosis. Both sodium arsenite and statins could be efficient inducers of apoptosis in some melanoma cell lines, but often exhibited only modest proapoptotic activity in others, due to numerous protective mechanisms. We demonstrated in the present study that treatment by sodium arsenite or statins with an additional inhibition of HO-1 expression (or activation) caused a substantial upregulation of apoptosis in melanoma cells. Sodium arsenite- or statin-induced apoptosis was independent of BRAF status (wild type versus V600E) in melanoma lines. Monotreatment required high doses of statins (20–40 μM) for effective induction of apoptosis. As an alternative approach, pretreatment of melanoma cells with statin at decreased doses (5–20 μM) dramatically enhanced TRAIL-induced apoptosis, due to suppression of the NF-κB and STAT3-transcriptional targets (including COX-2) and downregulation of cFLIP-L (a caspase-8 inhibitor) protein levels. Furthermore, combined treatment with sodium arsenite and TRAIL or simvastatin and TRAIL efficiently induced apoptotic commitment in human neuroblastoma cells. In summary, our findings on enhancing effects of combined treatment of cancer cells using statin and TRAIL provide the rationale for further preclinical evaluation. PMID:21910007

  19. Multiple controls affect arsenite oxidase gene expression in Herminiimonas arsenicoxydans

    Directory of Open Access Journals (Sweden)

    Coppée Jean-Yves

    2010-02-01

    Full Text Available Abstract Background Both the speciation and toxicity of arsenic are affected by bacterial transformations, i.e. oxidation, reduction or methylation. These transformations have a major impact on environmental contamination and more particularly on arsenic contamination of drinking water. Herminiimonas arsenicoxydans has been isolated from an arsenic- contaminated environment and has developed various mechanisms for coping with arsenic, including the oxidation of As(III to As(V as a detoxification mechanism. Results In the present study, a differential transcriptome analysis was used to identify genes, including arsenite oxidase encoding genes, involved in the response of H. arsenicoxydans to As(III. To get insight into the molecular mechanisms of this enzyme activity, a Tn5 transposon mutagenesis was performed. Transposon insertions resulting in a lack of arsenite oxidase activity disrupted aoxR and aoxS genes, showing that the aox operon transcription is regulated by the AoxRS two-component system. Remarkably, transposon insertions were also identified in rpoN coding for the alternative N sigma factor (σ54 of RNA polymerase and in dnaJ coding for the Hsp70 co-chaperone. Western blotting with anti-AoxB antibodies and quantitative RT-PCR experiments allowed us to demonstrate that the rpoN and dnaJ gene products are involved in the control of arsenite oxidase gene expression. Finally, the transcriptional start site of the aoxAB operon was determined using rapid amplification of cDNA ends (RACE and a putative -12/-24 σ54-dependent promoter motif was identified upstream of aoxAB coding sequences. Conclusion These results reveal the existence of novel molecular regulatory processes governing arsenite oxidase expression in H. arsenicoxydans. These data are summarized in a model that functionally integrates arsenite oxidation in the adaptive response to As(III in this microorganism.

  20. Constitutive arsenite oxidase expression detected in arsenic-hypertolerant Pseudomonas xanthomarina S11.

    Science.gov (United States)

    Koechler, Sandrine; Arsène-Ploetze, Florence; Brochier-Armanet, Céline; Goulhen-Chollet, Florence; Heinrich-Salmeron, Audrey; Jost, Bernard; Lièvremont, Didier; Philipps, Muriel; Plewniak, Frédéric; Bertin, Philippe N; Lett, Marie-Claire

    2015-04-01

    Pseudomonas xanthomarina S11 is an arsenite-oxidizing bacterium isolated from an arsenic-contaminated former gold mine in Salsigne, France. This bacterium showed high resistance to arsenite and was able to oxidize arsenite to arsenate at concentrations up to 42.72 mM As[III]. The genome of this strain was sequenced and revealed the presence of three ars clusters. One of them is located on a plasmid and is organized as an "arsenic island" harbouring an aio operon and genes involved in phosphorous metabolism, in addition to the ars genes. Neither the aioXRS genes nor a specific sigma-54-dependent promoter located upstream of aioBA genes, both involved in regulation of arsenite oxidase expression in other arsenite-oxidizing bacteria, could be identified in the genome. This observation is in accordance with the fact that no difference was observed in expression of arsenite oxidase in P. xanthomarina S11, whether or not the strain was grown in the presence of As[III].

  1. Development of a biosorbent for arsenite

    Energy Technology Data Exchange (ETDEWEB)

    Teixeira, Monica Cristina [Ouro Preto Univ. (UFOP), MG (Brazil). Dept. de Farmacia; Ciminelli, Virginia S.T. [Minas Gerais Univ.(UFMG), Belo Horizonte, MG (Brazil). Dept. de Engenharia Metalurgica e de Materiais

    2005-07-01

    The understanding of the interaction mechanism of arsenite with biological molecules, and more specifically the biochemical fundamentals that explain arsenic toxicity, was applied to the development of a bio material capable of selectively removing As (III) from aqueous environments. The results of this original approach to the treatment of arsenic-containing solution demonstrated that a cysteine-rich biomass - a residue from the poultry industry - was highly selective for arsenic removal in its trivalent form, and advantage over the conventional techniques for As uptake, which usually require a previous oxidation stage. Arsenic uptake reaches values of up to 270 {mu}mol As (III){sub I}g of biomass. The observed selectivity towards As(III) was explained by the adsorption mechanism. (author)

  2. Arsenite exposure accelerates aging process regulated by the transcription factor DAF-16/FOXO in Caenorhabditis elegans.

    Science.gov (United States)

    Yu, Chan-Wei; How, Chun Ming; Liao, Vivian Hsiu-Chuan

    2016-05-01

    Arsenic is a known human carcinogen and high levels of arsenic contamination in food, soils, water, and air are of toxicology concerns. Nowadays, arsenic is still a contaminant of emerging interest, yet the effects of arsenic on aging process have received little attention. In this study, we investigated the effects and the underlying mechanisms of chronic arsenite exposure on the aging process in Caenorhabditis elegans. The results showed that prolonged arsenite exposure caused significantly decreased lifespan compared to non-exposed ones. In addition, arsenite exposure (100 μM) caused significant changes of age-dependent biomarkers, including a decrease of defecation frequency, accumulations of intestinal lipofuscin and lipid peroxidation in an age-dependent manner in C. elegans. Further evidence revealed that intracellular reactive oxygen species (ROS) level was significantly increased in an age-dependent manner upon 100 μM arsenite exposure. Moreover, the mRNA levels of transcriptional makers of aging (hsp-16.1, hsp-16.49, and hsp-70) were increased in aged worms under arsenite exposure (100 μM). Finally, we showed that daf-16 mutant worms were more sensitive to arsenite exposure (100 μM) on lifespan and failed to induce the expression of its target gene sod-3 in aged daf-16 mutant under arsenite exposure (100 μM). Our study demonstrated that chronic arsenite exposure resulted in accelerated aging process in C. elegans. The overproduction of intracellular ROS and the transcription factor DAF-16/FOXO play roles in mediating the accelerated aging process by arsenite exposure in C. elegans. This study implicates a potential ecotoxicological and health risk of arsenic in the environment.

  3. Protective effect of arjunolic acid against arsenic-induced oxidative stress in mouse brain.

    Science.gov (United States)

    Sinha, Mahua; Manna, Prasenjit; Sil, Parames C

    2008-02-01

    Arsenic, a notoriously poisonous metalloid, is ubiquitous in the environment, and it affects nearly all organ systems of animals including humans. The present study was designed to investigate the preventive role of a triterpenoid saponin, arjunolic acid against arsenic-induced oxidative damage in murine brain. Sodium arsenite was selected as a source of arsenic for this study. The free-radical-scavenging activity and the in vivo antioxidant power of arjunolic acid were determined from its 2,2-diphenyl-1-picryl hydrazyl radical scavenging ability and ferric reducing/antioxidant power assay, respectively. Oral administration of sodium arsenite at a dose of 10 mg/kg body weight for 2 days significantly decreased the activities of antioxidant enzymes, superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase, the level of cellular metabolites, reduced glutathione, total thiols and increased the level of oxidized glutathione. In addition, it enhanced the levels of lipid peroxidation end products and protein carbonyl content. Treatment with arjunolic acid at a dose of 20 mg/kg body weight for 4 days prior to arsenic administration almost normalized above indices. Histological findings due to arsenic intoxication and arjunolic acid treatment supported the other biochemical changes in murine brains. Results of 2,2-diphenyl-1-picryl hydrazyl radical scavenging and ferric reducing/antioxidant power assays clearly showed the in vitro radical scavenging as well as the in vivo antioxidant power of arjunolic acid, respectively. The effect of a well-established antioxidant, vitamin C, has been included in the study as a positive control. Combining all, results suggest that arjunolic acid possessed the ability to ameliorate arsenic-induced oxidative insult in murine brain and is probably due to its antioxidant activity.

  4. 土壤中砷氧化菌的生理生化及转化砷特性研究%Arsenite Transformation Characteristics and Molecular Identification of Arsenic-oxidizing Bacteria Isolated from Soil

    Institute of Scientific and Technical Information of China (English)

    宋卫锋; 罗丽丽; 林梓河; 严明; 邓琪; 莫于婷

    2011-01-01

    [目的]通过外加砷源驯化肇庆市鼎湖山自然保护区土壤中细菌,研究砷氧化菌的生理生化及转化砷特性.[方法]采用富集、稀释平板、硝酸盐漫过、生理生化指标的测定等.[结果]从中分离、鉴定出具有氧化砷功能的产碱杆菌和土壤杆菌2种菌株.[结论]这2种菌株最适氧化砷温度为30℃,最适氧化砷pH为9.培养基中乳酸钠浓度对菌株氧化砷有一定的影响.%[ Objective ] Through domesticated bacteria from the applied arsenic source soil in Dinghushan Nature Reserve of Zhaoqing City,physiological,biochemical and transformation characteristics of arsenic oxide bacteria were studied. [ Method]The methods of concentration,plates serial dilution, silver nitrate overflowed, physiological characteristic were adopted. [ Result ] They were identified as alcaligenes castellani and agrobacterium conn respectively, which were able to oxidize arsenite ( As (Ⅲ) ) into arsenate ( As (Ⅴ) ). [ Conclusion ] The optimal temperature and pH were 30 ℃ and 9 respectively for two bacterial strains. In addition,sodium Lactate medium concentration had a certain impact to arsenicoxidizing.

  5. Chronic Arsenic Exposure-Induced Oxidative Stress is Mediated by Decreased Mitochondrial Biogenesis in Rat Liver.

    Science.gov (United States)

    Prakash, Chandra; Kumar, Vijay

    2016-09-01

    The present study was executed to study the effect of chronic arsenic exposure on generation of mitochondrial oxidative stress and biogenesis in rat liver. Chronic sodium arsenite treatment (25 ppm for 12 weeks) decreased mitochondrial complexes activity in rat liver. There was a decrease in mitochondrial superoxide dismutase (MnSOD) activity in arsenic-treated rats that might be responsible for increased protein and lipid oxidation as observed in our study. The messenger RNA (mRNA) expression of mitochondrial and nuclear-encoded subunits of complexes I (ND1 and ND2) and IV (COX I and COX IV) was downregulated in arsenic-treated rats only. The protein and mRNA expression of MnSOD was reduced suggesting increased mitochondrial oxidative damage after arsenic treatment. There was activation of Bax and caspase-3 followed by release of cytochrome c from mitochondria suggesting induction of apoptotic pathway under oxidative stress. The entire phenomenon was associated with decrease in mitochondrial biogenesis as evident by decreased protein and mRNA expression of nuclear respiratory factor 1 (NRF-1), nuclear respiratory factor 2 (NRF-2), peroxisome proliferator activator receptor gamma-coactivator 1α (PGC-1α), and mitochondrial transcription factor A (Tfam) in arsenic-treated rat liver. The results of the present study indicate that arsenic-induced mitochondrial oxidative stress is associated with decreased mitochondrial biogenesis in rat liver that may present one of the mechanisms for arsenic-induced hepatotoxicity.

  6. Anaerobic arsenite oxidation with an electrode serving as the sole electron acceptor: A novel approach to the bioremediation of arsenic-polluted groundwater

    Energy Technology Data Exchange (ETDEWEB)

    Pous, Narcis [Laboratory of Chemical and Environmental Engineering (LEQUiA), Institute of the Environment, University of Girona, C/Maria Aurèlia Capmany, 69 E-17071 Girona (Spain); Casentini, Barbara; Rossetti, Simona; Fazi, Stefano [Water Research Institute (IRSA-CNR), National Research Council, Via Salaria Km 29.300, 00015 Monterotondo (Italy); Puig, Sebastià [Laboratory of Chemical and Environmental Engineering (LEQUiA), Institute of the Environment, University of Girona, C/Maria Aurèlia Capmany, 69 E-17071 Girona (Spain); Aulenta, Federico, E-mail: aulenta@irsa.cnr.it [Water Research Institute (IRSA-CNR), National Research Council, Via Salaria Km 29.300, 00015 Monterotondo (Italy)

    2015-02-11

    Highlights: • As(III) was oxidized to As(V) in a bioelectrochemical system. • A polarized graphite electrode served as electron acceptor. • Gammaproteobacteria were the dominating organisms at the electrode. - Abstract: Arsenic contamination of soil and groundwater is a serious problem worldwide. Here we show that anaerobic oxidation of As(III) to As(V), a form which is more extensively and stably adsorbed onto metal-oxides, can be achieved by using a polarized (+497 mV vs. SHE) graphite anode serving as terminal electron acceptor in the microbial metabolism. The characterization of the microbial populations at the electrode, by using in situ detection methods, revealed the predominance of gammaproteobacteria. In principle, the proposed bioelectrochemical oxidation process would make it possible to provide As(III)-oxidizing microorganisms with a virtually unlimited, low-cost and low-maintenance electron acceptor as well as with a physical support for microbial attachment.

  7. Sorption of Arsenite onto Mackinawite Coated Sand

    Science.gov (United States)

    Gallegos, T. J.; Hayes, K. F.; Abriola, L. M.

    2004-05-01

    Arsenic contamination of groundwater is a widespread problem affecting aquifers in the United States as well as abroad. Recent strengthening of the US EPA MCL for arsenic has prompted the need for technology capable of removing both arsenite and arsenate from solution. Arsenite, the more toxic form of arsenic, is more difficult to remove from anoxic zones in the subsurface. Studies by others have demonstrated the affinity of some types of iron sulfides for arsenite, such as troilite, pyrite, amorphous iron sulfide and mackinawite. However, these studies have not provided a comprehensive investigation of the macroscopic behavior of arsenite in the presence of crystalline mackinawite in a form that can be readily applied to real-world treatment technologies. This study examines the behavior of arsenite in the presence of mackinawite coated sand. PH edge results demonstrate that arsenite sorption onto mackinawite coated sand increases with increasing pH, reaching maximum removal at pH 10. Arsenite removal, albeit slight, occurring below pH 5 is independent of pH indicative of a different removal mechanism. Isotherm studies show that at low concentrations, removal is Langmuirian in nature. Arsenite sorption abruptly converts to linear behavior at high concentrations, possibly attributed to the saturation of the monolayer. Ionic strength effects were assessed by comparing pH edge data developed for three different concentrations of NaCl background electrolyte solution. Increases in ionic strength enhance the removal of arsenite from solution, suggesting possible inner-sphere surface complexation removal mechanisms. Information gathered in this study can be used to further develop surface complexation models to describe and predict reactivity of arsenite in the presence of mackinawite coated sands in anoxic regions. Mackinawite coated sands investigated here may provide a feasible reactive medium for implementation in above-ground sorption reactors or subsurface

  8. Protection of arsenic-induced testicular oxidative stress by arjunolic acid.

    Science.gov (United States)

    Manna, Prasenjit; Sinha, Mahua; Sil, Parames C

    2008-01-01

    Arsenic-induced tissue damage is a major concern to the human population. An impaired antioxidant defense mechanism followed by oxidative stress is the major cause of arsenic-induced toxicity, which can lead to reproductive failure. The present study was carried out to investigate the preventive role of arjunolic acid, a triterpenoid saponin isolated from the bark of Terminalia arjuna, against arsenic-induced testicular damage in mice. Administration of arsenic (in the form of sodium arsenite, NaAsO(2), at a dose of 10 mg/kg body weight) for 2 days significantly decreased the intracellular antioxidant power, the activities of the antioxidant enzymes, as well as the levels of cellular metabolites. In addition, arsenic intoxication enhanced testicular arsenic content, lipid peroxidation, protein carbonylation and the level of glutathione disulfide (GSSG). Exposure to arsenic also caused significant degeneration of the seminiferous tubules with necrosis and defoliation of spermatocytes. Pretreatment with arjunolic acid at a dose of 20 mg/kg body weight for 4 days could prevent the arsenic-induced testicular oxidative stress and injury to the histological structures of the testes. Arjunolic acid had free radical scavenging activity in a cell-free system and antioxidant power in vivo. In summary, the results suggest that the chemopreventive role of arjunolic acid against arsenic-induced testicular toxicity may be due to its intrinsic antioxidant property.

  9. Effects of cultivation conditions on the uptake of arsenite and arsenic chemical species accumulated by Pteris vittata in hydroponics.

    Science.gov (United States)

    Hatayama, Masayoshi; Sato, Takahiko; Shinoda, Kozo; Inoue, Chihiro

    2011-03-01

    The physiological responses of the arsenic-hyperaccumulator, Pteris vittata, such as arsenic uptake and chemical transformation in the fern, have been investigated. However, a few questions remain regarding arsenic treatment in hydroponics. Incubation conditions such as aeration, arsenic concentration, and incubation period might affect those responses of P. vittata in hydroponics. Arsenite uptake was low under anaerobic conditions, as previously reported. However, in an arsenite uptake experiment, phosphorous (P) starvation-dependent uptake of arsenate was observed under aerobic conditions. Time course-dependent analysis of arsenite oxidation showed that arsenite was gradually oxidized to arsenate during incubation. Arsenite oxidation was not observed in any of the control conditions, such as exposure to a nutrient solution or to culture medium only, or with the use of dried root; arsenite oxidation was only observed when live root was used. This result suggests that sufficient aeration allows the rhizosphere system to oxidize arsenite and enables the fern to efficiently take up arsenite as arsenate. X-ray absorption near edge structure (XANES) analyses showed that long-duration exposure to arsenic using a hydroponic system led to the accumulation of arsenate as the dominant species in the root tips, but not in the whole roots, partly because up-regulation of arsenate uptake by P starvation of the fern was caused and retained by long-time incubation. Analysis of concentration-dependent arsenate uptake by P. vittata showed that the uptake switched from a high-affinity transport system to a low-affinity system at high arsenate concentrations, which partially explains the increased arsenate abundance in the whole root. Copyright © 2010 The Society for Biotechnology, Japan. Published by Elsevier B.V. All rights reserved.

  10. Effect of Sodium Arsenite Dose Administered in the Drinking Water on the Urinary Bladder Epithelium of Female Arsenic (+3 oxidation state) Methyltransferase Knockout Mice

    Science.gov (United States)

    The enzyme arsenic (+3 oxidation state) methyltransferase (As3mt) catalyzes reactions converting inorganic arsenic to methylated metabolites, some of which are highly cytotoxic. In a previous study, we evaluated whether the As3mt null genotype in mice modified cytotoxic and proli...

  11. Sodium arsenite down-regulates the expression of X-linked inhibitor of apoptosis protein via translational and post-translational mechanisms in hepatocellular carcinoma

    Energy Technology Data Exchange (ETDEWEB)

    Chen, Hong; Hao, Yuqing; Wang, Lijing; Jia, Dongwei [Gene Research Center, Shanghai Medical College, Fudan University, Shanghai 200032 (China); Ruan, Yuanyuan, E-mail: yuanyuanruan@fudan.edu.cn [Gene Research Center, Shanghai Medical College, Fudan University, Shanghai 200032 (China); Gu, Jianxin [Gene Research Center, Shanghai Medical College, Fudan University, Shanghai 200032 (China)

    2012-06-15

    Highlights: Black-Right-Pointing-Pointer Sodium arsenite down-regulates the protein expression level of XIAP in HCC. Black-Right-Pointing-Pointer Sodium arsenite inhibits the de novo XIAP synthesis and its IRES activity. Black-Right-Pointing-Pointer Sodium arsenite decreases XIAP stability and promotes its proteasomal degradation. Black-Right-Pointing-Pointer Overexpression of XIAP attenuates the pro-apoptotic effect of sodium arsenite. -- Abstract: X-linked inhibitor of apoptosis protein (XIAP) is a member of the inhibitors of apoptosis protein (IAP) family, and has been reported to exhibit elevated expression levels in hepatocellular carcinoma (HCC) and promote cell survival, metastasis and tumor recurrence. Targeting XIAP has proven effective for the inhibition of cancer cell proliferation and restoration of cancer cell chemosensitivity. Arsenic (or sodium arsenite) is a potent anti-tumor agent used to treat patients with acute promyelocytic leukemia (APL). Additionally, arsenic induces cell growth inhibition, cell cycle arrest and apoptosis in human HCC cells. In this study, we identified XIAP as a target for sodium arsenite-induced cytotoxicity in HCC. The exposure of HCC cell lines to sodium arsenite resulted in inhibition of XIAP expression in both a dose- and time-dependent manner. Sodium arsenite blocked the de novo XIAP synthesis and the activity of its internal ribosome entry site (IRES) element. Moreover, treatment with sodium arsenite decreased the protein stability of XIAP and induced its ubiquitin-proteasomal degradation. Overexpression of XIAP attenuated the pro-apoptotic effect of sodium arsenite in HCC. Taken together, our data demonstrate that sodium arsenite suppresses XIAP expression via translational and post-translational mechanisms in HCC.

  12. Protective effect of nitric oxide against arsenic-induced oxidative ...

    African Journals Online (AJOL)

    STORAGESEVER

    2010-03-15

    Mar 15, 2010 ... alleviating arsenic-induced oxidative damage in tall fescue leaves were investigated. Arsenic (25 ... and it is distributed widely in natural environment. It occurred in a ... fertilizers, pesticides and sewage (Roberto et al., 2002).

  13. Arsenite evokes IL-6 secretion, autocrine regulation of STAT3 signaling, and miR-21 expression, processes involved in the EMT and malignant transformation of human bronchial epithelial cells

    Energy Technology Data Exchange (ETDEWEB)

    Luo, Fei; Xu, Yuan [Institute of Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China); The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China); Ling, Min [Jiangsu Center for Disease Control and Prevention, Nanjing 211166, Jiangsu (China); Zhao, Yue; Xu, Wenchao [Institute of Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China); The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China); Liang, Xiao [Mental Health Center of Xuhui-CDC, Shanghai 200232 (China); Jiang, Rongrong; Wang, Bairu [Institute of Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China); The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China); Bian, Qian [Jiangsu Center for Disease Control and Prevention, Nanjing 211166, Jiangsu (China); Liu, Qizhan, E-mail: drqzliu@hotmail.com [Institute of Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China); The Key Laboratory of Modern Toxicology, Ministry of Education, School of Public Health, Nanjing Medical University (China)

    2013-11-15

    Arsenite is an established human carcinogen, and arsenite-induced inflammation contributes to malignant transformation of cells, but the molecular mechanisms by which cancers are produced remain to be established. The present results showed that, evoked by arsenite, secretion of interleukin-6 (IL-6), a pro-inflammatory cytokine, led to the activation of STAT3, a transcription activator, and to increased levels of a microRNA, miR-21. Blocking IL-6 with anti-IL-6 antibody and inhibiting STAT3 activation reduced miR-21 expression. For human bronchial epithelial cells, cultured in the presence of anti-IL-6 antibody for 3 days, the arsenite-induced EMT and malignant transformation were reversed. Thus, IL-6, acting on STAT3 signaling, which up-regulates miR-21in an autocrine manner, contributes to the EMT induced by arsenite. These data define a link from inflammation to EMT in the arsenite-induced malignant transformation of HBE cells. This link, mediated through miRNAs, establishes a mechanism for arsenite-induced lung carcinogenesis. - Highlights: • Arsenite evokes IL-6 secretion. • IL-6 autocrine mediates STAT3 signaling and up-regulates miR-21expression. • Inflammation is involved in arsenite-induced EMT.

  14. Lipid oxidation induced oxidative degradation of cereal beta-glucan.

    Science.gov (United States)

    Wang, Yu-Jie; Mäkelä, Noora; Maina, Ndegwa Henry; Lampi, Anna-Maija; Sontag-Strohm, Tuula

    2016-04-15

    In food systems, lipid oxidation can cause oxidation of other molecules. This research for the first time investigated oxidative degradation of β-glucan induced by lipid oxidation using an oil-in-water emulsion system which simulated a multi-phased aqueous food system containing oil and β-glucan. Lipid oxidation was monitored using peroxide value and hexanal production while β-glucan degradation was evaluated by viscosity and molecular weight measurements. The study showed that while lipid oxidation proceeded, β-glucan degradation occurred. Emulsions containing β-glucan, oil and ferrous ion showed significant viscosity and molecular weight decrease after 1 week of oxidation at room temperature. Elevated temperature (40°C) enhanced the oxidation reactions causing higher viscosity drop. In addition, the presence of β-glucan appeared to retard the hexanal production in lipid oxidation. The study revealed that lipid oxidation may induce the degradation of β-glucan in aqueous food systems where β-glucan and lipids co-exist.

  15. Effects of oxidative and thermal stresses on stress granule formation in human induced pluripotent stem cells.

    Science.gov (United States)

    Palangi, Freshteh; Samuel, Samson M; Thompson, I Richard; Triggle, Chris R; Emara, Mohamed M

    2017-01-01

    Stress Granules (SGs) are dynamic ribonucleoprotein aggregates, which have been observed in cells subjected to environmental stresses, such as oxidative stress and heat shock (HS). Although pluripotent stem cells (PSCs) are highly sensitive to oxidative stress, the role of SGs in regulating PSC self-renewal and differentiation has not been fully elucidated. Here we found that sodium arsenite (SA) and HS, but not hydrogen peroxide (H2O2), induce SG formation in human induced (hi) PSCs. Particularly, we found that these granules contain the well-known SG proteins (G3BP, TIAR, eIF4E, eIF4A, eIF3B, eIF4G, and PABP), were found in juxtaposition to processing bodies (PBs), and were disassembled after the removal of the stress. Moreover, we showed that SA and HS, but not H2O2, promote eIF2α phosphorylation in hiPSCs forming SGs. Analysis of pluripotent protein expression showed that HS significantly reduced all tested markers (OCT4, SOX2, NANOG, KLF4, L1TD1, and LIN28A), while SA selectively reduced the expression levels of NANOG and L1TD1. Finally, in addition to LIN28A and L1TD1, we identified DPPA5 (pluripotent protein marker) as a novel component of SGs. Collectively, these results provide new insights into the molecular cues of hiPSCs responses to environmental insults.

  16. Label-free signal-on aptasensor for sensitive electrochemical detection of arsenite.

    Science.gov (United States)

    Cui, Lin; Wu, Jie; Ju, Huangxian

    2016-05-15

    A signal-on aptasensor was fabricated for highly sensitive and selective electrochemical detection of arsenite with a label-free Ars-3 aptamer self-assembled on a screen-printed carbon electrode (SPCE) via Au-S bond. The Ars-3 aptamer could adsorb cationic polydiallyldimethylammonium (PDDA) via electrostatic interaction to repel other cationic species. In the presence of arsenite, the change of Ars-3 conformation due to the formation of Ars-3/arsenite complex led to less adsorption of PDDA, and the complex could adsorb more positively charged [Ru(NH3)6](3+) as an electrochemically active indicator on the aptasensor surface, which produced a sensitive "turn-on" response. The target-induced structure switching could be used for sensitive detection of arsenite with a linear range from 0.2 nM to 100 nM and a detection limit down to 0.15 nM. Benefiting from Ars-3 aptamer, the proposed system exhibited excellent specificity against other heavy metal ions. The SPCE-based aptasensor exhibited the advantages of low cost and simple fabrication, providing potential application of arsenite detection in environment.

  17. Isolation and characterization of arsenite oxidizing Pseudomonas ...

    African Journals Online (AJOL)

    STORAGESEVER

    2010-03-08

    Mar 8, 2010 ... African Journal of Biotechnology Vol. 9(10), pp. 1493-1498, 8 .... Industrial wastewater samples were collected in screw capped sterilized bottles from .... similarity), Pseudomonas alcaliphila strain Q1-3 EU. 144361.1 (gi/ ...

  18. Inducible nitric oxide synthase in renal transplantation

    NARCIS (Netherlands)

    Joles, JA; Vos, IH; Grone, HJ; Rabelink, TJ

    2002-01-01

    The importance of the endothelial isoform of nitric oxide synthase (eNOS) has been well established. Endothelium-derived nitric oxide has been shown to be essential for vascular homeostasis and modulation of eNOS has thus become a target in prevention of cardiovascular disease. The role of the induc

  19. Drug-Induced Oxidative Stress and Toxicity

    Directory of Open Access Journals (Sweden)

    Damian G. Deavall

    2012-01-01

    Full Text Available Reactive oxygen species (ROS are a byproduct of normal metabolism and have roles in cell signaling and homeostasis. Species include oxygen radicals and reactive nonradicals. Mechanisms exist that regulate cellular levels of ROS, as their reactive nature may otherwise cause damage to key cellular components including DNA, protein, and lipid. When the cellular antioxidant capacity is exceeded, oxidative stress can result. Pleiotropic deleterious effects of oxidative stress are observed in numerous disease states and are also implicated in a variety of drug-induced toxicities. In this paper, we examine the nature of ROS-induced damage on key cellular targets of oxidative stress. We also review evidence implicating ROS in clinically relevant, drug-related side effects including doxorubicin-induced cardiac damage, azidothymidine-induced myopathy, and cisplatin-induced ototoxicity.

  20. Oxidants and antioxidants relevance in rats' pulmonary induced oxidative stress

    Science.gov (United States)

    Zamfir, C; Eloaie Zugun, F; Cojocaru, E; Tocan, L

    2011-01-01

    Introduction: Even if the reactive oxygen species were discovered, described and detailed a long time ago, there is still little data about the mechanisms of oxidative stress, their tissular effects and about an efficient antioxidant strategy, involving animal experimental models. It has been shown that the lung is one of the most exposed organs to the oxidative stress. The particular effects of different types of oxidative stress on lungs were investigated in this experimental study, in order to quantify the intensity and the extent of the pulmonary damage, featuring the antioxidant enzymatic protective role. Methods: The study of lung injury was performed on four distinct groups of Wistar rats: a control group versus a group exposed to continuous light deprivation versus a group exposed to nitrofurantoin versus a group exposed to continuous light deprivation, to nitrofurantoin and vitamin C. Pulmonary samples were taken and treated for microscopic analysis. A qualitative immunohistochemical estimation of pulmonary superoxide dismutase 1(SOD 1) was performed. Blood tests were used in order to reveal the presence and intensity of oxidative stress. Results: Continuous light deprivation and the chronic administration of nitrofurantoin acted as oxidants with a certain involvement in lung damage– vascular and alveolar wall disturbances. Adding an antioxidant, such as vitamin C, considerably improved lung reactivity to oxidative stress. Conclusion: The chronic exposure to oxidants in the induced oxidative stress sustains the development of specific lung alterations. SOD 1 positive reaction underlines the complex enzymatic defense in oxidative stress. PMID:22567046

  1. Safrole oxide inhibits angiogenesis by inducing apoptosis.

    Science.gov (United States)

    Zhao, Jing; Miao, Junying; Zhao, Baoxiang; Zhang, Shangli; Yin, Deling

    2005-06-01

    Our previous studies indicate that 3, 4-(methylenedioxy)-1-(2', 3'-epoxypropyl)-benzene (safrole oxide), a newly synthesized compound, induces apoptosis in vascular endothelial cells (VECs) and A549 lung cancer cells. To our knowledge, the inhibition of angiogenesis by safrole oxide has not been reported yet. We report here that cultured rat aorta treated with safrole oxide exhibited a significant microvessel reduction as determined by counting the number of microvessels in a phase contrast microscope. There were more microvessels formed in the presence of A549 lung cancer cells in rat aorta model, while a dramatic inhibition of angiogenesis was obtained by adding 220-450 micromol l(-1) of safrole oxide to the growth medium (Psafrole oxide produced only some abortive endothelial cells but not microvessels. Furthermore, safrole oxide induced antiangiogenic effect in the chorioallantoic membranes (CAM) as a dose dependent manner. Eggs treated with 2-11 micromol 100 microl(-1) per egg of the safrole oxide for 48 h exhibited a significant reduction in blood vessel area of the CAM, a process likely mediated by apoptosis as demonstrated by DNA fragmentation. Our results suggest that safrole oxide has antiangiogenic activity and this effect might occur by induction of cellular apoptosis.

  2. Arsenite release on enzymic transformation of arsonomethyl substrate analogues: a potentially lethal synthesis by glycerol-3-phosphate dehydrogenase.

    Science.gov (United States)

    Mutenda, E K; Sparkes, M J; Dixon, H B

    1995-09-15

    The isosteric arsenical analogue of glycerol 3-phosphate, 3,4-dihydroxybutylarsonic acid, is a good substrate for rabbit muscle glycerol-3-phosphate dehydrogenase. Its oxidation is accompanied by release of arsenite. This release seems to be due to a spontaneous elimination of arsenite by 3-oxoalkylarsonic acids, as it is also observed in (1) the oxidation of 3-hydroxypropylarsonic acid by yeast alcohol dehydrogenase, (2) treatment of 3,4-dihydroxybutylarsonic acid with periodate and (3) nonenzymic transamination of the glutamate analogue 2-amino-4-arsonobutyric acid. Enzymic formation of 3-oxoalkylarsonic acids in cells can therefore be lethal, as arsenite is poisonous to most organisms because of its high affinity for dithiols such as dihydrolipoyl groups.

  3. Diabetic Cardiovascular Disease Induced by Oxidative Stress

    Directory of Open Access Journals (Sweden)

    Yosuke Kayama

    2015-10-01

    Full Text Available Cardiovascular disease (CVD is the leading cause of morbidity and mortality among patients with diabetes mellitus (DM. DM can lead to multiple cardiovascular complications, including coronary artery disease (CAD, cardiac hypertrophy, and heart failure (HF. HF represents one of the most common causes of death in patients with DM and results from DM-induced CAD and diabetic cardiomyopathy. Oxidative stress is closely associated with the pathogenesis of DM and results from overproduction of reactive oxygen species (ROS. ROS overproduction is associated with hyperglycemia and metabolic disorders, such as impaired antioxidant function in conjunction with impaired antioxidant activity. Long-term exposure to oxidative stress in DM induces chronic inflammation and fibrosis in a range of tissues, leading to formation and progression of disease states in these tissues. Indeed, markers for oxidative stress are overexpressed in patients with DM, suggesting that increased ROS may be primarily responsible for the development of diabetic complications. Therefore, an understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of diabetes-induced CVD. The current review focuses on the relationship between diabetes-induced CVD and oxidative stress, while highlighting the latest insights into this relationship from findings on diabetic heart and vascular disease.

  4. Diabetic Cardiovascular Disease Induced by Oxidative Stress.

    Science.gov (United States)

    Kayama, Yosuke; Raaz, Uwe; Jagger, Ann; Adam, Matti; Schellinger, Isabel N; Sakamoto, Masaya; Suzuki, Hirofumi; Toyama, Kensuke; Spin, Joshua M; Tsao, Philip S

    2015-10-23

    Cardiovascular disease (CVD) is the leading cause of morbidity and mortality among patients with diabetes mellitus (DM). DM can lead to multiple cardiovascular complications, including coronary artery disease (CAD), cardiac hypertrophy, and heart failure (HF). HF represents one of the most common causes of death in patients with DM and results from DM-induced CAD and diabetic cardiomyopathy. Oxidative stress is closely associated with the pathogenesis of DM and results from overproduction of reactive oxygen species (ROS). ROS overproduction is associated with hyperglycemia and metabolic disorders, such as impaired antioxidant function in conjunction with impaired antioxidant activity. Long-term exposure to oxidative stress in DM induces chronic inflammation and fibrosis in a range of tissues, leading to formation and progression of disease states in these tissues. Indeed, markers for oxidative stress are overexpressed in patients with DM, suggesting that increased ROS may be primarily responsible for the development of diabetic complications. Therefore, an understanding of the pathophysiological mechanisms mediated by oxidative stress is crucial to the prevention and treatment of diabetes-induced CVD. The current review focuses on the relationship between diabetes-induced CVD and oxidative stress, while highlighting the latest insights into this relationship from findings on diabetic heart and vascular disease.

  5. Laser induced single spot oxidation of titanium

    Energy Technology Data Exchange (ETDEWEB)

    Jwad, Tahseen, E-mail: taj355@bham.ac.uk; Deng, Sunan; Butt, Haider; Dimov, S.

    2016-11-30

    Highlights: • A new high resolution laser induced oxidation (colouring) method is proposed (single spot oxidation). • The method is applied to control oxide films thicknesses and hence colours on titanium substrates in micro-scale. • The method enable imprinting high resolution coloured image on Ti substrate. • Optical and morphological periodic surface structures are also produced by an array of oxide spots using the proposed method. • Colour coding of two colours into one field is presented. - Abstract: Titanium oxides have a wide range of applications in industry, and they can be formed on pure titanium using different methods. Laser-induced oxidation is one of the most reliable methods due to its controllability and selectivity. Colour marking is one of the main applications of the oxidation process. However, the colourizing process based on laser scanning strategies is limited by the relative large processing area in comparison to the beam size. Single spot oxidation of titanium substrates is proposed in this research in order to increase the resolution of the processed area and also to address the requirements of potential new applications. The method is applied to produce oxide films with different thicknesses and hence colours on titanium substrates. High resolution colour image is imprinted on a sheet of pure titanium by converting its pixels’ colours into laser parameter settings. Optical and morphological periodic surface structures are also produced by an array of oxide spots and then analysed. Two colours have been coded into one field and the dependencies of the reflected colours on incident and azimuthal angles of the light are discussed. The findings are of interest to a range of application areas, as they can be used to imprint optical devices such as diffusers and Fresnel lenses on metallic surfaces as well as for colour marking.

  6. Acetylation and methylation patterns of core histones are modified after heat or arsenite treatment of Drosophila tissue culture cells

    OpenAIRE

    Arrigo, André-Patrick

    1983-01-01

    Exposure of Drosophilamelanogaster tissue culture cells to 37°C (heat shock) or to arsenite induces a severe deacetylation of core histones and blocks the methylation of histone H3 and H4. Heat shock induces the methylation of histone H2b. These results are discussed in view of chromatin structure and function.

  7. Induced effects of advanced oxidation processes.

    Science.gov (United States)

    Liu, Peng; Li, Chaolin; Zhao, Zhuanjun; Lu, Gang; Cui, Haibo; Zhang, Wenfang

    2014-02-07

    Hazardous organic wastes from industrial, military, and commercial activities represent one of the greatest challenges to human beings. Advanced oxidation processes (AOPs) are alternatives to the degradation of those organic wastes. However, the knowledge about the exact mechanisms of AOPs is still incomplete. Here we report a phenomenon in the AOPs: induced effects, which is a common property of combustion reaction. Through analysis EDTA oxidation processes by Fenton and UV-Fenton system, the results indicate that, just like combustion, AOPs are typical induction reactions. One most compelling example is that pre-feeding easily oxidizable organic matter can promote the oxidation of refractory organic compound when it was treated by AOPs. Connecting AOPs to combustion, it is possible to achieve some helpful enlightenment from combustion to analyze, predict and understand AOPs. In addition, we assume that maybe other oxidation reactions also have induced effects, such as corrosion, aging and passivation. Muchmore research is necessary to reveal the possibilities of induced effects in those fields.

  8. Silibinin ameliorates arsenic induced nephrotoxicity by abrogation of oxidative stress, inflammation and apoptosis in rats.

    Science.gov (United States)

    Prabu, S Milton; Muthumani, M

    2012-12-01

    Arsenic (As) is an environmental and industrial pollutant that affects various organs in human and experimental animals. Silibinin is a naturally occurring plant bioflavonoid found in the milk thistle of Silybum marianum, which has been reported to have a wide range of pharmacological properties. A body of evidence has accumulated implicating the free radical generation with subsequent oxidative stress in the biochemical and molecular mechanisms of As toxicity. Since kidney is the critical target organ of chronic As toxicity, we carried out this study to investigate the effects of silibinin on As-induced toxicity in the kidney of rats. In experimental rats, oral administration of sodium arsenite [NaAsO(2), 5 mg/(kg day)] for 4 weeks significantly induced renal damage which was evident from the increased levels of serum urea, uric acid, creatinine with a significant (p rats. Co-administration of silibinin (75 mg/kg day) along with As resulted in a reversal of As-induced biochemical changes in kidney accompanied by a significant decrease in lipid peroxidation and an increase in the level of renal antioxidant defense system. The histopathological and immunohistochemical studies in the kidney of rats also shows that silibinin (75 mg/kg day) markedly reduced the toxicity of As and preserved the normal histological architecture of the renal tissue, inhibited the caspase-3 mediated tubular cell apoptosis and decreased the NADPH oxidase, iNOS and NF-κB over expression by As and upregulated the Nrf2 expression in the renal tissue. The present study suggests that the nephroprotective potential of silibinin in As toxicity might be due to its antioxidant and metal chelating properties, which could be useful for achieving optimum effects in As-induced renal damage.

  9. Arsenite Sorption by Drinking-Water Treatment Residuals: Redox Effects

    Science.gov (United States)

    Makris, K. C.; Sarkar, D.; Datta, R.

    2005-05-01

    Arsenic (As) is a major human carcinogen and could pose a serious human health risk at concentrations as low as 50 ppb in drinking water. Elevated As concentrations in soils currently used for residential purposes (located on former agricultural lands amended with arsenical pesticides) have increased the possibility of human contact with soil-As. Studies have shown that As bioavailability in the environment is primarily a function of its chemical speciation, which depends upon the redox potential. Arsenic toxicity and carcinogenicity to living organisms is primarily due to exposure to the reduced species of As - arsenite, i.e., As(III), rather than the oxidized species - arsenate, i.e., As(V); the mobility of As(III) is much higher than As(V). One of the most promising methods to decrease the mobility of arsenite in the soil-water system is promoting its retention onto amorphous Fe/Al hydroxides. Drinking-Water Treatment Residuals (WTRs) are an inexpensive source of such Fe/Al hydroxides, which can be land-applied following the USEPA-regulated biosolids application rules. The WTRs are byproducts of drinking-water purification processes and generally contain sediment, organic carbon, and Al/Fe hydroxides. The hydroxides are typically amorphous and have tremendous affinity for oxyanions (e.g., arsenate). Preliminary work showed that WTRs are characterized by large internal surface area and porosity that partly explains their high affinity for As(V). The current study examines the potential of two WTRs (Fe-based and Al-based) to adsorb arsenite from solution. We hypothesize that As(III) adsorption onto the Fe-based WTR (whose stability is highly redox-sensitive) would be vastly different from the adsorption of As(III) onto the redox-insensitive Al-based WTR. Our main objective is to characterize As(III) sorption by both Fe- and Al-based WTRs by changing critical factors, such as the solid:solution ratio, contact time, and initial As(III) load. Results from this study

  10. Short-term exposure of arsenite disrupted thyroid endocrine system and altered gene transcription in the HPT axis in zebrafish.

    Science.gov (United States)

    Sun, Hong-Jie; Li, Hong-Bo; Xiang, Ping; Zhang, Xiaowei; Ma, Lena Q

    2015-10-01

    Arsenic (As) pollution in aquatic environment may adversely impact fish health by disrupting their thyroid hormone homeostasis. In this study, we explored the effect of short-term exposure of arsenite (AsIII) on thyroid endocrine system in zebrafish. We measured As concentrations, As speciation, and thyroid hormone thyroxine levels in whole zebrafish, oxidative stress (H2O2) and damage (MDA) in the liver, and gene transcription in hypothalamic-pituitary-thyroid (HPT) axis in the brain and liver tissues of zebrafish after exposing to different AsIII concentrations for 48 h. Result indicated that exposure to AsIII increased inorganic As in zebrafish to 0.46-0.72 mg kg(-1), induced oxidative stress with H2O2 being increased by 1.4-2.5 times and caused oxidative damage with MDA being augmented by 1.6 times. AsIII exposure increased thyroxine levels by 1.3-1.4 times and modulated gene transcription in HPT axis. Our study showed AsIII caused oxidative damage, affected thyroid endocrine system and altered gene transcription in HPT axis in zebrafish.

  11. Laser induced single spot oxidation of titanium

    Science.gov (United States)

    Jwad, Tahseen; Deng, Sunan; Butt, Haider; Dimov, S.

    2016-11-01

    Titanium oxides have a wide range of applications in industry, and they can be formed on pure titanium using different methods. Laser-induced oxidation is one of the most reliable methods due to its controllability and selectivity. Colour marking is one of the main applications of the oxidation process. However, the colourizing process based on laser scanning strategies is limited by the relative large processing area in comparison to the beam size. Single spot oxidation of titanium substrates is proposed in this research in order to increase the resolution of the processed area and also to address the requirements of potential new applications. The method is applied to produce oxide films with different thicknesses and hence colours on titanium substrates. High resolution colour image is imprinted on a sheet of pure titanium by converting its pixels' colours into laser parameter settings. Optical and morphological periodic surface structures are also produced by an array of oxide spots and then analysed. Two colours have been coded into one field and the dependencies of the reflected colours on incident and azimuthal angles of the light are discussed. The findings are of interest to a range of application areas, as they can be used to imprint optical devices such as diffusers and Fresnel lenses on metallic surfaces as well as for colour marking.

  12. Facile Access to Graphene Oxide from Ferro-Induced Oxidation

    Science.gov (United States)

    Yu, Chao; Wang, Cai-Feng; Chen, Su

    2016-01-01

    Methods allowing the oxidation of graphite to graphene oxide (GO) are vital important for the production of graphene from GO. This oxidation reaction has mainly relied on strong acid strategy for 174 years, which circumvents issues associated with toxicity of reagent and product, complex post-treatment, high cost and waste generation. Here, we report a green route for performing this oxidization reaction via a ferro-induced strategy, with use of water, potassium ferrate (Fe(VI)) and hydrogen peroxide (H2O2) as reagents, to produce about 65% yield of GO (vs. 40% for Hummers’ method, the most commonly used concentrated acid strategy) and non-toxic by-products. Moreover, GO produced from this new method shows equivalent performance to those reported previously. This H2SO4-free strategy makes it possible to process graphite into GO in a safe, low-cost, time-saving, energy-efficient and eco-friendly pathway, opening a promising avenue for the large-scale production of GO and GO-based materials.

  13. Arsenite oxidase from Ralstonia sp. 22: characterization of the enzyme and its interaction with soluble cytochromes.

    Science.gov (United States)

    Lieutaud, Aurélie; van Lis, Robert; Duval, Simon; Capowiez, Line; Muller, Daniel; Lebrun, Régine; Lignon, Sabrina; Fardeau, Marie-Laure; Lett, Marie-Claire; Nitschke, Wolfgang; Schoepp-Cothenet, Barbara

    2010-07-02

    We characterized the aro arsenite oxidation system in the novel strain Ralstonia sp. 22, a beta-proteobacterium isolated from soil samples of the Salsigne mine in southern France. The inducible aro system consists of a heterodimeric membrane-associated enzyme reacting with a dedicated soluble cytochrome c(554). Our biochemical results suggest that the weak association of the enzyme to the membrane probably arises from a still unknown interaction partner. Analysis of the phylogeny of the aro gene cluster revealed that it results from a lateral gene transfer from a species closely related to Achromobacter sp. SY8. This constitutes the first clear cut case of such a transfer in the Aro phylogeny. The biochemical study of the enzyme demonstrates that it can accommodate in vitro various cytochromes, two of which, c(552) and c(554,) are from the parent species. Cytochrome c(552) belongs to the sox and not the aro system. Kinetic studies furthermore established that sulfite and sulfide, substrates of the sox system, are both inhibitors of Aro activity. These results reinforce the idea that sulfur and arsenic metabolism are linked.

  14. Accumulation of heme oxygenase-1 (HSP32) in Xenopus laevis A6 kidney epithelial cells treated with sodium arsenite, cadmium chloride or proteasomal inhibitors.

    Science.gov (United States)

    Music, Ena; Khan, Saad; Khamis, Imran; Heikkila, John J

    2014-11-01

    The present study examined the effect of sodium arsenite, cadmium chloride, heat shock and the proteasomal inhibitors MG132, withaferin A and celastrol on heme oxygenase-1 (HO-1; also known as HSP32) accumulation in Xenopus laevis A6 kidney epithelial cells. Immunoblot analysis revealed that HO-1 accumulation was not induced by heat shock but was enhanced by sodium arsenite and cadmium chloride in a dose- and time-dependent fashion. Immunocytochemistry revealed that these metals induced HO-1 accumulation in a granular pattern primarily in the cytoplasm. Additionally, in 20% of the cells arsenite induced the formation of large HO-1-containing perinuclear structures. In cells recovering from sodium arsenite or cadmium chloride treatment, HO-1 accumulation initially increased to a maximum at 12h followed by a 50% reduction at 48 h. This initial increase in HO-1 levels was likely the result of new synthesis as it was inhibited by cycloheximide. Interestingly, treatment of cells with a mild heat shock enhanced HO-1 accumulation induced by low concentrations of sodium arsenite and cadmium chloride. Finally, we determined that HO-1 accumulation was induced in A6 cells by the proteasomal inhibitors, MG132, withaferin A and celastrol. An examination of heavy metal and proteasomal inhibitor-induced HO-1 accumulation in amphibians is of importance given the presence of toxic heavy metals in aquatic habitats.

  15. Effects of Arsenite Resistance on the Growth and Functional Gene Expression of Leptospirillum ferriphilum and Acidithiobacillus thiooxidans in Pure Culture and Coculture

    Directory of Open Access Journals (Sweden)

    Huidan Jiang

    2015-01-01

    Full Text Available The response of iron-oxidizing Leptospirillum ferriphilum YSK and sulfur-oxidizing Acidithiobacillus thiooxidans A01 to arsenite under pure culture and coculture was investigated based on biochemical characterization (concentration of iron ion and pH value and related gene expression. L. ferriphilum YSK and At. thiooxidans A01 in pure culture could adapt up to 400 mM and 800 mM As(III after domestication, respectively, although arsenite showed a negative effect on both strains. The coculture showed a stronger sulfur and ferrous ion oxidation activity when exposed to arsenite. In coculture, the pH value showed no significant difference when under 500 mM arsenite stress, and the cell number of At. thiooxidans was higher than that in pure culture benefiting from the interaction with L. ferriphilum. The expression profile showed that the arsenic efflux system in the coculture was more active than that in pure culture, indicating that there is a synergetic interaction between At. thiooxidans A01 and L. ferriphilum YSK. In addition, a model was proposed to illustrate the interaction between arsenite and the ars operon in L. ferriphilum YSK and At. thiooxidans A01. This study will facilitate the effective application of coculture in the bioleaching process by taking advantage of strain-strain communication and coordination.

  16. Effects of Arsenite Resistance on the Growth and Functional Gene Expression of Leptospirillum ferriphilum and Acidithiobacillus thiooxidans in Pure Culture and Coculture.

    Science.gov (United States)

    Jiang, Huidan; Liang, Yili; Yin, Huaqun; Xiao, Yunhua; Guo, Xue; Xu, Ying; Hu, Qi; Liu, Hongwei; Liu, Xueduan

    2015-01-01

    The response of iron-oxidizing Leptospirillum ferriphilum YSK and sulfur-oxidizing Acidithiobacillus thiooxidans A01 to arsenite under pure culture and coculture was investigated based on biochemical characterization (concentration of iron ion and pH value) and related gene expression. L. ferriphilum YSK and At. thiooxidans A01 in pure culture could adapt up to 400 mM and 800 mM As(III) after domestication, respectively, although arsenite showed a negative effect on both strains. The coculture showed a stronger sulfur and ferrous ion oxidation activity when exposed to arsenite. In coculture, the pH value showed no significant difference when under 500 mM arsenite stress, and the cell number of At. thiooxidans was higher than that in pure culture benefiting from the interaction with L. ferriphilum. The expression profile showed that the arsenic efflux system in the coculture was more active than that in pure culture, indicating that there is a synergetic interaction between At. thiooxidans A01 and L. ferriphilum YSK. In addition, a model was proposed to illustrate the interaction between arsenite and the ars operon in L. ferriphilum YSK and At. thiooxidans A01. This study will facilitate the effective application of coculture in the bioleaching process by taking advantage of strain-strain communication and coordination.

  17. Arsenite Regulates Prolongation of Glycan Residues of Membrane Glycoprotein: A Pivotal Study via Wax Physisorption Kinetics and FTIR Imaging

    Directory of Open Access Journals (Sweden)

    Chih-Hung Lee

    2016-03-01

    Full Text Available Arsenic exposure results in several human cancers, including those of the skin, lung, and bladder. As skin cancers are the most common form, epidermal keratinocytes (KC are the main target of arsenic exposure. The mechanisms by which arsenic induces carcinogenesis remains unclear, but aberrant cell proliferation and dysregulated energy homeostasis play a significant role. Protein glycosylation is involved in many key physiological processes, including cell proliferation and differentiation. To evaluate whether arsenite exposure affected protein glycosylation, the alteration of chain length of glycan residues in arsenite treated skin cells was estimated. Herein we demonstrated that the protein glycosylation was adenosine triphosphate (ATP-dependent and regulated by arsenite exposure by using Fourier transform infrared (FTIR reflectance spectroscopy, synchrotron-radiation-based FTIR (SR-FTIR microspectroscopy, and wax physisorption kinetics coupled with focal-plane-array-based FTIR (WPK-FPA-FTIR imaging. We were able to estimate the relative length of surface protein-linked glycan residues on arsenite-treated skin cells, including primary KC and two skin cancer cell lines, HSC-1 and HaCaT cells. Differential physisorption of wax adsorbents adhered to long-chain (elongated type and short-chain (regular type glycan residues of glycoprotein of skin cell samples treated with various concentration of arsenite was measured. The physisorption ratio of beeswax remain/n-pentacosane remain for KC cells was increased during arsenite exposure. Interestingly, this increase was reversed after oligomycin (an ATP synthase inhibitor pretreatment, suggesting the chain length of protein-linked glycan residues is likely ATP-dependent. This is the first study to demonstrate the elongation and termination of surface protein-linked glycan residues using WPK-FPA-FTIR imaging in eukaryotes. Herein the result may provide a scientific basis to target surface protein

  18. Arsenite Regulates Prolongation of Glycan Residues of Membrane Glycoprotein: A Pivotal Study via Wax Physisorption Kinetics and FTIR Imaging.

    Science.gov (United States)

    Lee, Chih-Hung; Hsu, Chia-Yen; Huang, Pei-Yu; Chen, Ching-Iue; Lee, Yao-Chang; Yu, Hsin-Su

    2016-03-22

    Arsenic exposure results in several human cancers, including those of the skin, lung, and bladder. As skin cancers are the most common form, epidermal keratinocytes (KC) are the main target of arsenic exposure. The mechanisms by which arsenic induces carcinogenesis remains unclear, but aberrant cell proliferation and dysregulated energy homeostasis play a significant role. Protein glycosylation is involved in many key physiological processes, including cell proliferation and differentiation. To evaluate whether arsenite exposure affected protein glycosylation, the alteration of chain length of glycan residues in arsenite treated skin cells was estimated. Herein we demonstrated that the protein glycosylation was adenosine triphosphate (ATP)-dependent and regulated by arsenite exposure by using Fourier transform infrared (FTIR) reflectance spectroscopy, synchrotron-radiation-based FTIR (SR-FTIR) microspectroscopy, and wax physisorption kinetics coupled with focal-plane-array-based FTIR (WPK-FPA-FTIR) imaging. We were able to estimate the relative length of surface protein-linked glycan residues on arsenite-treated skin cells, including primary KC and two skin cancer cell lines, HSC-1 and HaCaT cells. Differential physisorption of wax adsorbents adhered to long-chain (elongated type) and short-chain (regular type) glycan residues of glycoprotein of skin cell samples treated with various concentration of arsenite was measured. The physisorption ratio of beeswax remain/n-pentacosane remain for KC cells was increased during arsenite exposure. Interestingly, this increase was reversed after oligomycin (an ATP synthase inhibitor) pretreatment, suggesting the chain length of protein-linked glycan residues is likely ATP-dependent. This is the first study to demonstrate the elongation and termination of surface protein-linked glycan residues using WPK-FPA-FTIR imaging in eukaryotes. Herein the result may provide a scientific basis to target surface protein-linked glycan

  19. Voltage-induced reduction of graphene oxide

    Science.gov (United States)

    Faucett, Austin C.

    Graphene Oxide (GO) is being widely researched as a precursor for the mass production of graphene, and as a versatile material in its own right for flexible electronics, chemical sensors, and energy harvesting applications. Reduction of GO, an electrically insulating material, into reduced graphene oxide (rGO) restores electrical conductivity via removal of oxygen-containing functional groups. Here, a reduction method using an applied electrical bias, known as voltage-induced reduction, is explored. Voltage-induced reduction can be performed under ambient conditions and avoids the use of hazardous chemicals or high temperatures common with standard methods, but little is known about the reduction mechanisms and the quality of rGO produced with this method. This work performs extensive structural and electrical characterization of voltage-reduced GO (V-rGO) and shows that it is competitive with standard methods. Beyond its potential use as a facile and eco-friendly processing approach, V-rGO reduction also offers record high-resolution patterning capabilities. In this work, the spatial resolution limits of voltage-induced reduction, performed using a conductive atomic force microscope probe, are explored. It is shown that arbitrary V-rGO conductive features can be patterned into insulating GO with nanoscale resolution. The localization of voltage-induced reduction to length scales < 10 nm allows studies of reduction reaction kinetics, using electrical current obtained in-situ, with statistical robustness. Methods for patterning V-rGO nanoribbons are then developed. After presenting sub-10nm patterning of V-rGO nanoribbons in GO single sheets and films, the performance of V-rGO nanoribbon field effect transistors (FETs) are demonstrated. Preliminary measurements show an increase in electrical current on/off ratios as compared to large-area rGO FETs, indicating transport gap modulation that is possibly due to quantum confinement effects.

  20. Melamine Induces Oxidative Stress in Mouse Ovary.

    Science.gov (United States)

    Dai, Xiao-Xin; Duan, Xing; Cui, Xiang-Shun; Kim, Nam-Hyung; Xiong, Bo; Sun, Shao-Chen

    2015-01-01

    Melamine is a nitrogen heterocyclic triazine compound which is widely used as an industrial chemical. Although melamine is not considered to be acutely toxic with a high LD50 in animals, food contaminated with melamine expose risks to the human health. Melamine has been reported to be responsible for the renal impairment in mammals, its toxicity on the reproductive system, however, has not been adequately assessed. In the present study, we examined the effect of melamine on the follicle development and ovary formation. The data showed that melamine increased reactive oxygen species (ROS) levels, and induced granulosa cell apoptosis as well as follicle atresia. To further analyze the mechanism by which melamine induces oxidative stress, the expression and activities of two key antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) were analyzed, and the concentration of malondialdehyde (MDA) were compared between control and melamine-treated ovaries. The result revealed that melamine changed the expression and activities of SOD and GPX in the melamine-treated mice. Therefore, we demonstrate that melamine causes damage to the ovaries via oxidative stress pathway.

  1. Melamine Induces Oxidative Stress in Mouse Ovary.

    Directory of Open Access Journals (Sweden)

    Xiao-Xin Dai

    Full Text Available Melamine is a nitrogen heterocyclic triazine compound which is widely used as an industrial chemical. Although melamine is not considered to be acutely toxic with a high LD50 in animals, food contaminated with melamine expose risks to the human health. Melamine has been reported to be responsible for the renal impairment in mammals, its toxicity on the reproductive system, however, has not been adequately assessed. In the present study, we examined the effect of melamine on the follicle development and ovary formation. The data showed that melamine increased reactive oxygen species (ROS levels, and induced granulosa cell apoptosis as well as follicle atresia. To further analyze the mechanism by which melamine induces oxidative stress, the expression and activities of two key antioxidant enzymes superoxide dismutase (SOD and glutathione peroxidase (GPX were analyzed, and the concentration of malondialdehyde (MDA were compared between control and melamine-treated ovaries. The result revealed that melamine changed the expression and activities of SOD and GPX in the melamine-treated mice. Therefore, we demonstrate that melamine causes damage to the ovaries via oxidative stress pathway.

  2. Arsenic-induced mitochondrial oxidative damage is mediated by decreased PGC-1α expression and its downstream targets in rat brain.

    Science.gov (United States)

    Prakash, Chandra; Kumar, Vijay

    2016-08-25

    The present study was carried out to investigate the molecular mechanism of arsenic-induced mitochondrial oxidative damage and its relation to biogenesis in rat brain. Chronic sodium arsenite (25 ppm, orally) administration for 12 weeks decreased mitochondrial complexes activities and mRNA expression of selective complexes subunits. The expression of mitochondrial biogenesis regulator PGC-1α, and its downstream targets NRF-1, NRF-2 and Tfam were decreased significantly both at mRNA and protein levels suggesting impaired biogenesis following chronic arsenic-exposure. In addition to this, protein expression analysis also revealed activation of Bax and caspase-3, leading to translocation of cytochrome c from mitochondria to cytosol suggesting induction of apoptotic pathway under oxidative stress. This was further confirmed by electron microscopy study which depicted morphological changes in mitochondria in terms of altered nuclear and mitochondrial shape and chromatin condensation in arsenic-treated rats. The immunohistochemical studies showed both nuclear and cytosolic localization of NRF-1 and NRF-2 in arsenic-exposed rat brain further suggesting regulatory role of these transcription factors under arsenic neurotoxicity. The results of present study indicate that arsenic-induced mitochondrial oxidative damage is associated with decreased mitochondrial biogenesis in rat brain that may present as important target to reveal the mechanism for arsenic-induced neurotoxicity.

  3. An ArsR/SmtB family member is involved in the regulation by arsenic of the arsenite oxidase operon in Thiomonas arsenitoxydans.

    Science.gov (United States)

    Moinier, Danielle; Slyemi, Djamila; Byrne, Deborah; Lignon, Sabrina; Lebrun, Régine; Talla, Emmanuel; Bonnefoy, Violaine

    2014-10-01

    The genetic organization of the aioBA operon, encoding the arsenite oxidase of the moderately acidophilic and facultative chemoautotrophic bacterium Thiomonas arsenitoxydans, is different from that of the aioBA operon in the other arsenite oxidizers, in that it encodes AioF, a metalloprotein belonging to the ArsR/SmtB family. AioF is stabilized by arsenite, arsenate, or antimonite but not molybdate. Arsenic is tightly attached to AioF, likely by cysteine residues. When loaded with arsenite or arsenate, AioF is able to bind specifically to the regulatory region of the aio operon at two distinct positions. In Thiomonas arsenitoxydans, the promoters of aioX and aioB are convergent, suggesting that transcriptional interference occurs. These results indicate that the regulation of the aioBA operon is more complex in Thiomonas arsenitoxydans than in the other aioBA containing arsenite oxidizers and that the arsenic binding protein AioF is involved in this regulation. On the basis of these data, a model to explain the tight control of aioBA expression by arsenic in Thiomonas arsenitoxydans is proposed.

  4. Fate of arsenite and arsenate in flooded and not flooded soils of southwest Bangladesh irrigated with arsenic contaminated water.

    Science.gov (United States)

    Martin, Maria; Violante, Antonio; Barberis, Elisabetta

    2007-10-01

    In Bangladesh and West Bengal, India, tons of arsenic are added every year to wide extensions of agricultural soils after irrigation with arsenic polluted groundwater, and the fate of the added arsenic in these water-soil environments is not yet clear. This work was aimed to investigate the accumulation and potential release of arsenite [As(III)] and arsenate [As(V)] in two adjacent soils of Bangladesh, irrigated with arsenic contaminated groundwater and cultivated under flooded or not flooded conditions. Both soils showed a scarce As accumulation, in spite of a good adsorption capacity, higher for As(III) than for As(V). The poorly ordered Fe oxides dominated As adsorption in the topsoil of the flooded soil, whereas the crystalline forms were more important in the well aerated soil. A high percentage of the native arsenic was exchangeable with phosphate and the freshly added arsenate or arsenite were even much more mobile. In our experimental conditions, the high As mobility was not dependent on the surface coverage, and, in the flooded soil, 60-70% of the freshly added arsenite or arsenate were desorbed with an infinite sink method, while in the not flooded soil arsenate was less desorbed than arsenite. Depending on their characteristics, some soils, in particular when cultivated under flooded conditions, can represent only a temporary sink for the added As, that can be easily released to waters and possibly enter the food chain from the water-soil system.

  5. Arsenite in drinking water produces glucose intolerance in pregnant rats and their female offspring.

    Science.gov (United States)

    Bonaventura, María Marta; Bourguignon, Nadia Soledad; Bizzozzero, Marianne; Rodriguez, Diego; Ventura, Clara; Cocca, Claudia; Libertun, Carlos; Lux-Lantos, Victoria Adela

    2017-02-01

    Drinking water is the main source of arsenic exposure. Chronic exposure has been associated with metabolic disorders. Here we studied the effects of arsenic on glucose metabolism, in pregnant and post-partum of dams and their offspring. We administered 5 (A5) or 50 (A50) mg/L of sodium arsenite in drinking water to rats from gestational day 1 (GD1) until two months postpartum (2MPP), and to their offspring from weaning until 8 weeks old. Liver arsenic dose-dependently increased in arsenite-treated rats to levels similar to exposed population. Pregnant A50 rats gained less weight than controls and recovered normal weight at 2MPP. Arsenite-treated pregnant animals showed glucose intolerance on GD16-17, with impaired insulin secretion but normal insulin sensitivity; they showed dose-dependent increased pancreas insulin on GD18. All alterations reverted at 2MPP. Offspring from A50-treated mothers showed lower body weight at birth, 4 and 8 weeks of age, and glucose intolerance in adult females, probably due to insulin secretion and sensitivity alterations. Arsenic alters glucose homeostasis during pregnancy by altering beta-cell function, increasing risk of developing gestational diabetes. In pups, it induces low body weight from birth to 8 weeks of age, and glucose intolerance in females, demonstrating a sex specific response. Copyright © 2016 Elsevier Ltd. All rights reserved.

  6. Ion Chromatographic Estimation of Arsenite and Arsenate at Trace Level

    Directory of Open Access Journals (Sweden)

    Chetan Chavan

    2011-01-01

    Full Text Available Present method shows simple and specific determination of traces of inorganic arsenic in water. This method enables simultaneous determination of arsenite by electrochemical detection and arsenate by suppressed conductivity detection. The applicability of this method was illustrated by determining the inorganic arsenite and arsenate content from bore-well water and river water samples without any special pretreatment. The present method for direct determination of arsenite and arsenate shows good sensitivity, selectivity, precision and accuracy. Detection limits determined using this procedure was found to be 2.0 μg/L for arsenite and 30.0 μg/L for Arsenate. The simplicity, ease of use, low detection limit and low running cost of this method makes it appealing for increasing capability of testing in the lab.

  7. Industrial experiment of copper electrolyte purification by copper arsenite

    Institute of Scientific and Technical Information of China (English)

    ZHENG Ya-jie; XIAO Fa-xin; WANG Yong; LI Chun-hua; XU Wei; JIAN Hong-sheng; MA Yut-ian

    2008-01-01

    Copper electrolyte was purified by copper arsenite that was prepared with As2O3. And electrolysis experiments of purified electrolyte were carried out at 235 and 305 A/m2, respectively. The results show that the yield of copper arsenite is up to 98.64% when the molar ratio of Cu to As is 1.5 in the preparation of copper arsenite. The removal rates of Sb and Bi reach 74.11% and 65.60% respectively after copper arsenite is added in electrolyte. The concentrations of As, Sb and Bi in electrolyte nearly remain constant during electrolysis of 13 d. The appearances of cathode copper obtained at 235 and 305 A/m2 are slippery and even, and the qualification rate is 100% according to the Chinese standard of high-pure cathode copper(GB/T467-97).

  8. Inducible nitric oxide synthase mediates bone loss in ovariectomized mice.

    NARCIS (Netherlands)

    Cuzzocrea, S.; Mazzon, E.; Dugo, L.; Genovese, T.; Paola, R. Di; Ruggeri, Z.; Vegeto, E.; Caputi, A.P.; Loo, F.A.J. van de; Puzzolo, D.; Maggi, A.

    2003-01-01

    Several clinical studies have shown that bone loss may be attributed to osteoclast recruitment induced by mediators of inflammation. In different experimental paradigms we have recently demonstrated that estrogen exhibits antiinflammatory activity by preventing the induction of inducible nitric oxid

  9. Deficiencies in mitochondrial dynamics sensitize Caenorhabditis elegans to arsenite and other mitochondrial toxicants by reducing mitochondrial adaptability.

    Science.gov (United States)

    Luz, Anthony L; Godebo, Tewodros R; Smith, Latasha L; Leuthner, Tess C; Maurer, Laura L; Meyer, Joel N

    2017-07-15

    Mitochondrial fission, fusion, and mitophagy are interlinked processes that regulate mitochondrial shape, number, and size, as well as metabolic activity and stress response. The fundamental importance of these processes is evident in the fact that mutations in fission (DRP1), fusion (MFN2, OPA1), and mitophagy (PINK1, PARK2) genes can cause human disease (collectively >1/10,000). Interestingly, however, the age of onset and severity of clinical manifestations varies greatly between patients with these diseases (even those harboring identical mutations), suggesting a role for environmental factors in the development and progression of certain mitochondrial diseases. Using the model organism Caenorhabditis elegans, we screened ten mitochondrial toxicants (2, 4-dinitrophenol, acetaldehyde, acrolein, aflatoxin B1, arsenite, cadmium, cisplatin, doxycycline, paraquat, rotenone) for increased or decreased toxicity in fusion (fzo-1, eat-3)-, fission (drp-1)-, and mitophagy (pdr-1, pink-1)-deficient nematodes using a larval growth assay. In general, fusion-deficient nematodes were the most sensitive to toxicants, including aflatoxin B1, arsenite, cisplatin, paraquat, and rotenone. Because arsenite was particularly potent in fission- and fusion-deficient nematodes, and hundreds of millions of people are chronically exposed to arsenic, we investigated the effects of these genetic deficiencies on arsenic toxicity in more depth. We found that deficiencies in fission and fusion sensitized nematodes to arsenite-induced lethality throughout aging. Furthermore, low-dose arsenite, which acted in a "mitohormetic" fashion by increasing mitochondrial function (in particular, basal and maximal oxygen consumption) in wild-type nematodes by a wide range of measures, exacerbated mitochondrial dysfunction in fusion-deficient nematodes. Analysis of multiple mechanistic changes suggested that disruption of pyruvate metabolism and Krebs cycle activity underlie the observed arsenite-induced

  10. Sodium arsenite alters cell cycle and MTHFR, MT1/2, and c-Myc protein levels in MCF-7 cells.

    Science.gov (United States)

    Ruiz-Ramos, Ruben; López-Carrillo, Lizbeth; Albores, Arnulfo; Hernández-Ramírez, Raúl U; Cebrian, Mariano E

    2009-12-15

    There is limited available information on the effects of arsenic on enzymes participating in the folate cycle. Therefore, our aim was to evaluate the effects of sodium arsenite on the protein levels of methylenetetrahydrofolate reductase (MTHFR) and dihydrofolate reductase (DHFR) and its further relationship with the expression MT1/2 and c-myc in MCF-7 cells. Arsenite treatment (0-10 microM) for 4 h decreased MTHFR levels in a concentration-dependent fashion without significant effects on DHFR. The effects on MTHFR were observed at arsenite concentrations not significantly affecting cell viability. We also observed an increase in S-phase recruitment at all concentrations probed. Lower concentrations ( or =5 microM) or longer treatment periods induced apoptosis. Arsenite also induced dose-dependent increases in MT1/2 and c-Myc protein levels. The levels of MTHFR were inversely correlated to MT1/2 and c-Myc overexpression and increased S-phase recruitment. Our findings indicate that breast epithelial cells are responsive to arsenite and suggest that exposure may pose a risk for breast cancer. The reductions in MTHFR protein levels contribute to understand the mechanisms underlying the induction of genes influencing growth regulation, such as c-myc and MT1/2. However, further research is needed to ascertain if the effects here reported following short-time and high-dose exposure are relevant for human populations chronically exposed to low arsenic concentrations.

  11. Hypochlorous and peracetic acid induced oxidation of dairy proteins.

    Science.gov (United States)

    Kerkaert, Barbara; Mestdagh, Frédéric; Cucu, Tatiana; Aedo, Philip Roger; Ling, Shen Yan; De Meulenaer, Bruno

    2011-02-09

    Hypochlorous and peracetic acids, both known disinfectants in the food industry, were compared for their oxidative capacity toward dairy proteins. Whey proteins and caseins were oxidized under well controlled conditions at pH 8 as a function of the sanitizing concentration. Different markers for protein oxidation were monitored. The results established that the protein carbonyl content was a rather unspecific marker for protein oxidation, which did not allow one to differentiate the oxidant used especially at the lower concentrations. Cysteine, tryptophan, and methionine were proven to be the most vulnerable amino acids for degradation upon hypochlorous and peracetic acid treatment, while tyrosine was only prone to degradation in the presence of hypochlorous acid. Hypochlorous acid induced oxidation gave rise to protein aggregation, while during peracetic acid induced oxidation, no high molecular weight aggregates were observed. Protein aggregation upon hypochlorous acid oxidation could primarily be linked to tryptophan and tyrosine degradation.

  12. Myoglobin-induced lipid oxidation : A review

    DEFF Research Database (Denmark)

    Baron, Caroline; Andersen, H.J.

    2002-01-01

    An overview of myoglobin-initiated lipid oxidation in simple model systems, muscle, and muscle-based foods is presented. The potential role of myoglobin spin and redox states in initiating lipid oxidation is reviewed. Proposed mechanisms for myoglobin- initiated lipid oxidation in muscle tissue (p...

  13. Potential role of punicalagin against oxidative stress induced testicular damage

    Directory of Open Access Journals (Sweden)

    Faiza Rao

    2016-01-01

    Full Text Available Punicalagin is isolated from pomegranate and widely used for the treatment of different diseases in Chinese traditional medicine. This study aimed to evaluate the effect of Punicalagin (purity ≥98% on oxidative stress induced testicular damage and its effect on fertility. We detected the antioxidant potential of punicalagin in lipopolysaccharide (LPS induced oxidative stress damage in testes, also tried to uncover the boosting fertility effect of Punicalagin (PU against oxidative stress-induced infertility. Results demonstrated that 9 mg kg−1 for 7 days treatment significantly decreases LPS induced oxidative damage in testes and nitric oxide production. The administration of oxidative stress resulted in a significant reduction in testes antioxidants GSH, T-SOD, and CAT raised LPO, but treatment with punicalagin for 7 days increased antioxidant defense GSH, T-SOD, and CAT by the end of the experiment and reduced LPO level as well. PU also significantly activates Nrf2, which is involved in regulation of antioxidant defense systems. Hence, the present research categorically elucidates the protective effect of punicalagin against LPS induced oxidative stress induced perturbation in the process of spermatogenesis and significantly increased sperm health and number. Moreover, fertility success significantly decreased in LPS-injected mice compared to controls. Mice injected with LPS had fertility indices of 12.5%, while others treated with a combination of PU + LPS exhibited 75% indices. By promoting fertility and eliminating oxidative stress and inflammation, PU may be a useful nutrient for the treatment of infertility.

  14. Effect of vitamin E supplementation on arsenic induced alteration in blood biochemical profile, oxidant/antioxidant status, serum cortisol level and retention of arsenic and selenium in goats.

    Science.gov (United States)

    Mohanta, Ranjan Kumar; Garg, Anil Kumar; Dass, Ram Sharan

    2015-01-01

    Arsenic (As) exerts oxidative stress with depletion of body selenium in monogastric animals. But in ruminants this fact is not yet verified. Vitamin E is an effective dietary antioxidant. Thus, in this experiment, the protective effect of vitamin E against arsenic toxicity induced by sodium arsenite (60mg As/kg diet) was investigated in goat kids. For this, 21 male kids were divided into three equal groups and fed either basal diet as such (control), or supplemented with 60mg As/kg diet and 60mg As/kg diet+250IU vitamin E/kg diet for 180 days. Vitamin E supplementation alleviated the toxic effects caused by arsenic on serum alanine aminotransferase and aspartate aminotransferase and lipid peroxidation. It also prevented the depletion of reduced glutathione content and reduction in activity of catalase, superoxide dismutase and glutathione-s-transferase in erythrocytes resulted from arsenic intoxication. The elevated levels of arsenic and reduced levels of selenium in the serum and tissues in arsenic treated animals were attenuated by vitamin E supplementation, though not completely. However, serum cortisol level was not affected by arsenic. It was concluded that arsenic exerts cortisol independent stressor mechanism and supplementation of vitamin E at a level of 250IU/kg diet was partially effective in reducing tissue accumulation of arsenic in the body and protect the kids from oxidative stress induced by arsenic. Copyright © 2014 Elsevier GmbH. All rights reserved.

  15. Arsenite exposure compromises early embryonic development in the Golden hamster.

    Science.gov (United States)

    Unis, Dave; Osborne, Cassandra; Diawara, Moussa M

    2009-11-01

    The toxicity of arsenite to 8-cell stage hamster embryos was evaluated. Females were superovulated and mated; embryos were collected and grown for 72 h in culture medium containing vehicle control, 25, 50, 250, 500, or 750 nM arsenite. Morphological observations were taken at 0 and 24h increments. A TUNEL assay was used for determining DNA damage. Survival was expressed by the ability to undergo zona escape. The control group had 78% survival and no evidence of deformities. Embryos in the 25, 50 and 250 nM groups had survival rates of 63%, 55% and 27%, respectively. Arsenite exposure caused total embryo lethality, major deformities, complete failure to undergo zona lysis, and significantly higher number of cells with fragmented DNA in embryos at the 500 and 750 nM concentrations. The study underscores the sensitivity of preimplantation stage embryos to the presence of even relatively small amounts of arsenic in luminal fluid.

  16. Anti- and pro-oxidant effects of (+)-catechin on hemoglobin-induced protein oxidative damage.

    Science.gov (United States)

    Lu, Naihao; Chen, Puqing; Yang, Qin; Peng, Yi-Yuan

    2011-06-01

    Evidence to support the role of heme proteins as major inducers of oxidative damage is increasingly present. Flavonoids have been widely used to ameliorate oxidative damage in vivo and in vitro, where the mechanism of this therapeutic action was usually dependent on their anti-oxidant effects. In this study, we investigated the influence of (+)-catechin, a polyphenol identified in tea, cocoa, and red wine, on hemoglobin-induced protein oxidative damage. It was found that (+)-catechin had the capacities to act as a free radical scavenger and reducing agent to remove cytotoxic ferryl hemoglobin, demonstrating apparent anti-oxidant activities. However, the presence of (+)-catechin surprisingly promoted hemoglobin-induced protein oxidation, which was probably due to the ability of this anti-oxidant to rapidly trigger the oxidative degradation of normal hemoglobin. In addition, hemoglobin-H2O2-induced protein carbonyl formation was significantly enhanced by (+)-catechin at lower concentrations, while it was efficiently inhibited when higher concentrations were used. These novel results showed that the dietary intake and therapeutic use of catechins might possess pro-oxidant activity through aggravating hemoglobin-related oxidative damage. The dual effects on hemoglobin redox reactions may provide new insights into the physiological implications of tea extract and wine (catechins) with cellular heme proteins.

  17. Magnesium Oxide Induced Metabolic Alkalosis in Cattle

    OpenAIRE

    Ogilvie, T H; Butler, D G; Gartley, C J; Dohoo, I. R.

    1983-01-01

    A study was designed to compare the metabolic alkalosis produced in cattle from the use of an antacid (magnesium oxide) and a saline cathartic (magnesium sulphate). Six, mature, normal cattle were treated orally with a magnesium oxide (MgO) product and one week later given a comparable cathartic dose of magnesium sulphate (MgSO4).

  18. Acrylonitrile-induced oxidative DNA damage in rat astrocytes.

    Science.gov (United States)

    Pu, Xinzhu; Kamendulis, Lisa M; Klaunig, James E

    2006-10-01

    Chronic administration of acrylonitrile results in a dose-related increase in astrocytomas in rat brain, but the mechanism of acrylonitrile carcinogenicity is not fully understood. The potential of acrylonitrile or its metabolites to induce direct DNA damage as a mechanism for acrylonitrile carcinogenicity has been questioned, and recent studies indicate that the mechanism involves the induction of oxidative stress in rat brain. The present study examined the ability of acrylonitrile to induce DNA damage in the DI TNC1 rat astrocyte cell line using the alkaline Comet assay. Oxidized DNA damage also was evaluated using formamidopyrimidine DNA glycosylase treatment in the modified Comet assay. No increase in direct DNA damage was seen in astrocytes exposed to sublethal concentrations of acrylonitrile (0-1.0 mM) for 24 hr. However, acrylonitrile treatment resulted in a concentration-related increase in oxidative DNA damage after 24 hr. Antioxidant supplementation in the culture media (alpha-tocopherol, (-)-epigallocathechin-3 gallate, or trolox) reduced acrylonitrile-induced oxidative DNA damage. Depletion of glutathione using 0.1 mM DL-buthionine-[S,R]-sulfoximine increased acrylonitrile-induced oxidative DNA damage (22-46%), while cotreatment of acrylonitrile with 2.5 mM L-2-oxothiazolidine-4-carboxylic acid, a precursor for glutathione biosynthesis, significantly reduced acrylonitrile-induced oxidative DNA damage (7-47%). Cotreatment of acrylonitrile with 0.5 mM 1-aminobenzotriazole, a suicidal inhibitor of cytochrome P450, prevented the oxidative DNA damage produced by acrylonitrile. Cyanide (0.1-0.5 mM) increased oxidative DNA damage (44-160%) in astrocytes. These studies demonstrate that while acrylonitrile does not directly damage astrocyte DNA, it does increase oxidative DNA damage. The oxidative DNA damage following acrylonitrile exposure appears to arise mainly through the P450 metabolic pathway; moreover, glutathione depletion may contribute to the

  19. Oxidant-induced corticosteroid unresponsiveness in human bronchial epithelial cells

    NARCIS (Netherlands)

    Heijink, Irene; van Oosterhout, Antoon; Kliphuis, Nathalie; Jonker, Marnix; Hoffmann, Roland; Telenga, Eef; Klooster, Karin; Slebos, Dirk-Jan; ten Hacken, Nick; Postma, Dirkje; van den Berge, Maarten

    2014-01-01

    Background We hypothesised that increased oxidative stress, as present in the airways of asthma and chronic obstructive pulmonary disease (COPD) patients, induces epithelial damage and reduces epithelial responsiveness to suppressive effects of corticosteroids on proinflammatory cytokine production

  20. Effects of thyroid dysfunction-induced liver oxidative

    African Journals Online (AJOL)

    Unicornis

    of micronutrients such as selenium (Se) and zinc (Zn) prevented MD-induced hepatic damage. Rats ..... Acute exposure to pesticides can cause oxidative damage. The current ..... Effect of chronic intake of arsenic contaminated water on liver.

  1. Oxidant-induced corticosteroid unresponsiveness in human bronchial epithelial cells

    NARCIS (Netherlands)

    Heijink, Irene; van Oosterhout, Antoon; Kliphuis, Nathalie; Jonker, Marnix; Hoffmann, Roland; Telenga, Eef; Klooster, Karin; Slebos, Dirk-Jan; ten Hacken, Nick; Postma, Dirkje; van den Berge, Maarten

    2014-01-01

    Background We hypothesised that increased oxidative stress, as present in the airways of asthma and chronic obstructive pulmonary disease (COPD) patients, induces epithelial damage and reduces epithelial responsiveness to suppressive effects of corticosteroids on proinflammatory cytokine production

  2. Density of oxidation-induced stacking faults in damaged silicon

    NARCIS (Netherlands)

    Kuper, F.G.; Hosson, J.Th.M. De; Verwey, J.F.

    1986-01-01

    A model for the relation between density and length of oxidation-induced stacking faults on damaged silicon surfaces is proposed, based on interactions of stacking faults with dislocations and neighboring stacking faults. The model agrees with experiments.

  3. Protective Effects of Combined Selenium and Punica granatum Treatment on Some Inflammatory and Oxidative Stress Markers in Arsenic-Induced Hepatotoxicity in Rats.

    Science.gov (United States)

    Shafik, Noha M; El Batsh, Maha M

    2016-01-01

    Oxidative stress is one of the major mechanisms implicated in inorganic arsenic poisoning. Punica granatum is known by its free radical scavenging properties. The aim of this study was to evaluate the protective role of combined selenium and P. granatum against arsenic-induced liver injury. Seventy-five female albino rats were divided into five groups (of 15 rats each). Toxicity was induced by oral sodium arsenite (5.5 mg/kg body weight (bw) daily) (group ІІ). Treatment of arsenic-intoxicated rats was induced by daily oral administration of sodium selenite (3 mg/kg bw) (group ІІІ), 100 mg of P. granatum ethanol extract per kilogram body weight dissolved in 300 mL distilled water in three divided doses (100 mL of this suspension every 8 h) (group IV), and combined daily oral treatment with both selenite and P. granatum ethanol extract (group V). After 3 weeks, serum and liver tissues were obtained from the decapitated rats for different estimations. Hepatotoxicity was demonstrated by significant elevation in liver weights and activities of liver enzymes, alanine aminotransferase (ALT) and aspartate aminotransferase (AST), and decrease in serum total proteins and albumin (p hepatotoxicity led to an increased values of malondialdehyde, advanced oxidation protein products, nitric oxide, and interleukin-6 (IL-6) (p rat group treated with both P. granatum and selenium. It was concluded that combined P. granatum and selenium treatment had a synergistic hepatoprotective effect against arsenic toxicity through activation of Nrf2 anti-oxidant pathway.

  4. Altered Gravity Induces Oxidative Stress in Drosophila Melanogaster

    Science.gov (United States)

    Bhattacharya, Sharmila; Hosamani, Ravikumar

    2015-01-01

    Altered gravity environments can induce increased oxidative stress in biological systems. Microarray data from our previous spaceflight experiment (FIT experiment on STS-121) indicated significant changes in the expression of oxidative stress genes in adult fruit flies after spaceflight. Currently, our lab is focused on elucidating the role of hypergravity-induced oxidative stress and its impact on the nervous system in Drosophila melanogaster. Biochemical, molecular, and genetic approaches were combined to study this effect on the ground. Adult flies (2-3 days old) exposed to acute hypergravity (3g, for 1 hour and 2 hours) showed significantly elevated levels of Reactive Oxygen Species (ROS) in fly brains compared to control samples. This data was supported by significant changes in mRNA expression of specific oxidative stress and antioxidant defense related genes. As anticipated, a stress-resistant mutant line, Indy302, was less vulnerable to hypergravity-induced oxidative stress compared to wild-type flies. Survival curves were generated to study the combined effect of hypergravity and pro-oxidant treatment. Interestingly, many of the oxidative stress changes that were measured in flies showed sex specific differences. Collectively, our data demonstrate that altered gravity significantly induces oxidative stress in Drosophila, and that one of the organs where this effect is evident is the brain.

  5. Biotransformation of arsenite and bacterial aox activity in drinking water produced from surface water of floating houses: Arsenic contamination in Cambodia.

    Science.gov (United States)

    Chang, Jin-Soo

    2015-11-01

    The potential arsenite bioteansformation activity of arsenic was investigated by examining bacterial arsenic arsenite-oxidizing gene such as aoxS, aoxR, aoxA, aoxB, aoxC, and aoxD in high arsenic-contaminated drinking water produced from the surface water of floating houses. There is a biogeochemical cycle of activity involving arsenite oxidase aox system and the ars (arsenic resistance system) gene operon and aoxR leader gene activity in Alcaligenes faecalis SRR-11 and aoxS leader gene activity in Achromobacter xylosoxidans TSL-66. Batch experiments showed that SRR-11 and TSL-66 completely oxidized 1 mM of As (III) to As (V) within 35-40 h. The leaders of aoxS and aoxR are important for gene activity, and their effects in arsenic bioremediation and mobility in natural water has a significant ecological role because it allows arsenite oxidase in bacteria to control the biogeochemical cycle of arsenic-contaminated drinking water produced from surface water of floating houses. Copyright © 2015 Elsevier Ltd. All rights reserved.

  6. Quercitrin protects skin from UVB-induced oxidative damage

    Energy Technology Data Exchange (ETDEWEB)

    Yin, Yuanqin [Cancer Institute, The First Affiliated Hospital, China Medical University, Shenyang (China); Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Li, Wenqi; Son, Young-Ok; Sun, Lijuan; Lu, Jian; Kim, Donghern; Wang, Xin [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Yao, Hua [Department of Stomatology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, Zhejiang (China); Wang, Lei; Pratheeshkumar, Poyil; Hitron, Andrew J. [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Luo, Jia [Department of Internal Medicine, University of Kentucky, 800 Rose Street, Lexington, KY (United States); Gao, Ning [Department of Pharmacognos, College of Pharmacy, 3rd Military Medical University, Chongqing (China); Shi, Xianglin [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States); Zhang, Zhuo, E-mail: zhuo.zhang@uky.edu [Graduate Center for Toxicology, University of Kentucky, 1095 VA Drive, Lexington, KY (United States)

    2013-06-01

    Exposure of the skin to ultraviolet B (UVB) radiation causes oxidative damage to skin, resulting in sunburn, photoaging, and skin cancer. It is generally believed that the skin damage induced by UV irradiation is a consequence of generation of reactive oxygen species (ROS). Recently, there is an increased interest in the use of natural products as chemopreventive agents for non-melanoma skin cancer (NMSC) due to their antioxidants and anti-inflammatory properties. Quercitrin, glycosylated form of quercetin, is the most common flavonoid in nature with antioxidant properties. The present study investigated the possible beneficial effects of quercitrin to inhibit UVB irradiation-induced oxidative damage in vitro and in vivo. Our results showed that quercitrin decreased ROS generation induced by UVB irradiation in JB6 cells. Quercitrin restored catalase expression and GSH/GSSG ratio reduced by UVB exposure, two major antioxidant enzymes, leading to reductions of oxidative DNA damage and apoptosis and protection of the skin from inflammation caused by UVB exposure. The present study demonstrated that quercitrin functions as an antioxidant against UVB irradiation-induced oxidative damage to skin. - Highlights: • Oxidative stress plays a key role in UV-induced cell and tissue injuries. • Quercitrin decreases ROS generation and restores antioxidants irradiated by UVB. • Quercitrin reduces UVB-irradiated oxidative DNA damage, apoptosis, and inflammation. • Quercitrin functions as an antioxidant against UVB-induced skin injuries.

  7. The Respiratory Arsenite Oxidase: Structure and the Role of Residues Surrounding the Rieske Cluster

    Science.gov (United States)

    Warelow, Thomas P.; Oke, Muse; Schoepp-Cothenet, Barbara; Dahl, Jan U.; Bruselat, Nicole; Sivalingam, Ganesh N.; Leimkühler, Silke; Thalassinos, Konstantinos; Kappler, Ulrike; Naismith, James H.; Santini, Joanne M.

    2013-01-01

    The arsenite oxidase (Aio) from the facultative autotrophic Alphaproteobacterium Rhizobium sp. NT-26 is a bioenergetic enzyme involved in the oxidation of arsenite to arsenate. The enzyme from the distantly related heterotroph, Alcaligenes faecalis, which is thought to oxidise arsenite for detoxification, consists of a large α subunit (AioA) with bis-molybdopterin guanine dinucleotide at its active site and a 3Fe-4S cluster, and a small β subunit (AioB) which contains a Rieske 2Fe-2S cluster. The successful heterologous expression of the NT-26 Aio in Escherichia coli has resulted in the solution of its crystal structure. The NT-26 Aio, a heterotetramer, shares high overall similarity to the heterodimeric arsenite oxidase from A. faecalis but there are striking differences in the structure surrounding the Rieske 2Fe-2S cluster which we demonstrate explains the difference in the observed redox potentials (+225 mV vs. +130/160 mV, respectively). A combination of site-directed mutagenesis and electron paramagnetic resonance was used to explore the differences observed in the structure and redox properties of the Rieske cluster. In the NT-26 AioB the substitution of a serine (S126 in NT-26) for a threonine as in the A. faecalis AioB explains a −20 mV decrease in redox potential. The disulphide bridge in the A. faecalis AioB which is conserved in other betaproteobacterial AioB subunits and the Rieske subunit of the cytochrome bc1 complex is absent in the NT-26 AioB subunit. The introduction of a disulphide bridge had no effect on Aio activity or protein stability but resulted in a decrease in the redox potential of the cluster. These results are in conflict with previous data on the betaproteobacterial AioB subunit and the Rieske of the bc1 complex where removal of the disulphide bridge had no effect on the redox potential of the former but a decrease in cluster stability was observed in the latter. PMID:24023621

  8. The respiratory arsenite oxidase: structure and the role of residues surrounding the rieske cluster.

    Directory of Open Access Journals (Sweden)

    Thomas P Warelow

    Full Text Available The arsenite oxidase (Aio from the facultative autotrophic Alphaproteobacterium Rhizobium sp. NT-26 is a bioenergetic enzyme involved in the oxidation of arsenite to arsenate. The enzyme from the distantly related heterotroph, Alcaligenes faecalis, which is thought to oxidise arsenite for detoxification, consists of a large α subunit (AioA with bis-molybdopterin guanine dinucleotide at its active site and a 3Fe-4S cluster, and a small β subunit (AioB which contains a Rieske 2Fe-2S cluster. The successful heterologous expression of the NT-26 Aio in Escherichia coli has resulted in the solution of its crystal structure. The NT-26 Aio, a heterotetramer, shares high overall similarity to the heterodimeric arsenite oxidase from A. faecalis but there are striking differences in the structure surrounding the Rieske 2Fe-2S cluster which we demonstrate explains the difference in the observed redox potentials (+225 mV vs. +130/160 mV, respectively. A combination of site-directed mutagenesis and electron paramagnetic resonance was used to explore the differences observed in the structure and redox properties of the Rieske cluster. In the NT-26 AioB the substitution of a serine (S126 in NT-26 for a threonine as in the A. faecalis AioB explains a -20 mV decrease in redox potential. The disulphide bridge in the A. faecalis AioB which is conserved in other betaproteobacterial AioB subunits and the Rieske subunit of the cytochrome bc 1 complex is absent in the NT-26 AioB subunit. The introduction of a disulphide bridge had no effect on Aio activity or protein stability but resulted in a decrease in the redox potential of the cluster. These results are in conflict with previous data on the betaproteobacterial AioB subunit and the Rieske of the bc 1 complex where removal of the disulphide bridge had no effect on the redox potential of the former but a decrease in cluster stability was observed in the latter.

  9. The role of the rice aquaporin Lsi1 in arsenite efflux from roots.

    Science.gov (United States)

    Zhao, Fang-Jie; Ago, Yukiko; Mitani, Namiki; Li, Ren-Ying; Su, Yu-Hong; Yamaji, Naoki; McGrath, Steve P; Ma, Jian Feng

    2010-04-01

    *When supplied with arsenate (As(V)), plant roots extrude a substantial amount of arsenite (As(III)) to the external medium through as yet unidentified pathways. The rice (Oryza sativa) silicon transporter Lsi1 (OsNIP2;1, an aquaporin channel) is the major entry route of arsenite into rice roots. Whether Lsi1 also mediates arsenite efflux was investigated. *Expression of Lsi1 in Xenopus laevis oocytes enhanced arsenite efflux, indicating that Lsi1 facilitates arsenite transport bidirectionally. *Arsenite was the predominant arsenic species in arsenate-exposed rice plants. During 24-h exposure to 5 mum arsenate, rice roots extruded arsenite to the external medium rapidly, accounting for 60-90% of the arsenate uptake. A rice mutant defective in Lsi1 (lsi1) extruded significantly less arsenite than the wild-type rice and, as a result, accumulated more arsenite in the roots. By contrast, Lsi2 mutation had little effect on arsenite efflux to the external medium. *We conclude that Lsi1 plays a role in arsenite efflux in rice roots exposed to arsenate. However, this pathway accounts for only 15-20% of the total efflux, suggesting the existence of other efflux transporters.

  10. Nitroxides protect against peroxynitrite-induced nitration and oxidation.

    Science.gov (United States)

    Sadowska-Bartosz, Izabela; Gajewska, Agnieszka; Skolimowski, Janusz; Szewczyk, Rafał; Bartosz, Grzegorz

    2015-12-01

    Nitroxides are promising compounds for prevention of undesired protein modifications. The aim of this study was to compare the efficiency of 11 nitroxides, derivatives of 2,2,6,6-tetramethylpiperidine-1-oxide (TEMPO) and 2,2,5,5-tetramethylpirrolidine-1-oxyl (PROXYL) in prevention of nitration and oxidation of model compounds and human serum albumin (HSA). Most nitroxides were very efficient in preventing loss of fluorescein fluorescence induced by peroxynitrite (PN) (IC50 in the nanomolar range) and preventing HSA nitration. The loss of fluorescein fluorescence was demonstrated to be due to nitration. Nitroxides were more effective in prevention nitration than oxidation reactions. They showed a concentration window for preventing dihydrorhodamine (DHR) 123 oxidation but exerted a prooxidant effect at both high and low concentrations. No prooxidant effect of nitroxides was seen in prevention of DHR123 oxidation induced by SIN-1. In all essays hydrophobic nitroxides (especially 4-nonylamido-TEMPO and 3-carbamolyl-dehydroPROXYL) showed the lowest efficiency. An exception was the prevention of thiol group oxidation by PN and SIN-1 where hydrophobic nitroxides were the most effective, apparently due to binding to the protein. Nitroxides showed low toxicity to MCF-7 cells. Most nitroxides, except for the most hydrophobic ones, protected cells from the cytotoxic action of SIN-1 and SIN-1-induced protein nitration. These results point to potential usefulness of nitroxides for prevention of PN-induced oxidation and, especially, nitration. Copyright © 2015 Elsevier Inc. All rights reserved.

  11. Oxidative stress-induced autophagy: Role in pulmonary toxicity

    Energy Technology Data Exchange (ETDEWEB)

    Malaviya, Rama [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States); Laskin, Jeffrey D. [Department of Environmental and Occupational Medicine, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ 08854 (United States); Laskin, Debra L., E-mail: laskin@eohsi.rutgers.edu [Department of Pharmacology and Toxicology, Ernest Mario School of Pharmacy, Rutgers University, Piscataway, NJ 08854 (United States)

    2014-03-01

    Autophagy is an evolutionarily conserved catabolic process important in regulating the turnover of essential proteins and in elimination of damaged organelles and protein aggregates. Autophagy is observed in the lung in response to oxidative stress generated as a consequence of exposure to environmental toxicants. Whether autophagy plays role in promoting cell survival or cytotoxicity is unclear. In this article recent findings on oxidative stress-induced autophagy in the lung are reviewed; potential mechanisms initiating autophagy are also discussed. A better understanding of autophagy and its role in pulmonary toxicity may lead to the development of new strategies to treat lung injury associated with oxidative stress. - Highlights: • Exposure to pulmonary toxicants is associated with oxidative stress. • Oxidative stress is known to induce autophagy. • Autophagy is upregulated in the lung following exposure to pulmonary toxicants. • Autophagy may be protective or pathogenic.

  12. HCV-Induced Oxidative Stress: Battlefield-Winning Strategy

    Science.gov (United States)

    Rebbani, Khadija; Tsukiyama-Kohara, Kyoko

    2016-01-01

    About 150 million people worldwide are chronically infected with hepatitis C virus (HCV). The persistence of the infection is controlled by several mechanisms including the induction of oxidative stress. HCV relies on this strategy to redirect lipid metabolism machinery and escape immune response. The 3β-hydroxysterol Δ24-reductase (DHCR24) is one of the newly discovered host markers of oxidative stress. This protein, as HCV-induced oxidative stress responsive protein, may play a critical role in the pathogenesis of HCV chronic infection and associated liver diseases, when aberrantly expressed. The sustained expression of DHCR24 in response to HCV-induced oxidative stress results in suppression of nuclear p53 activity by blocking its acetylation and increasing its interaction with MDM2 in the cytoplasm leading to its degradation, which may induce hepatocarcinogenesis. PMID:27293514

  13. Arsenite tolerance and biotransformation potential in estuarine bacteria

    Digital Repository Service at National Institute of Oceanography (India)

    Nagvenkar, G.S.; Ramaiah, N.

    isolates tested in nutrient broth with 200 ppm Arsenite (A sup(3+)), many of them were able to attain log phase and substantial growth variously between 36 and 96 h. The isolates tolerating is greater than or equal to 200 ppm arsenic (As) were found...

  14. Sorption and desorption of arsenate and arsenite on calcite

    DEFF Research Database (Denmark)

    Sø, Helle Ugilt; Postma, Diederik Jan; Jakobsen, Rasmus

    2008-01-01

    The adsorption and desorption of arsenate (As(V)) and arsenite (As(111)) oil calcite was investigated in a series of batch experiments in calcite-equilibrated solutions. The solutions covered a broad range of pH, alkalinity, calcium concentration and ionic strength. The initial arsenic...

  15. Inhibition of mitotic-specific histone phophorylation by sodium arsenite

    Energy Technology Data Exchange (ETDEWEB)

    Cobo, J.M. [Universidad de Alcala de Henares, Madrid (Spain); Valdez, J.G.; Gurley, L.R. [Los Alamos National Lab., NM (United States)

    1994-10-01

    Synchronized cultures of Chinese hamster cells (line CHO) were used to measure the effects of 10{mu}M sodium arsenite on histone phosphorylation. This treatment caused cell proliferation to be temporarily arrested, after which the cells spontaneously resumed cell proliferation in a radiomimetric manner. Immediately following treatment, it was found that sodium arsenite affected only mitotic-specific HI and H3 phosphorylations. Neither interphase, nor mitotic, H2A and H4 phosphorylations were affected, nor was interphase HI Phosphorylation affected. The phosphorylation of HI was inhibited only in mitosis, reducing HI phosphorylation to 38.1% of control levels, which was the level of interphase HI phosphorylation. The phosphorylation of both H3 variants was inhibited in mitosis, the less hydrophobic H3 to 19% and the more hydrophobic H3 to 24% of control levels. These results suggest that sodium arsenite may inhibite cell proliferation by interfering with the cyclin B/p34{sup cdc2} histone kinase activity which is thought to play a key role in regulating the cell cycle. It has been proposed by our laboratory that HI and H3 phosphorylations play a role in restructuring interphase chromatin into metaphase chromosomes. Interference of this process by sodium arsenite may lead to structurally damaged chromosomes resulting in the increased cancer risks known to be produced by arsenic exposure from the environment.

  16. Synergism between arsenite and proteasome inhibitor MG132 over cell death in myeloid leukaemic cells U937 and the induction of low levels of intracellular superoxide anion

    Energy Technology Data Exchange (ETDEWEB)

    Lombardo, Tomás [Laboratorio de Immunotoxicologia (LaITO), IDEHU-CONICET, Hospital de Clínicas, José de San Martín, Universidad de Buenos Aires (UBA), Buenos Aires (Argentina); Cavaliere, Victoria; Costantino, Susana N. [Laboratorio de Inmunología Tumoral (LIT), IDEHU-CONICET, Facultad de Farmacia y Bioquímica, UBA, Buenos Aires (Argentina); Kornblihtt, Laura [Servicio de Hematología, Hospital de Clínicas, José de San Martín (UBA), Buenos Aires (Argentina); Alvarez, Elida M. [Laboratorio de Inmunología Tumoral (LIT), IDEHU-CONICET, Facultad de Farmacia y Bioquímica, UBA, Buenos Aires (Argentina); Blanco, Guillermo A., E-mail: gblanco@ffyb.uba.ar [Laboratorio de Immunotoxicologia (LaITO), IDEHU-CONICET, Hospital de Clínicas, José de San Martín, Universidad de Buenos Aires (UBA), Buenos Aires (Argentina)

    2012-02-01

    Increased oxygen species production has often been cited as a mechanism determining synergism on cell death and growth inhibition effects of arsenic-combined drugs. However the net effect of drug combination may not be easily anticipated solely from available knowledge of drug-induced death mechanisms. We evaluated the combined effect of sodium arsenite with the proteasome inhibitor MG132, and the anti-leukaemic agent CAPE, on growth-inhibition and cell death effect in acute myeloid leukaemic cells U937 and Burkitt's lymphoma-derived Raji cells, by the Chou–Talalay method. In addition we explored the association of cytotoxic effect of drugs with changes in intracellular superoxide anion (O{sub 2}{sup −}) levels. Our results showed that combined arsenite + MG132 produced low levels of O{sub 2}{sup −} at 6 h and 24 h after exposure and were synergic on cell death induction in U937 cells over the whole dose range, although the combination was antagonistic on growth inhibition effect. Exposure to a constant non-cytotoxic dose of 80 μM hydrogen peroxide together with arsenite + MG132 changed synergism on cell death to antagonism at all effect levels while increasing O{sub 2}{sup −} levels. Arsenite + hydrogen peroxide also resulted in antagonism with increased O{sub 2}{sup −} levels in U937 cells. In Raji cells, arsenite + MG132 also produced low levels of O{sub 2}{sup −} at 6 h and 24 h but resulted in antagonism on cell death and growth inhibition. By contrast, the combination arsenite + CAPE showed high levels of O{sub 2}{sup −} production at 6 h and 24 h post exposure but resulted in antagonism over cell death and growth inhibition effects in U937 and Raji cells. We conclude that synergism between arsenite and MG132 in U937 cells is negatively associated to O{sub 2}{sup −} levels at early time points after exposure. -- Highlights: ► Arsenic combined cytotoxic and anti-proliferative effects by Chou–Talalay method. ► Cytotoxic effect

  17. Oxidative stress in MeHg-induced neurotoxicity

    Energy Technology Data Exchange (ETDEWEB)

    Farina, Marcelo, E-mail: farina@ccb.ufsc.br [Departamento de Bioquimica, Centro de Ciencias Biologicas, Universidade Federal de Santa Catarina, Florianopolis, SC (Brazil); Aschner, Michael [Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN (United States); Department of Pharmacology, Vanderbilt University Medical Center, Nashville, TN (United States); Rocha, Joao B.T., E-mail: jbtrocha@yahoo.com.br [Departamento de Quimica, Centro de Ciencias Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, RS (Brazil)

    2011-11-15

    Methylmercury (MeHg) is an environmental toxicant that leads to long-lasting neurological and developmental deficits in animals and humans. Although the molecular mechanisms mediating MeHg-induced neurotoxicity are not completely understood, several lines of evidence indicate that oxidative stress represents a critical event related to the neurotoxic effects elicited by this toxicant. The objective of this review is to summarize and discuss data from experimental and epidemiological studies that have been important in clarifying the molecular events which mediate MeHg-induced oxidative damage and, consequently, toxicity. Although unanswered questions remain, the electrophilic properties of MeHg and its ability to oxidize thiols have been reported to play decisive roles to the oxidative consequences observed after MeHg exposure. However, a close examination of the relationship between low levels of MeHg necessary to induce oxidative stress and the high amounts of sulfhydryl-containing antioxidants in mammalian cells (e.g., glutathione) have led to the hypothesis that nucleophilic groups with extremely high affinities for MeHg (e.g., selenols) might represent primary targets in MeHg-induced oxidative stress. Indeed, the inhibition of antioxidant selenoproteins during MeHg poisoning in experimental animals has corroborated this hypothesis. The levels of different reactive species (superoxide anion, hydrogen peroxide and nitric oxide) have been reported to be increased in MeHg-exposed systems, and the mechanisms concerning these increments seem to involve a complex sequence of cascading molecular events, such as mitochondrial dysfunction, excitotoxicity, intracellular calcium dyshomeostasis and decreased antioxidant capacity. This review also discusses potential therapeutic strategies to counteract MeHg-induced toxicity and oxidative stress, emphasizing the use of organic selenocompounds, which generally present higher affinity for MeHg when compared to the classically

  18. Proteome oxidative carbonylation during oxidative stress-induced premature senescence of WI-38 human fibroblasts

    DEFF Research Database (Denmark)

    Le Boulch, Marine; Ahmed, Emad K; Rogowska-Wrzesinska, Adelina

    2017-01-01

    Accumulation of oxidatively damaged proteins is a hallmark of cellular and organismal ageing, and is also a phenotypic feature shared by both replicative senescence and stress-induced premature senescence of human fibroblasts. Moreover, proteins that are building up as oxidized (i.e. the "Oxi......-proteome") during ageing and age-related diseases represent a restricted set of cellular proteins, indicating that certain proteins are more prone to oxidative carbonylation and subsequent intracellular accumulation. The occurrence of specific carbonylated proteins upon oxidative stress induced premature senescence...... of WI-38 human fibroblasts and their follow-up identification have been addressed in this study. Indeed, it was expected that the identification of these proteins would give insights into the mechanisms by which oxidatively damaged proteins could affect cellular function. Among these proteins, some...

  19. Nitric oxide, inducible nitric oxide synthase and inflammation in veterinary medicine.

    Science.gov (United States)

    Hunter, Robert P

    2002-12-01

    Inflammation is a process consisting of a complex of cytological and chemical reactions which occur in and around affected blood vessels and adjacent tissues in response to an injury caused by a physical, chemical or biological insult. Much work has been performed in the past several years investigating inducible nitric oxide synthase (NOS, EC 1.14.13.39) and nitric oxide in inflammation. This has resulted in a rapid increase in knowledge about iNOS and nitric oxide. Nitric oxide formation from inducible NOS is regulated by numerous inflammatory mediators, often with contradictory effects, depending upon the type and duration of the inflammatory insult. Equine medicine appears to have benefited the most from the increased interest in this small, inflammatory mediator. Most of the information on nitric oxide in traditional veterinary species has been produced using models or naturally occurring inflammatory diseases of this species.

  20. Hypochlorite-induced oxidation of thiols

    DEFF Research Database (Denmark)

    Davies, Michael Jonathan; Hawkins, C L

    2000-01-01

    -molecular-weight thiols such as reduced glutathione (GSH), and sulfur-containing amino acids in proteins, are major targets for HOCl. Radicals have not generally been implicated as intermediates in thiol oxidation by HOCl, though there is considerable literature evidence for the involvement of radicals in the metal ion...... to the thiol, thiyl radicals are the major species detected by EPR spin trapping. When the HOCl is present in excess over the thiol, additional radicals are detected with compounds which contain amine functions; these additional radicals are assigned to nitrogen-centered species. Evidence is presented...... for the involvement of sulfenyl chlorides (RSCl) in the formation of these radicals, and studies with an authentic sulfenyl chloride have demonstrated that this compound readily decomposes in thermal-, metal-ion- or light-catalysed reactions to give thiyl radicals. The formation of thiyl radicals on oxidation...

  1. Apoptosis of wound fibroblasts induced by oxidative stress.

    Science.gov (United States)

    Takahashi, Atsushi; Aoshiba, Kazutetsu; Nagai, Atsushi

    2002-06-01

    Irreversible lung parenchymal injury is usually healed by fibrosis, which depends on the abilities of fibroblasts to proliferate, migrate into the wound, and survive. Because the lung is frequently exposed to increased oxidative stress, which is thought to mediate apoptosis, we examined whether oxidative stress induces apoptosis in fibroblasts during wound healing. We performed an in vitro scratch wound assay where cultured fibroblast monolayers were exposed to H2O2 (10-500 microM) after artificial wounding. Apoptosis was evaluated by nuclear staining with Hoechst33342 or terminal deoxynucleotidyl transferase (TdT)-mediated nucleotide nick end-labeling (TUNEL). Intracellular oxidants were assessed with the peroxide-sensitive fluorochrome carboxydichlorodihydrofluorescein (CDCF). We found that repopulating fibroblasts at the wound margin, but not quiescent fibroblasts at the intact site, selectively underwent oxidant accumulation and apoptosis in response to H2O2 exposure. Some of the apoptotic cells had incorporated bromodeoxyuridine (BrdU), an indicator of proliferating cells. These results suggest that oxidative stress selectively induces apoptosis in fibroblasts that are stimulated to proliferate and/or migrate into the wound. Fibroblast apoptosis induced by oxidative stress during wound repopulation may be relevant to intractable wound healing.

  2. Ovariectomy exacerbates oxidative stress and cardiopathy induced by adriamycin.

    Science.gov (United States)

    Muñoz-Castañeda, Juan Rafael; Muntané, Jordi; Herencia, Carmen; Muñoz, Maria C; Bujalance, Inmaculada; Montilla, Pedro; Túnez, Issac

    2006-02-01

    Ovarian hormone depletion in ovariectomized experimental animals is a useful model with which to study the physiopathological consequences of menopause in women. It has been suggested that menopause is a risk factor for the induction of several cardiovascular disorders. In the present study we analyzed the effects of ovarian hormone depletion by ovariectomy (OVX) in a model of oxidative stress and cardiopathy induced by adriamycin (AD). To evaluate these effects, we measured parameters related to cardiac damage (creatinine kinase, lactate dehydrogenase, aspartate aminotransferase and alanine aminotransferase) and oxidative stress (malondialdehyde, catalase, superoxide dismutase, glutathione peroxidase, reduced glutathione, nitric oxide and carbonyl proteins) in cardiac tissue and erythrocytes. OVX was found to alter all markers of oxidative stress and cell damage in cardiac tissue. Similarly, the OVX-derived loss of ovarian hormones enhanced cardiac damage and oxidative stress induced by AD. Our results suggest that antioxidant status in cardiac tissue and erythrocytes is seriously compromised by OVX during the cardiomyopathy induced by AD in experimental animals. In conclusion, the absence of hormones caused by OVX or menopause may induce or accelerate pre-existing cardiovascular dysfunctions.

  3. Mitochondrial oxidative stress significantly influences atherogenic risk and cytokine-induced oxidant production.

    Science.gov (United States)

    Harrison, Corey M; Pompilius, Melissa; Pinkerton, Kent E; Ballinger, Scott W

    2011-05-01

    Oxidative stress associated with cardiovascular disease (CVD) risk factors contributes to disease development. However, less is known whether specific subcellular components play a role in disease susceptibility. In this regard, it has been previously reported that vascular mitochondrial damage and dysfunction are associated with atherosclerosis. However, no studies have determined whether altered mitochondrial oxidant production directly influences atherogenic susceptibility and response in primary cells to atherogenic factors such as tumor necrosis factor-α (TNF-α). We undertook this study to determine whether increased mitochondrial oxidant production affects atherosclerotic lesion development associated with CVD risk factor exposure and endothelial cell response to TNF-α. We assessed atherosclerotic lesion formation, oxidant stress, and mitochondrial DNA damage in male apolipoprotein E (apoE)-null mice with normal and decreased levels of mitochondrial superoxide dismutase-2 (SOD2; apoE(-/-) and apoE(-/-), SOD2(+/-), respectively) exposed to environmental tobacco smoke or filtered air. Atherogenesis, oxidative stress, and mitochondrial damage were significantly higher in apoE(-/-), SOD2(+/-) mice than in apoE(-/-) controls. Furthermore, experiments with small interfering RNA in endothelial cells revealed that decreased SOD2 activity increased TNF-α-mediated cellular oxidant levels compared with controls. Endogenous mitochondrial oxidative stress is an important CVD risk factor that can modulate atherogenesis and cytokine-induced endothelial cell oxidant generation. Consequently, CVD risk factors that induce mitochondrial damage alter cellular response to endogenous atherogenic factors, increasing disease susceptibility.

  4. Oxidative stress and DNA damages induced by cadmium accumulation

    Institute of Scientific and Technical Information of China (English)

    LIN Ai-jun; ZHANG Xu-hong; CHEN Mei-mei; CAO Qing

    2007-01-01

    Experimental evidence shows that cadmium (Cd) could induce oxidative stress and then causes DNA damage in animal cells, however, whether such effect exists in plants is still unclear. In the present study, Vicia faba plants was exposed to 5 and 10 mg/L Cd for 4 d to investigate the distribution of Cd in plant, the metal effects on the cell lipids, antioxidative enzymes and DNA damages in leaves. Cd induced an increase in Cd concentrations in plants. An enhanced level of lipid peroxidation in leaves and an enhanced concentration of H2O2 in root tissues suggested that Cd caused oxidative stress in Vicia faba. Compared with control, Cd-induced enhancement in superoxide dismutase activity was significant at 5 mg/L than at 10 mg/kg in leaves, by contrast, catalase and peroxidaseactivities were significantly suppressed by Cd addition. DNA damage was detected by neutral/neutral, alkaline/neutral and alkaline/alkaline Comet assay. Increased levels of DNA damages induced by Cd occurred with reference to oxidative stress in leaves, therefore, oxidative stress induced by Cd accumulation in plants contributed to DNA damages and was possibly an important mechanism of Cd-phytotoxicity in Vicia faba plants.

  5. Mechanisms of Nanoparticle-Induced Oxidative Stress and Toxicity

    Directory of Open Access Journals (Sweden)

    Amruta Manke

    2013-01-01

    Full Text Available The rapidly emerging field of nanotechnology has offered innovative discoveries in the medical, industrial, and consumer sectors. The unique physicochemical and electrical properties of engineered nanoparticles (NP make them highly desirable in a variety of applications. However, these novel properties of NP are fraught with concerns for environmental and occupational exposure. Changes in structural and physicochemical properties of NP can lead to changes in biological activities including ROS generation, one of the most frequently reported NP-associated toxicities. Oxidative stress induced by engineered NP is due to acellular factors such as particle surface, size, composition, and presence of metals, while cellular responses such as mitochondrial respiration, NP-cell interaction, and immune cell activation are responsible for ROS-mediated damage. NP-induced oxidative stress responses are torch bearers for further pathophysiological effects including genotoxicity, inflammation, and fibrosis as demonstrated by activation of associated cell signaling pathways. Since oxidative stress is a key determinant of NP-induced injury, it is necessary to characterize the ROS response resulting from NP. Through physicochemical characterization and understanding of the multiple signaling cascades activated by NP-induced ROS, a systemic toxicity screen with oxidative stress as a predictive model for NP-induced injury can be developed.

  6. Exercise-Induced Oxidative Stress Responses in the Pediatric Population

    Directory of Open Access Journals (Sweden)

    Alexandra Avloniti

    2017-01-01

    Full Text Available Adults demonstrate an upregulation of their pro- and anti-oxidant mechanisms in response to acute exercise while systematic exercise training enhances their antioxidant capacity, thereby leading to a reduced generation of free radicals both at rest and in response to exercise stress. However, less information exists regarding oxidative stress responses and the underlying mechanisms in the pediatric population. Evidence suggests that exercise-induced redox perturbations may be valuable in order to monitor exercise-induced inflammatory responses and as such training overload in children and adolescents as well as monitor optimal growth and development. The purpose of this review was to provide an update on oxidative stress responses to acute and chronic exercise in youth. It has been documented that acute exercise induces age-specific transient alterations in both oxidant and antioxidant markers in children and adolescents. However, these responses seem to be affected by factors such as training phase, training load, fitness level, mode of exercise etc. In relation to chronic adaptation, the role of training on oxidative stress adaptation has not been adequately investigated. The two studies performed so far indicate that children and adolescents exhibit positive adaptations of their antioxidant system, as adults do. More studies are needed in order to shed light on oxidative stress and antioxidant responses, following acute exercise and training adaptations in youth. Available evidence suggests that small amounts of oxidative stress may be necessary for growth whereas the transition to adolescence from childhood may promote maturation of pro- and anti-oxidant mechanisms. Available evidence also suggests that obesity may negatively affect basal and exercise-related antioxidant responses in the peripubertal period during pre- and early-puberty.

  7. Phosphine-induced oxidative damage in rats: role of glutathione.

    Science.gov (United States)

    Hsu, Ching-Hung; Chi, Bei-Ching; Liu, Ming-Yie; Li, Jih-Heng; Chen, Chiou-Jong; Chen, Ruey-Yu

    2002-09-30

    Phosphine (PH(3)), generated from aluminium, magnesium and zinc phosphide, is a widely used pesticide. PH(3) induces oxidative stress in insects, mammalian cells, animals, and humans. The involvement of glutathione (GSH) in PH(3)-induced oxidative toxicity is controversial. GSH levels in various tested tissues were reduced in aluminium phosphide-poisoned rats and humans, while the levels remained unchanged in insects and mammalian cells. This study examines the effectiveness of endogenous GSH as a protective agent against PH(3)-induced oxidative damage in rats. The association of PH(3)-induced nephrotoxicity and cardiotoxicity with free radical production was also tested. Male Wistar rats, administered intraperitoneally (I.P.) with PH(3) at 4 mg/kg, were evaluated 30 min after treatment for PH(3) toxicity to organs. PH(3) significantly decreased GSH, GSH peroxidase and catalase, while significantly increased lipid peroxidation (as malondialdehyde and 4-hydroxyalkenals), DNA oxidation (as 8-hydroxydeoxyguaonsoine) and superoxide dismutase (SOD) levels in kidney and heart. These changes were significantly alleviated by melatonin (10 mg/kg I.P., 30 min before PH(3)), with the exception of SOD activity in heart tissue. The study also found that buthionine sulfoximine (1 g/kg I.P., 24 h before PH(3)) significantly enhanced the effect of PH(3) on GSH loss and lipid peroxidation elevation in lung. These findings indicate that (1) endogenous GSH plays a crucial role as a protective factor in modulating PH(3)-induced oxidative damage, and (2) PH(3) could injure kidney and heart (as noted earlier with brain, liver and lung) via oxidative stress and the antioxidant melatonin effectively prevents the damage.

  8. Mangiferin induces cell death against rhabdomyosarcoma through sustained oxidative stress

    OpenAIRE

    Vishwanadha Vijaya Padma; Palanisamy Kalaiselvi; Rangasamy Yuvaraj; M. Rabeeth

    2015-01-01

    Background: Embryonic rhabdomyosarcoma (RD) is the most prevalent type of cancer among children. The present study aimed to investigate cell death induced by mangiferin in RD cells. Methods: The Inhibitory concentration (IC50) value of mangiferin was determined by an MTT (3-(4,5-Dimethylthiazol-2-yl)-2,5-Diphenyltetrazolium Bromide) assay. Cell death induced by mangiferin against RD cells was determined through lactate dehydrogenase and nitric oxide release, intracellular calcium levels, r...

  9. Oxidative stress induces mitochondrial fragmentation in frataxin-deficient cells

    Energy Technology Data Exchange (ETDEWEB)

    Lefevre, Sophie [Mitochondria, Metals and Oxidative Stress Laboratory, Institut Jacques Monod, CNRS-Universite Paris-Diderot, Sorbonne Paris Cite, 15 rue Helene Brion, 75205 Paris cedex 13 (France); ED515 UPMC, 4 place Jussieu 75005 Paris (France); Sliwa, Dominika [Mitochondria, Metals and Oxidative Stress Laboratory, Institut Jacques Monod, CNRS-Universite Paris-Diderot, Sorbonne Paris Cite, 15 rue Helene Brion, 75205 Paris cedex 13 (France); Rustin, Pierre [Inserm, U676, Physiopathology and Therapy of Mitochondrial Disease Laboratory, 75019 Paris (France); Universite Paris-Diderot, Faculte de Medecine Denis Diderot, IFR02 Paris (France); Camadro, Jean-Michel [Mitochondria, Metals and Oxidative Stress Laboratory, Institut Jacques Monod, CNRS-Universite Paris-Diderot, Sorbonne Paris Cite, 15 rue Helene Brion, 75205 Paris cedex 13 (France); Santos, Renata, E-mail: santos.renata@ijm.univ-paris-diderot.fr [Mitochondria, Metals and Oxidative Stress Laboratory, Institut Jacques Monod, CNRS-Universite Paris-Diderot, Sorbonne Paris Cite, 15 rue Helene Brion, 75205 Paris cedex 13 (France)

    2012-02-10

    Highlights: Black-Right-Pointing-Pointer Yeast frataxin-deficiency leads to increased proportion of fragmented mitochondria. Black-Right-Pointing-Pointer Oxidative stress induces complete mitochondrial fragmentation in {Delta}yfh1 cells. Black-Right-Pointing-Pointer Oxidative stress increases mitochondrial fragmentation in patient fibroblasts. Black-Right-Pointing-Pointer Inhibition of mitochondrial fission in {Delta}yfh1 induces oxidative stress resistance. -- Abstract: Friedreich ataxia (FA) is the most common recessive neurodegenerative disease. It is caused by deficiency in mitochondrial frataxin, which participates in iron-sulfur cluster assembly. Yeast cells lacking frataxin ({Delta}yfh1 mutant) showed an increased proportion of fragmented mitochondria compared to wild-type. In addition, oxidative stress induced complete fragmentation of mitochondria in {Delta}yfh1 cells. Genetically controlled inhibition of mitochondrial fission in these cells led to increased resistance to oxidative stress. Here we present evidence that in yeast frataxin-deficiency interferes with mitochondrial dynamics, which might therefore be relevant for the pathophysiology of FA.

  10. Developmental mechanisms of arsenite toxicity in zebrafish (Danio rerio) embryos

    Energy Technology Data Exchange (ETDEWEB)

    Li Dan [Department of Genetics, National Research Institute for Family Planning, Beijing (China); Graduate School of Peking Union Medical College, Beijing (China); Lu Cailing [Department of Genetics, National Research Institute for Family Planning, Beijing (China); Wang Ju; Hu Wei; Cao Zongfu; Sun Daguang [Department of Genetics, National Research Institute for Family Planning, Beijing (China); Graduate School of Peking Union Medical College, Beijing (China); Xia Hongfei [Department of Genetics, National Research Institute for Family Planning, Beijing (China); Ma Xu [Department of Genetics, National Research Institute for Family Planning, Beijing (China) and Graduate School of Peking Union Medical College, Beijing (China) and Department of Reproductive Genetics, WHO Collaborative Center for Research in Human Reproduction, Beijing (China)], E-mail: genetic@263.net.cn

    2009-02-19

    Arsenic usually accumulates in soil, water and airborne particles, from which it is taken up by various organisms. Exposure to arsenic through food and drinking water is a major public health problem affecting some countries. At present there are limited laboratory data on the effects of arsenic exposure on early embryonic development and the mechanisms behind its toxicity. In this study, we used zebrafish as a model system to investigate the effects of arsenite on early development. Zebrafish embryos were exposed to a range of sodium arsenite concentrations (0-10.0 mM) between 4 and 120 h post-fertilization (hpf). Survival and early development of the embryos were not obviously influenced by arsenite concentrations below 0.5 mM. However, embryos exposed to higher concentrations (0.5-10.0 mM) displayed reduced survival and abnormal development including delayed hatching, retarded growth and changed morphology. Alterations in neural development included weak tactile responses to light (2.0-5.0 mM, 30 hpf), malformation of the spinal cord and disordered motor axon projections (2.0 mM, 48 hpf). Abnormal cardiac function was observed as bradycardia (0.5-2.0 mM, 60 hpf) and altered ventricular shape (2.0 mM, 48 hpf). Furthermore, altered cell proliferation (2.0 mM, 24 hpf) and apoptosis status (2.0 mM, 24 and 48 hpf), as well as abnormal genomic DNA methylation patterning (2.0 mM, 24 and 48 hpf) were detected in the arsenite-treated embryos. All of these indicate a possible relationship between arsenic exposure and developmental failure in early embryogenesis. Our studies suggest that the negative effects of arsenic on vertebrate embryogenesis are substantial.

  11. Electron beam induced oxidation of Al–Mg alloy surfaces

    NARCIS (Netherlands)

    Palasantzas, G.; Agterveld, D.T.L. van; Hosson, J.Th.M. De

    2002-01-01

    Electron beam currents of a few nanoamperes, currently used in nanometer scale scanning Auger/electron microscopy, induces severe oxidation of Al–Mg alloy surfaces at room temperature. Auger peak-to-peak oxygen curves for Al–Mg surfaces support the hypothesis that the electron beam creates

  12. Deficiency of nitric oxide in polycation-induced airway hyperreactivity

    NARCIS (Netherlands)

    Meurs, Herman; Schuurman, F.E; Duyvendak, M; Zaagsma, Hans

    1999-01-01

    Using a perfused guinea-pig tracheal tube preparation, we investigated the role of endogenous nitric oxide (NO) in polycation-induced airway hyperreactivity (AHR) to methacholine. Intraluminal (IL) administration of the NO synthase inhibitor N-omega-nitro-L-arginine methyl ester (L-NAME; 100 mu M) c

  13. Light-Induced Absorption in Nominally Pure Bismuth Silicon Oxide

    Institute of Scientific and Technical Information of China (English)

    李飞飞; 许京军; 孔勇发; 黄辉; 张光寅; 杨春晖; 徐玉恒

    2001-01-01

    Light-induced absorption in the nominally pure bismuth silicon oxide is investigated experimentally and the result shows that it consists of transient and persistent parts. The experimental evidence is analysed based on the model of three groups of trap (donor) centres.

  14. Electron beam induced oxidation of Al–Mg alloy surfaces

    NARCIS (Netherlands)

    Palasantzas, G.; Agterveld, D.T.L. van; Hosson, J.Th.M. De

    2002-01-01

    Electron beam currents of a few nanoamperes, currently used in nanometer scale scanning Auger/electron microscopy, induces severe oxidation of Al–Mg alloy surfaces at room temperature. Auger peak-to-peak oxygen curves for Al–Mg surfaces support the hypothesis that the electron beam creates additiona

  15. extract attenuates MPTP-induced oxidative stress and behavioral ...

    African Journals Online (AJOL)

    on oxidative stress levels were assessed by estimating enzyme status, ... Results: MPTP (25 mg/kg, i.p.)-treated mice resulted in a significant (p ... Conclusion: CCY extract exhibits strong protection against MPTP-induced behavioral deficit through ..... cuminol, cymine, cuminaldehyde, limonene, ... Antibacterial effect of plant.

  16. Quercitrin protects skin from UVB-induced oxidative damage.

    Science.gov (United States)

    Yin, Yuanqin; Li, Wenqi; Son, Young-Ok; Sun, Lijuan; Lu, Jian; Kim, Donghern; Wang, Xin; Yao, Hua; Wang, Lei; Pratheeshkumar, Poyil; Hitron, Andrew J; Luo, Jia; Gao, Ning; Shi, Xianglin; Zhang, Zhuo

    2013-06-01

    Exposure of the skin to ultraviolet B (UVB) radiation causes oxidative damage to skin, resulting in sunburn, photoaging, and skin cancer. It is generally believed that the skin damage induced by UV irradiation is a consequence of generation of reactive oxygen species (ROS). Recently, there is an increased interest in the use of natural products as chemopreventive agents for non-melanoma skin cancer (NMSC) due to their antioxidants and anti-inflammatory properties. Quercitrin, glycosylated form of quercetin, is the most common flavonoid in nature with antioxidant properties. The present study investigated the possible beneficial effects of quercitrin to inhibit UVB irradiation-induced oxidative damage in vitro and in vivo. Our results showed that quercitrin decreased ROS generation induced by UVB irradiation in JB6 cells. Quercitrin restored catalase expression and GSH/GSSG ratio reduced by UVB exposure, two major antioxidant enzymes, leading to reductions of oxidative DNA damage and apoptosis and protection of the skin from inflammation caused by UVB exposure. The present study demonstrated that quercitrin functions as an antioxidant against UVB irradiation-induced oxidative damage to skin.

  17. Arsenite tolerance in rice (Oryza sativa L.) involves coordinated role of metabolic pathways of thiols and amino acids.

    Science.gov (United States)

    Tripathi, Preeti; Tripathi, Rudra Deo; Singh, Rana Pratap; Dwivedi, Sanjay; Chakrabarty, Debasis; Trivedi, Prabodh K; Adhikari, Bijan

    2013-02-01

    Thiolic ligands and several amino acids (AAs) are known to build up in plants against heavy metal stress. In the present study, alteration of various AAs in rice and its synchronized role with thiolic ligand was explored for arsenic (As) tolerance and detoxification. To understand the mechanism of As tolerance and stress response, rice seedlings of one tolerant (Triguna) and one sensitive (IET-4786) cultivar were exposed to arsenite (0-25 μM) for 7 days for various biochemical analyses using spectrophotometer, HPLC and ICPMS. Tolerant and sensitive cultivars respond differentially in terms of thiol metabolism, essential amino acids (EEAs) and nonessential amino acids (NEEAs) vis-á-vis As accumulation. Thiol biosynthesis-related enzymes were positively correlated to As accumulation in Triguna. Conversely, these enzymes, cysteine content and GSH/GSSG ratio declined significantly in IET-4786 upon As exposure. The level of identified phytochelatin (PC) species (PC(2), PC(3) and PC(4)) and phytochelatin synthase activity were also more pronounced in Triguna than IET-4786. Nearly all EAAs were negatively affected by As-induced oxidative stress (except phenylalanine in Triguna), but more significantly in IET-4786 than Triguna. However, most of the stress-responsive NEAAs like glutamic acid, histidine, alanine, glycine, tyrosine, cysteine and proline were enhanced more prominently in Triguna than IET-4786 upon As exposure. The study suggests that IET-4786 appears sensitive to As due to reduction of AAs and thiol metabolic pathway. However, a coordinated response of thiolic ligands and stress-responsive AAs seems to play role for As tolerance in Triguna to achieve the effective complexation of As by PCs.

  18. Intense and exhaustive exercise induce oxidative stress in skeletal muscle

    Directory of Open Access Journals (Sweden)

    T Thirumalai

    2011-03-01

    Full Text Available Objective: To assess the oxidative stress and antioxidant defense system in the skeletal muscle of male albino rats subjected to strenuous exercise programme. Methods: Wistar strain albino rats were subjected to exhaustive swimming exercise programme daily for a period of five days. The thiobarbituric acid reactive substances (TBARS, conjugated dienes, superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase were measured in the gastrocnemius muscle of the exercised animals. Results: The elevated levels of TBARS and conjugated dienes indicated the oxidative stress in the gastrocemius muscle of the exercised animals. The depleted activity levels of superoxide dismutase, catalase, glutathione peroxidase and glutathione-S-transferase in the exercise animals indicated the increased oxidative stress and decreased antioxidative defense system in the muscle. Conclusions: The study suggests that prolonged strenuous exercise programme can induce oxidative stress and therefore an optimal level of exercise schedule should be advocated to obtain the maximum benefit of exercise programme.

  19. Statins lower calcium-induced oxidative stress in isolated mitochondria.

    Science.gov (United States)

    Parihar, A; Parihar, M S; Zenebe, W J; Ghafourifar, P

    2012-04-01

    Statins are widely used cholesterol-lowering agents that exert cholesterol-independent effects including antioxidative. The present study delineates the effects of statins, atorvastatin, and simvastatin on oxidative stress and functions of mitochondria that are the primary cellular sources of oxidative stress. In isolated rat liver mitochondria, both the statins prevented calcium-induced cytochrome c release, lipid peroxidation, and opening of the mitochondrial membrane permeability transition (MPT). Both the statins decreased the activity of mitochondrial nitric oxide synthase (mtNOS), lowered the intramitochondrial ionized calcium, and increased the mitochondrial transmembrane potential. Our findings suggest that statins lower intramitochondrial ionized calcium that decreases mtNOS activity, lowers oxidative stress, prevents MPT opening, and prevents the release of cytochrome c from the mitochondria. These results provide a novel framework for understanding the antioxidative properties of statins and their effects on mitochondrial functions.

  20. Nitric oxide damages neuronal mitochondria and induces apoptosis in neurons

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    The cytotoxic effect of nitric oxide on primarily cultured rat cerebellar granule cells was studied,and the mechanisms were discussed.The results showed that nitric oxide donor S-nitroso-N-acetyl-penicillamine (SNAP; 500 μmol/L) could induce apoptosis in immature cultures of cerebellar granule cells.Flow cytometry and HPLC analyses revealed that after treatment with SNAP,the mitochondrial transmembrane potential and the cellular ATP content decreased significantly.Nitric oxide scavenger hemoglobin could effectively prevent the neuronal mitochondria from dysfunction and attenuate apoptosis.The results suggested that nitric oxide activated the apoptotic program by inhibiting the activity of mitochondrial respiratory chain and thus decreasing the cellular ATP content.

  1. Microbially Induced Iron Oxidation: What, Where, How

    Energy Technology Data Exchange (ETDEWEB)

    SCHIERMEYER,ELISA M.; PROVENCIO,PAULA P.; NORTHUP,DIANA E.

    2000-08-15

    From the results of the different bacterial cells seen, it is fairly certain that Gallionella is present because of the bean-shaped cells and twisted stalks found with the TEM. The authors cannot confirm, though, what other iron-oxidizing genera exist in the tubes, since the media was only preferential and not one that isolated a specific genus of bacteria. Based on the environment in which they live and the source of the water, they believe their cultures contain Gallionella, Leptothrix, and possibly Crenothrix and Sphaerotilus. They believe the genus Leptothrix rather than Sphaerotilus exist in the tubes because the water source was fresh, unlike the polluted water in which Sphaerotilus are usually found. The TEM preparations worked well. The cryogenic method rapidly froze the cells in place and allowed them to view their morphology. The FAA method, as stated previously, was the best of the three methods because it gave the best contrast. The gluteraldehyde samples did not come out as well. It is possible that the gluteraldehyde the authors prepared was still too concentrated and did not mix well. Although these bacteria were collected from springs and then cultured in an environment containing a presumably pure iron-bearing metal, it seems the tube already containing Manganese Gradient Medium could be used with a piece of metal containing these bacteria. A small piece of corroding metal could then be inserted into the test tube and cultured to study the bacteria.

  2. Enhanced oxidative stress is responsible for TRPV4-induced neurotoxicity

    Directory of Open Access Journals (Sweden)

    Zhiwen Hong

    2016-10-01

    Full Text Available Transient receptor potential vanilloid 4 (TRPV4 has been reported to be responsible for neuronal injury in pathological conditions. Excessive oxidative stress can lead to neuronal damage, and activation of TRPV4 increases the production of reactive oxygen species and nitric oxide (NO in many types of cells. The present study explored whether TRPV4-induced neuronal injury is mediated through enhancing oxidative stress. We found that intracerebroventricular injection of the TRPV4 agonist GSK1016790A increased the content of methane dicarboxylic aldehyde (MDA and NO in the hippocampus, which was blocked by administration of the TRPV4 specific antagonist HC-067047. The activities of catalase (CAT and glutathione peroxidase (GSH-Px were decreased by GSK1016790A, whereas the activity of superoxide dismutase remained unchanged. Moreover, the protein level and activity of neuronal nitric oxide synthase (nNOS were increased by GSK1016790A, and the GSK1016790A-induced increase in NO content was blocked by an nNOS specific antagonist ARL-17477. The GSK1016790A-induced modulations of CAT, GSH-Px and nNOS activities and the protein level of nNOS were significantly inhibited by HC-067047. Finally, GSK1016790A-induced neuronal death and apoptosis in the hippocampal CA1 area were markedly attenuated by administration of a reactive oxygen species scavenger Trolox or ARL-17477. We conclude that activation of TRPV4 enhances oxidative stress by inhibiting CAT and GSH-Px and increasing nNOS, which is responsible, at least in part, for TRPV4-induced neurotoxicity.

  3. Oxidative stress induces senescence in human mesenchymal stem cells

    Energy Technology Data Exchange (ETDEWEB)

    Brandl, Anita [Department of Anesthesiology, University Medical Center Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg (Germany); Meyer, Matthias; Bechmann, Volker [Department of Trauma Surgery, University Medical Center Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg (Germany); Nerlich, Michael [Department of Anesthesiology, University Medical Center Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg (Germany); Angele, Peter, E-mail: Peter.Angele@klinik.uni-regensburg.de [Department of Trauma Surgery, University Medical Center Regensburg, Franz-Josef-Strauss-Allee 11, 93042 Regensburg (Germany)

    2011-07-01

    Mesenchymal stem cells (MSCs) contribute to tissue repair in vivo and form an attractive cell source for tissue engineering. Their regenerative potential is impaired by cellular senescence. The effects of oxidative stress on MSCs are still unknown. Our studies were to investigate into the proliferation potential, cytological features and the telomere linked stress response system of MSCs, subject to acute or prolonged oxidant challenge with hydrogen peroxide. Telomere length was measured using the telomere restriction fragment assay, gene expression was determined by rtPCR. Sub-lethal doses of oxidative stress reduced proliferation rates and induced senescent-morphological features and senescence-associated {beta}-galactosidase positivity. Prolonged low dose treatment with hydrogen peroxide had no effects on cell proliferation or morphology. Sub-lethal and prolonged low doses of oxidative stress considerably accelerated telomere attrition. Following acute oxidant insult p21 was up-regulated prior to returning to initial levels. TRF1 was significantly reduced, TRF2 showed a slight up-regulation. SIRT1 and XRCC5 were up-regulated after oxidant insult and expression levels increased in aging cells. Compared to fibroblasts and chondrocytes, MSCs showed an increased tolerance to oxidative stress regarding proliferation, telomere biology and gene expression with an impaired stress tolerance in aged cells.

  4. Prednisolone reduces nitric oxide-induced migraine

    DEFF Research Database (Denmark)

    Tfelt-Hansen, P; Daugaard, D; Lassen, L H

    2009-01-01

    BACKGROUND AND PURPOSE: Glyceryl trinitrate (GTN) induces delayed migraine attacks in migraine patients. The purpose of this study was to investigate whether pre-treatment with prednisolon could decrease this effect of GTN. METHODS: In this double-blind, randomized and placebo-controlled, crossover...... study 15 migraineurs with migraine without aura were pre-treated with 150 mg of prednisolone or placebo followed by a 20-min infusion of GTN (0.5 ug/kg/min). One hour after the GTN-infusion, the participants were sent home, but continued to rate headache and possible associated symptoms by filling out...... a headache diary every hour for 12 h. There were two equal primary efficacy end-points: frequency of delayed migraine and intensity of delayed headache. RESULTS: Nine patients experienced a GTN headache fulfilling the diagnostic criteria for migraine without aura on the placebo day compared with four...

  5. Lycopene Protects the Diabetic Rat Kidney Against Oxidative Stress-mediated Oxidative Damage Induced by Furan

    OpenAIRE

    Dilek Pandir; Betul Unal; Hatice Bas

    2016-01-01

    Furan is a food and environmental contaminant and a potent carcinogen in animals. Lycopene is one dietary carotenoid found in fruits such as tomato, watermelon and grapefruit. The present study was designed to explore the protective effect of lycopene against furan-induced oxidative damage in streptozotocin (STZ)-induced diabetic rat kidney. At the end of the experimental period (28 days), we found that lycopene markedly decreased the malondialdehide (MDA) levels in the kidney, urea, uric aci...

  6. Acute heat stress induces oxidative stress in broiler chickens.

    Science.gov (United States)

    Lin, Hai; Decuypere, Eddy; Buyse, Johan

    2006-05-01

    The stress responses and possible oxidative damage in plasma, liver and heart were investigated in broiler chickens acutely exposed to high temperature. Eighty 5-week old broiler chickens were exposed to 32 degrees C for 6h. The extent of lipid peroxidation, activities of superoxide dismutase and total antioxidant power in plasma, liver and heart tissues were investigated. Meanwhile, the blood metabolites such as glucose, urate, triiodothyronine, thyroxine, corticosterone, ceruloplasmin and creatine kinase were measured before and after 3 and 6h of heat exposure. The results showed that oxidative stress could be induced in 5-week old broiler chickens by acute heat exposure (32 degrees C, 6h). The results suggest that the elevated body temperature can induce the metabolic changes that are involved in the induction of oxidative stress. The liver is more susceptible to oxidative stress than heart during acute heat exposure in broiler chickens. The oxidative stress should be considered as part of the stress response of broiler chickens to heat exposure.

  7. Gentamicin induced nitric oxide-related oxidative damages on vestibular afferents in the guinea pig.

    Science.gov (United States)

    Hong, Sung Hwa; Park, Sook Kyung; Cho, Yang-Sun; Lee, Hyun-Seok; Kim, Ki Ryung; Kim, Myung Gu; Chung, Won-Ho

    2006-01-01

    Gentamicin is a well-known ototoxic aminoglycoside. However, the mechanism underlying this ototoxicity remains unclear. One of the mechanisms which may be responsible for this ototoxicity is excitotoxic damage to hair cells. The overstimulation of the N-methyl-d-aspartate (NMDA) receptors increases the production of nitric oxide (NO), which induces oxidative stress on hair cells. In order to determine the mechanism underlying this excitotoxicity, we treated guinea pigs with gentamicin by placing gentamicin (0.5 mg) pellets into a round window niche. After the sacrifice of the animals, which occurred at 3, 7 and 14 days after the treatment, the numbers of hair cells in the animals were counted with a scanning electron microscope. We then performed immunostaining using neuronal nitric oxide synthase (nNOS), inducible NOS (iNOS) and nitrotyrosine antibodies. The number of hair cells in the animals was found to decrease significantly after 7 days. nNOS and iNOS expression levels were observed to have increased 3 days after treatment. Nitrotyrosine was expressed primarily at the calyceal afferents of the type I hair cells 3 days after treatment. Terminal deoxynucleotidyl transferase biotin-dUTP nick end labeling (TUNEL) staining revealed positive hair cells 3 days after treatment. Our results suggest that inner ear treatment with gentamicin may upregulate nNOS and iNOS to induce oxidative stress in the calyceal afferents of type I hair cells, via nitric oxide overproduction.

  8. Obesity Exacerbates Sepsis-Induced Oxidative Damage in Organs.

    Science.gov (United States)

    Petronilho, Fabricia; Giustina, Amanda Della; Nascimento, Diego Zapelini; Zarbato, Graciela Freitas; Vieira, Andriele Aparecida; Florentino, Drielly; Danielski, Lucinéia Gainski; Goldim, Mariana Pereira; Rezin, Gislaine Tezza; Barichello, Tatiana

    2016-12-01

    Sepsis progression is linked to the imbalance between reactive oxygen species and antioxidant enzymes. Sepsis affects multiple organs, but when associated with a chronic inflammatory disease, such as obesity, it may be exacerbated. We hypothesized that obesity could aggravate the oxidative damage to peripheral organs of rats submitted to an animal model of sepsis. Male Wistar rats aged 8 weeks received hypercaloric nutrition for 2 months to induce obesity. Sepsis was induced by cecal ligation and puncture (CLP) procedure, and sham-operated rats were considered as control group. The experimental groups were divided into sham + eutrophic, sham + obese, CLP + eutrophic, and CLP + obese. Twelve and 24 h after surgery, oxidative damage to lipids and proteins and superoxide dismutase (SOD) and catalase (CAT) activities were evaluated in the liver, lung, kidney, and heart. The data indicate that obese rats subjected to sepsis present oxidative stress mainly in the lung and liver. This alteration reflected an oxidative damage to lipids and proteins and an imbalance of SOD and CAT levels, especially 24 h after sepsis. It follows that obesity due to its pro-inflammatory phenotype can aggravate sepsis-induced damage in peripheral organs.

  9. Simvastatin Attenuates Contrast-Induced Nephropathy through Modulation of Oxidative Stress, Proinflammatory Myeloperoxidase, and Nitric Oxide

    Directory of Open Access Journals (Sweden)

    Ketab E. Al-Otaibi

    2012-01-01

    Full Text Available Contrast media- (CM- induced nephropathy is a serious complication of radiodiagnostic procedures. Available data suggests that the development of prophylaxis strategies is limited by poor understanding of pathophysiology of CM-induced nephropathy. Present study was designed to determine the role of oxidative stress, myeloperoxidase, and nitric oxide in the pathogenesis of iohexol model of nephropathy and its modification with simvastatin (SSTN. Adult Sprague Dawley rats were divided into seven groups. After 24 h of water deprivation, all the rats except in control and SSTN-only groups were injected (10 ml/kg with 25% glycerol. After 30 min, SSTN (15, 30, and 60 mg/kg was administered orally, daily for 4 days. Twenty-four hours after the glycerol injection, iohexol was infused (8 ml/kg through femoral vein over a period of 2 min. All the animals were sacrificed on day 5 and blood and kidneys were collected for biochemical and histological studies. The results showed that SSTN dose dependently attenuated CM-induced rise of creatinine, urea, and structural abnormalities suggesting its nephroprotective effect. A significant increase in oxidative stress (increased lipid hydroperoxides and reduced glutathione levels and myeloperoxidase (MPO and decreased nitric oxide in CM group were reversed by SSTN. These findings support the use of SSTN to combat CM-induced nephrotoxicity.

  10. Ultraviolet-induced erasable photochromism in bilayer metal oxide films

    Science.gov (United States)

    Terakado, Nobuaki; Tanaka, Keiji; Nakazawa, Akira

    2011-09-01

    We demonstrate that the optical transmittance of bilayer samples consisting of pyrolytically coated amorphous Mg-Sn-O and metal oxide films such as In 2O 3 and SnO 2 decreases upon ultraviolet illumination, but can be recovered by annealing in air at ˜300 ∘C. Spectral, structural, and compositional studies suggest that this photochromic phenomenon is induced by photoelectronic excitation in the Mg-Sn-O film, electron injection into the metal oxide, which becomes negatively charged, and subsequent formation of metallic particles, which absorb and/or scatter visible light.

  11. Investigation of the Interaction Between Sodium(meta) Arsenite and Catechin via ESI Tandem Mass Spectrometry

    Institute of Scientific and Technical Information of China (English)

    CUI Sheng-yun; WEN Jin-feng; KIM Seung-jin; LEE Yong-ill

    2007-01-01

    Catechin, one of the main components of green tea, is considered to have the remedy effect of arsenic poison,although the chemical mechanism is not well known. In this study, sodium(meta) selenite, which is used as herbisolution to investigate the interaction between toxic inorganic arsenic compound and catechin via ESI tandem mass spectrometry. The interaction products of mono-methylated arsenic with catechin in the presence of methanol were identified in the negative mode. Collission induced dissociation(CID) mass spectrometric measurements indicate that monomethylated arsenic was "alkylated" strongly by conjugation at the sites of C2' and C5' in the phenyl ring B of the catechin. The interaction mechanism between sodium(meta) arsenite and catechin was proposed. The results provide useful information to understand the chemical pathway of the detoxification of the arsenic toxicity by catechin.

  12. Enzymatic adaptations to arsenic-induced oxidative stress in Zea mays and genotoxic effect of arsenic in root tips of Vicia faba and Zea mays.

    Science.gov (United States)

    Duquesnoy, Isabelle; Champeau, Gabrielle Marie; Evray, Germaine; Ledoigt, Gérard; Piquet-Pissaloux, Agnès

    2010-01-01

    Agronomic plant species may display physiological and biochemical responses to oxidative stress caused by heavy metals and metalloids. Zea mays plants were grown hydroponically for eight days at different concentrations of As (0, 134 and 668 μM) and at different pH (4, 7 and 9). Metabolic variations in response to As toxicity were measured using physiological parameters and antioxidant enzymatic activities. A significant decrease in SOD activity was observed in the leaves and roots of Z. mays with the majority of As treatments. As decreased G-POX activity less in leaves than in roots. An increase in the concentration of As increased APX activity in leaves and roots, except As(V) at pH 4 and pH 9 in the leaves and As(III) at pH 9 in the roots, when there was a significant decrease in APX activity at low As concentrations. After exposure to As(V), CAT activity was the same as in the control. As(III) led to an increase in CAT activity in leaves and to a decrease in roots. With increasing concentrations of As(III), CAT activity increased in both leaves and roots whatever the pH. To obtain more detailed knowledge on the effects of arsenate and arsenite exposure on Vicia faba and Z. mays, root meristems were also examined. Roots were fed hydroponically with 134, 334, 534 and 668 μM arsenate or arsenite and 4 × 10(-3)M of maleic hydrazide as positive control, at three different pH. Physiological parameters, the mitotic index and micronuclei frequencies were evaluated in root meristems. At all three pH, the highest As(V) and As(III) concentrations induced a substantial modification in root colour, increased root thickness with stiffening, and reduced root length. High concentrations also caused a significant decrease in the mitotic index, and micronucleus chromosomic aberrations were observed in the root meristems of both species. 2010 Académie des sciences. Published by Elsevier SAS. All rights reserved.

  13. Nivalenol induces oxidative stress and increases deoxynivalenol pro-oxidant effect in intestinal epithelial cells

    Energy Technology Data Exchange (ETDEWEB)

    Del Regno, Marisanta; Adesso, Simona; Popolo, Ada [Department of Pharmacy, School of Pharmacy, University of Salerno, Via Giovanni Paolo II, 132–84084 Fisciano, Salerno (Italy); Quaroni, Andrea [Department of Biomedical Sciences, Cornell University, Veterinary Research Tower, Cornell University, Ithaca, NY 14853–6401 (United States); Autore, Giuseppina [Department of Pharmacy, School of Pharmacy, University of Salerno, Via Giovanni Paolo II, 132–84084 Fisciano, Salerno (Italy); Severino, Lorella [Department of Pathology and Animal Health, Division of Toxicology, School of Veterinary Medicine, University of Naples “Federico II”, Via Delpino 1, 80137 Naples (Italy); Marzocco, Stefania, E-mail: smarzocco@unisa.it [Department of Pharmacy, School of Pharmacy, University of Salerno, Via Giovanni Paolo II, 132–84084 Fisciano, Salerno (Italy)

    2015-06-01

    Mycotoxins are secondary fungal metabolites often found as contaminants in almost all agricultural commodities worldwide, and the consumption of food or feed contaminated by mycotoxins represents a major risk for human and animal health. Reactive oxygen species are normal products of cellular metabolism. However, disproportionate generation of reactive oxygen species poses a serious problem to bodily homeostasis and causes oxidative tissue damage. In this study we analyzed the effect of two trichothecenes mycotoxins: nivalenol and deoxynivalenol, alone and in combination, on oxidative stress in the non-tumorigenic intestinal epithelial cell line IEC-6. Our results indicate the pro-oxidant nivalenol effect in IEC-6, the stronger pro-oxidant effect of nivalenol when compared to deoxynivalenol and, interestingly, that nivalenol increases deoxynivalenol pro-oxidative effects. Mechanistic studies indicate that the observed effects were mediated by NADPH oxidase, calcium homeostasis alteration, NF-kB and Nrf2 pathways activation and by iNOS and nitrotyrosine formation. The toxicological interaction by nivalenol and deoxynivalenol reported in this study in IEC-6, points out the importance of the toxic effect of these mycotoxins, mostly in combination, further highlighting the risk assessment process of these toxins that are of growing concern. - Highlights: • Nivalenol induces oxidative stress in intestinal epithelial cells (IECs). • Nivalenol increases deoxynivalenol pro-oxidant effects in IECs. • Nivalenol and deoxynivalenol trigger antioxidant response IECs. • These results indicate the importance of mycotoxins co-contamination.

  14. Complexation of arsenite with phytochelatins reduces arsenite efflux and translocation from roots to shoots in Arabidopsis.

    Science.gov (United States)

    Liu, Wen-Ju; Wood, B Alan; Raab, Andrea; McGrath, Steve P; Zhao, Fang-Jie; Feldmann, Jörg

    2010-04-01

    Complexation of arsenite [As(III)] with phytochelatins (PCs) is an important mechanism employed by plants to detoxify As; how this complexation affects As mobility was little known. We used high-resolution inductively coupled plasma-mass spectrometry and accurate mass electrospray ionization-mass spectrometry coupled to HPLC to identify and quantify As(III)-thiol complexes and free thiol compounds in Arabidopsis (Arabidopsis thaliana) exposed to arsenate [As(V)]. As(V) was efficiently reduced to As(III) in roots. In wild-type roots, 69% of As was complexed as As(III)-PC4, As(III)-PC3, and As(III)-(PC2)2. Both the glutathione (GSH)-deficient mutant cad2-1 and the PC-deficient mutant cad1-3 were approximately 20 times more sensitive to As(V) than the wild type. In cad1-3 roots, only 8% of As was complexed with GSH as As(III)-(GS)3 and no As(III)-PCs were detected, while in cad2-1 roots, As(III)-PCs accounted for only 25% of the total As. The two mutants had a greater As mobility, with a significantly higher accumulation of As(III) in shoots and 4.5 to 12 times higher shoot-to-root As concentration ratio than the wild type. Roots also effluxed a substantial proportion of the As(V) taken up as As(III) to the external medium, and this efflux was larger in the two mutants. Furthermore, when wild-type plants were exposed to l-buthionine sulfoximine or deprived of sulfur, both As(III) efflux and root-to-shoot translocation were enhanced. The results indicate that complexation of As(III) with PCs in Arabidopsis roots decreases its mobility for both efflux to the external medium and for root-to-shoot translocation. Enhancing PC synthesis in roots may be an effective strategy to reduce As translocation to the edible organs of food crops.

  15. Cerebrolysin protects against rotenone-induced oxidative stress and neurodegeneration

    Directory of Open Access Journals (Sweden)

    Abdel-Salam OME

    2014-05-01

    Full Text Available Omar ME Abdel-Salam,1 Nadia A Mohammed,2 Eman R Youness,2 Yasser A Khadrawy,3 Enayat A Omara,4 Amany A Sleem51Department of Toxicology and Narcotics, 2Department of Medical Biochemistry, 3Department of Physiology, 4Department of Pathology, 5Department of Pharmacology, National Research Centre, Dokki, Cairo, EgyptAbstract: We investigated the effect of cerebrolysin, a peptide mixture used for promoting memory and recovery from cerebral stroke, on the development of oxidative stress and nigrostriatal cell injury induced by rotenone administration in rats. Rotenone 1.5 mg/kg was given subcutaneously three times weekly either alone or in combination with cerebrolysin at 21.5, 43, or 86 mg/kg. Rats were euthanized 14 days after starting the rotenone injection. Lipid peroxidation (malondialdehyde, reduced glutathione (GSH, nitric oxide (nitrite concentrations, paraoxonase 1 (PON1, and acetylcholinesterase (AChE activities – as well as the monocyte chemoattractant protein-1 (MCP-1 and the antiapoptotic protein Bcl-2 – were measured in the brain. Histopathology, tyrosine hydroxylase, inducible nitric oxide synthase (iNOS, tumor necrosis factor-α (TNF-α, and cleaved caspase-3 immunohistochemistry were also performed. Rotenone caused a significantly elevated oxidative stress and proinflammatory response in the different brain regions. Malondialdehyde and nitric oxide concentrations were significantly increased, while GSH markedly decreased in the cerebral cortex, striatum, hippocampus, and in the rest of the brain. PON1 and AChE activities significantly decreased with respect to the control levels after rotenone application. Striatal Bcl-2 was significantly decreased while MCP-1 increased following rotenone injection. Rotenone caused prominent iNOS, TNF-α, and caspase-3 immunostaining in the striatum and resulted in markedly decreased tyrosine hydroxylase immunoreactivity in the substantia nigra and striatum. Cerebrolysin coadministered with

  16. Increased Oxidative Stress in Women With Pregnancy-induced Hypertension

    Institute of Scientific and Technical Information of China (English)

    JUN-FU ZHOU; XIN-YU WANG; XUE-JUN SHANGGUAN; ZU-MING GAO; SHU-MEI ZHANG; WEI-QIANG XIAO; CHANG-GUI CHEN

    2005-01-01

    Objective To investigate whether pregnancy-induced hypertension (PIH) may increase oxidative stress in women with PIH, and to explore the mechanisms by which PIH may increase oxidative stress and potential free radical damage. Methods Seventy women with PIH and seventy women with uncomplicated normotensive pregnancy (UNP) whose age, nutritional conditions, levels of hemoglobin and albumin were all matched, were enrolled in a randomized controlled trial. Their plasma concentrations of nitric oxide (NO), vitamin C (VC), vitamin E (VE), and β-carotene (β-CAR) as well as their erythrocyte malondialdehyde (MDA), and activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPX)were determined by spectrophotometry. Results Compared with average values of the above experimental parameters in the women with UNP, the average value of erythrocyte MDA in the women with PIH significantly increased (P<0.0001), while the average values of plasma NO, VC, VE, and β-CAR as well as those of erythrocyte SOD, CAT, and GPX in the women with PIH significantly decreased (P<0.0005-0.0001). The findings from partial correlation analysis (controlling for age) for 70women with PIH showed that with elevated systolic blood pressure (SBP) and diastolic blood pressure (DBP), MDA value gradually increased (P<0.001), and NO, VC, VE, β-CAR, SOD, CAT, and GPX values gradually decreased (P<0.02-0.001).The fmdings from reliability analysis for NO, VC, VE, β-CAR, SOD, CAT, GPX, and MDA values used to reflect increased oxidative stress and potential free radical damage in women with PIH showed that the reliability coefficients (alpha, 8 items) =0.7062, P< 0.0001, and the standardized item alpha = 0.9116, P< 0.0001. Conclusion The findings in the present research suggest that pregnancy-induced hypertension can increase oxidative stress and potential free radical damage in women with pregnancy-induced hypertension.

  17. THz-Pulse-Induced Selective Catalytic CO Oxidation on Ru

    Science.gov (United States)

    LaRue, Jerry L.; Katayama, Tetsuo; Lindenberg, Aaron; Fisher, Alan S.; Ã-ström, Henrik; Nilsson, Anders; Ogasawara, Hirohito

    2015-07-01

    We demonstrate the use of intense, quasi-half-cycle THz pulses, with an associated electric field component comparable to intramolecular electric fields, to direct the reaction coordinate of a chemical reaction by stimulating the nuclear motions of the reactants. Using a strong electric field from a THz pulse generated via coherent transition radiation from an ultrashort electron bunch, we present evidence that CO oxidation on Ru(0001) is selectively induced, while not promoting the thermally induced CO desorption process. The reaction is initiated by the motion of the O atoms on the surface driven by the electric field component of the THz pulse, rather than thermal heating of the surface.

  18. Diaphragmatic Breathing Reduces Exercise-Induced Oxidative Stress

    Directory of Open Access Journals (Sweden)

    Daniele Martarelli

    2011-01-01

    Full Text Available Diaphragmatic breathing is relaxing and therapeutic, reduces stress, and is a fundamental procedure of Pranayama Yoga, Zen, transcendental meditation and other meditation practices. Analysis of oxidative stress levels in people who meditate indicated that meditation correlates with lower oxidative stress levels, lower cortisol levels and higher melatonin levels. It is known that cortisol inhibits enzymes responsible for the antioxidant activity of cells and that melatonin is a strong antioxidant; therefore, in this study, we investigated the effects of diaphragmatic breathing on exercise-induced oxidative stress and the putative role of cortisol and melatonin hormones in this stress pathway. We monitored 16 athletes during an exhaustive training session. After the exercise, athletes were divided in two equivalent groups of eight subjects. Subjects of the studied group spent 1 h relaxing performing diaphragmatic breathing and concentrating on their breath in a quiet place. The other eight subjects, representing the control group, spent the same time sitting in an equivalent quite place. Results demonstrate that relaxation induced by diaphragmatic breathing increases the antioxidant defense status in athletes after exhaustive exercise. These effects correlate with the concomitant decrease in cortisol and the increase in melatonin. The consequence is a lower level of oxidative stress, which suggests that an appropriate diaphragmatic breathing could protect athletes from long-term adverse effects of free radicals.

  19. Aluminium oxide nanoparticles induced morphological changes, cytotoxicity and oxidative stress in Chinook salmon (CHSE-214) cells.

    Science.gov (United States)

    Srikanth, Koigoora; Mahajan, Amit; Pereira, Eduarda; Duarte, Armando Costa; Venkateswara Rao, Janapala

    2015-10-01

    Aluminium oxide nanoparticles (Al2 O3 NPs) are increasingly used in diverse applications that has raised concern about their safety. Recent studies suggested that Al2 O3 NPs induced oxidative stress may be the cause of toxicity in algae, Ceriodaphnia dubia, Caenorhabditis elegans and Danio rerio. However, there is paucity on the toxicity of Al2 O3 NPs on fish cell lines. The current study was aimed to investigate Al2 O3 NPs induced cytotoxicity, oxidative stress and morphological abnormality of Chinnok salmon cells (CHSE-214). A dose-dependent decline in cell viability was observed in CHSE-214 cells exposed to Al2 O3 NPs. Oxidative stress induced by Al2 O3 NPs in CHSE-214 cells has resulted in the significant reduction of superoxide dismutase, catalase and glutathione in a dose-dependent manner. However, a significant increase in glutathione sulfo-transferase and lipid peroxidation was observed in CHSE-214 cells exposed to Al2 O3 NPs in a dose-dependent manner. Significant morphological changes in CHSE-214 cells were observed when exposed to Al2 O3 NPs at 6, 12 and 24 h. The cells started to detach and appear spherical at 6 h followed by loss of cellular contents resulting in the shrinking of the cells. At 24 h, the cells started to disintegrate and resulted in cell death. Our data demonstrate that Al2 O3 NPs induce cytotoxicity and oxidative stress in a dose-dependent manner in CHSE-214 cells. Thus, our current work may serve as a base-line study for future evaluation of toxicity studies using CHSE-214 cells.

  20. Phosphine-induced oxidative damage in rats: attenuation by melatonin.

    Science.gov (United States)

    Hsu, C; Han, B; Liu, M; Yeh, C; Casida, J E

    2000-02-15

    Phosphine (PH(3)), from hydrolysis of aluminum, magnesium and zinc phosphide, is an insecticide and rodenticide. Earlier observations on PH(3)-poisoned insects, mammals and a mammalian cell line led to the proposed involvement of oxidative damage in the toxic mechanism. This investigation focused on PH(3)-induced oxidative damage in rats and antioxidants as candidate protective agents. Male Wistar rats were treated ip with PH(3) at 2 mg/kg. Thirty min later the brain, liver, and lung were analyzed for glutathione (GSH) levels and lipid peroxidation (as malondialdehyde and 4-hydroxyalkenals) and brain and lung for 8-hydroxydeoxyguanosine (8-OH-dGuo) in DNA. PH(3) caused a significant decrease in GSH concentration and elevation in lipid peroxidation in brain (36-42%), lung (32-38%) and liver (19-25%) and significant increase of 8-OH-dGuo in DNA of brain (70%) and liver (39%). Antioxidants administered ip 30 min before PH(3) were melatonin, vitamin C, and beta-carotene at 10, 30, and 6 mg/kg, respectively. The PH(3)-induced changes were significantly or completely blocked by melatonin while vitamin C and beta-carotene were less effective or inactive. These findings establish that PH(3) induces and melatonin protects against oxidative damage in the brain, lung and liver of rats and suggest the involvement of reactive oxygen species in the genotoxicity of PH(3).

  1. Azadirachta indica Attenuates Cisplatin-Induced Nephrotoxicity and Oxidative Stress

    Directory of Open Access Journals (Sweden)

    Ahmed E. Abdel Moneim

    2014-01-01

    Full Text Available We investigated the effects of methanolic leaves extract of Azadirachta indica (MLEN, 500 mg/kg bwt on cisplatin- (CP- induced nephrotoxicity and oxidative stress in rats. CP (5 mg/kg bwt was injected intraperitoneally and MLEN was given by gastric gavage for 5 days before or after CP injection. After 5 days of CP injection, CP-induced injury of the renal tissue was evidenced (i as histopathological damage of the renal tissue, (ii as increases in serum uric acid, urea, and creatinine, (iii as increases in malondialdehyde (MDA and nitric oxide (NO, (iv as decreases in the level of glutathione and activities of superoxide dismutase, catalase, glutathione reductase, glutathione-S-transferase, and glutathione peroxidase, and (v as increase in the expression of nuclear factor kappa B and apoptosis in kidney tissues. However, the oral administration of MLEN to CP-intoxicated rats for 5 days brought back MDA, NO production, and enzymatic and nonenzymatic antioxidants to near normalcy. Moreover, the histological observations evidenced that neem extract effectively rescues the kidney from CP-mediated oxidative damage. Furthermore, PCR results for caspase-3 and caspase-9 and Bax genes showed downregulation in MLEN treated groups. Therefore, Azadirachta indica can be considered a potential candidate for protection of nephrotoxicity induced by cisplatin.

  2. Hypochlorite-induced oxidation of proteins in plasma

    DEFF Research Database (Denmark)

    Hawkins, C L; Davies, Michael Jonathan

    1999-01-01

    Activated phagocyte cells generate hypochlorite (HOCl) via the release of H2O2 and the enzyme myeloperoxidase. Plasma proteins are major targets for HOCl, although little information is available about the mechanism(s) of oxidation. In this study the reaction of HOCl (at least 50 microM) with dil......Activated phagocyte cells generate hypochlorite (HOCl) via the release of H2O2 and the enzyme myeloperoxidase. Plasma proteins are major targets for HOCl, although little information is available about the mechanism(s) of oxidation. In this study the reaction of HOCl (at least 50 micro......M) with diluted fresh human plasma has been shown to generate material that oxidizes 5-thio-2-nitrobenzoic acid; these oxidants are believed to be chloramines formed from the reaction of HOCl with protein amine groups. Chloramines have also been detected with isolated plasma proteins treated with HOCl. In both....... These results are consistent with protein-derived chloramines, and the radicals derived from them, as contributing agents in HOCl-induced plasma protein oxidation....

  3. Oxidative-stress-induced epigenetic changes in chronic diabetic complications.

    Science.gov (United States)

    Feng, Biao; Ruiz, Michael Anthony; Chakrabarti, Subrata

    2013-03-01

    Oxidative stress plays an important role in the development and progression of chronic diabetic complications. Diabetes causes mitochondrial superoxide overproduction in the endothelial cells of both large and small vessels. This increased superoxide production causes the activation of several signal pathways involved in the pathogenesis of chronic complications. In particular, endothelial cells are major targets of glucose-induced oxidative damage in the target organs. Oxidative stress activates cellular signaling pathways and transcription factors in endothelial cells including protein kinase C (PKC), c-Jun-N-terminal kinase (JNK), p38 mitogen-activated protein kinase (MAPK), forkhead box O (FOXO), and nuclear factor kappa-B (NF-κB). Oxidative stress also causes DNA damage and activates DNA nucleotide excision repair enzymes including the excision repair cross complimenting 1(ERCC1), ERCC4, and poly(ADP-ribose) polymerase (PARP). Augmented production of histone acetyltransferase p300, and alterations of histone deacetylases, including class III deacetylases sirtuins, are also involved in this process. Recent research has found that small noncoding RNAs, like microRNA, are a new kind of regulator associated with chronic diabetic complications. There are extensive and complicated interactions and among these molecules. The purpose of this review is to demonstrate the role of oxidative stress in the development of diabetic complications in relation to epigenetic changes such as acetylation and microRNA alterations.

  4. Influence of a thiazole derivative on ethanol and thermally oxidized sunflower oil-induced oxidative stress.

    Science.gov (United States)

    Kode, Aruna; Rajagopalan, Rukkumani; Penumathsa, Suresh Varma; Menon, Venugopal P

    2004-10-01

    The present work describes the protective influence of the dendrodoine analogue (DA) [4-amino-5-benzoyl-2-(4-methoxy phenylamino) thiazole] on thermally oxidized sunflower oil and ethanol-induced oxidative stress. Ethanol was fed to animals at a level of 20% [(7.9 g/kg body weight (bw)] and thermally oxidized sunflower oil at a level of 15% (15 mL/100 g feed). Hepatotoxicity was assessed by measuring the activity of plasma aspartate transaminase (AST), alkaline phosphatase (ALP) and gamma-glutamyl transferase (GGT), which were elevated in thermally oxidized oil, and ethanol fed rats when compared with normal control rats. Tissue damage was associated with increased lipid peroxidation and disruption in the antioxidant defence mechanism in thermally oxidized oil- and ethanol-fed groups when compared with normal control group. The activity of liver marker enzymes (AST, ALP and GGT) and the level of lipid peroxidation decreased when DA was administered along with ethanol and thermally oxidized oil. The antioxidant status was near normal in DA-administered groups. Thus we propose that DA exerts antioxidant properties by modulating the activity of hepatic marker enzymes, level of lipid peroxidation and antioxidant status.

  5. X-ray crystal structure of arsenite-inhibited xanthine oxidase: μ-sulfido,μ-oxo double bridge between molybdenum and arsenic in the active site.

    Science.gov (United States)

    Cao, Hongnan; Hall, James; Hille, Russ

    2011-08-17

    Xanthine oxidoreductase is a molybdenum-containing enzyme that catalyzes the hydroxylation reaction of sp(2)-hybridized carbon centers of a variety of substrates, including purines, aldehydes, and other heterocyclic compounds. The complex of arsenite-inhibited xanthine oxidase has been characterized previously by UV-vis, electron paramagnetic resonance, and X-ray absorption spectroscopy (XAS), and the catalytically essential sulfido ligand of the square-pyrimidal molybdenum center has been suggested to be involved in arsenite binding through either a μ-sulfido,μ-oxo double bridge or a single μ-sulfido bridge. However, this is contrary to the crystallographically observed single μ-oxo bridge between molybdenum and arsenic in the desulfo form of aldehyde oxidoreductase from Desulfovibrio gigas (an enzyme closely related to xanthine oxidase), whose molybdenum center has an oxo ligand replacing the catalytically essential sulfur, as seen in the functional form of xanthine oxidase. Here we use X-ray crystallography to characterize the molybdenum center of arsenite-inhibited xanthine oxidase and solve the structures of the oxidized and reduced inhibition complexes at 1.82 and 2.11 Å resolution, respectively. We observe μ-sulfido,μ-oxo double bridges between molybdenum and arsenic in the active sites of both complexes. Arsenic is four-coordinate with a distorted trigonal-pyramidal geometry in the oxidized complex and three-coordinate with a distorted trigonal-planar geometry in the reduced complex. The doubly bridged binding mode is in agreement with previous XAS data indicating that the catalytically essential sulfur is also essential for the high affinity of reduced xanthine oxidoreductase for arsenite.

  6. Arsenic responsive microRNAs in vivo and their potential involvement in arsenic-induced oxidative stress

    Energy Technology Data Exchange (ETDEWEB)

    Ren, Xuefeng, E-mail: xuefengr@buffalo.edu [Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, The State University of New York, Buffalo, NY 14214 (United States); Department of Pharmacology and Toxicology, School of Biomedical Sciences, The State University of New York, Buffalo, NY 14214 (United States); Gaile, Daniel P. [Department of Biostatistics, School of Public Health and Health Professions, the State University of New York, Buffalo, NY 14214 (United States); Gong, Zhihong [Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, The State University of New York, Buffalo, NY 14214 (United States); Qiu, Wenting [School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035 (China); Ge, Yichen [Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, The State University of New York, Buffalo, NY 14214 (United States); Zhang, Chuanwu; Huang, Chenping; Yan, Hongtao [School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035 (China); Olson, James R. [Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, The State University of New York, Buffalo, NY 14214 (United States); Department of Pharmacology and Toxicology, School of Biomedical Sciences, The State University of New York, Buffalo, NY 14214 (United States); Kavanagh, Terrance J. [Department of Environmental and Occupational Health Sciences, University of Washington, Seattle, WA 98195 (United States); Wu, Hongmei, E-mail: hongmeiwwu@hotmail.com [School of Public Health, Wenzhou Medical University, Wenzhou, Zhejiang 325035 (China)

    2015-03-15

    Arsenic exposure is postulated to modify microRNA (miRNA) expression, leading to changes of gene expression and toxicities, but studies relating the responses of miRNAs to arsenic exposure are lacking, especially with respect to in vivo studies. We utilized high-throughput sequencing technology and generated miRNA expression profiles of liver tissues from Sprague Dawley (SD) rats exposed to various concentrations of sodium arsenite (0, 0.1, 1, 10 and 100 mg/L) for 60 days. Unsupervised hierarchical clustering analysis of the miRNA expression profiles clustered the SD rats into different groups based on the arsenic exposure status, indicating a highly significant association between arsenic exposure and cluster membership (p-value of 0.0012). Multiple miRNA expressions were altered by arsenic in an exposure concentration-dependent manner. Among the identified arsenic-responsive miRNAs, several are predicted to target Nfe2l2-regulated antioxidant genes, including glutamate–cysteine ligase (GCL) catalytic subunit (GCLC) and modifier subunit (GCLM) which are involved in glutathione (GSH) synthesis. Exposure to low concentrations of arsenic increased mRNA expression for Gclc and Gclm, while high concentrations significantly reduced their expression, which were correlated to changes in hepatic GCL activity and GSH level. Moreover, our data suggested that other mechanisms, e.g., miRNAs, rather than Nfe2l2-signaling pathway, could be involved in the regulation of mRNA expression of Gclc and Gclm post-arsenic exposure in vivo. Together, our findings show that arsenic exposure disrupts the genome-wide expression of miRNAs in vivo, which could lead to the biological consequence, such as an altered balance of antioxidant defense and oxidative stress. - Highlights: • Chronic arsenic exposure induces changes of hepatic miRNA expression profiles. • Hepatic GCL activity and GSH level in rats are altered following arsenic exposure. • Arsenic induced GCL expression change is

  7. Oxidation-induced loss of the ability of HDL to counteract the inhibitory effect of oxidized LDL on vasorelaxation.

    Science.gov (United States)

    Perségol, Laurence; Brindisi, Marie-Claude; Rageot, David; Pais de Barros, Jean-Paul; Monier, Serge; Vergès, Bruno; Duvillard, Laurence

    2015-11-01

    Several current diseases are associated with an increase in the oxidation of HDL, which is likely to impair their functionality. Our aim was to identify whether oxidation could change the protective effect of HDL against the deleterious effect on vasoreactivity induced by oxidative stress. HDL from healthy subjects were oxidized in vitro by Cu(2+), and the ability of oxidized HDL to counteract the inhibitory effect of oxidized LDL on acetylcholine-induced vasodilation was tested on isolated rabbit aorta rings. Oxidation of HDL was evidenced by the increase in the 7-oxysterols/cholesterol ratio (3.20 ± 1.12 vs 0.02 ± 0.01 % in native HDL, p HDL counteracted this inhibition (E max = 72.4 ± 4.8 vs 50.2 ± 5.0 % p HDL had no effect on oxidized LDL-induced inhibition on endothelium-dependent vasorelaxation (E max = 53.7 ± 4.8 vs 50.2 ± 5.0 %, NS). HDL oxidation is associated with a decreased ability of HDL to remove 7-oxysterols from oxidized LDL. In conclusion, these results show that oxidation of HDL induces the loss of their protective effect against endothelial dysfunction, which could promote atherosclerosis in diseases associated with increased oxidative stress.

  8. Increased nitric oxide release and expression of endothelial and inducible nitric oxide synthases in mildly changed porcine mitral valve leaflets

    DEFF Research Database (Denmark)

    Moesgaard, Sophia G; Olsen, Lisbeth H; Viuff, Birgitte M

    2007-01-01

    BACKGROUND AND AIM OF THE STUDY: Little is known of the local role of nitric oxide (NO) in heart valves in relation to heart valve diseases. The study aim was to examine NO release and the expression of both endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS) in re...

  9. Increased nitric oxide release and expression of endothelial and inducible nitric oxide synthases in mildly changed porcine mitral valve leaflets

    DEFF Research Database (Denmark)

    Moesgaard, Sophia Gry; Olsen, Lisbeth Høier; Viuff, Birgitte;

    2007-01-01

    Background and aim of the study: Little is known of the local role of nitric oxide (NO) in heart valves in relation to heart valve diseases. The study aim was to examine NO release and the expression of both endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (i...

  10. Expression of inducible nitric oxide in human lung epithelial cells.

    Science.gov (United States)

    Robbins, R A; Barnes, P J; Springall, D R; Warren, J B; Kwon, O J; Buttery, L D; Wilson, A J; Geller, D A; Polak, J M

    1994-08-30

    Nitric oxide (NO) is increased in the exhaled air of subjects with several airway disorders. To determine if cytokines could stimulate epithelial cells accounting for the increased NO, the capacity of the proinflammatory cytokines (cytomix: tumor necrosis factor-alpha, interleukin-1 beta, and interferon-gamma) to increase inducible nitric oxide synthase (iNOS) was investigated in A549 and primary cultures of human bronchial epithelial cells. Cytomix induced a time-dependent increase in nitrite levels in culture supernatant fluids (p < 0.05). Increased numbers of cells stained for iNOS and increased iNOS mRNA was detected in the cytokine-stimulated cells compared to control (p < 0.05). Dexamethasone diminished the cytokine-induced increase in nitrite, iNOS by immunocytochemistry, and iNOS mRNA. These data demonstrate that cytokines, such as those released by mononuclear cells, can induce lung epithelial iNOS expression and NO release, and that this is attenuated by dexamethasone.

  11. Visible light induced oxidation of water by rare earth manganites, cobaltites and related oxides

    Science.gov (United States)

    Naidu, B. S.; Gupta, Uttam; Maitra, Urmimala; Rao, C. N. R.

    2014-01-01

    A study of the visible light induced oxidation of water by perovskite oxides of the formula LaMO3 (M = transition metal) has revealed the best activity with LaCoO3 which contains Co3+ in the intermediate-spin (IS) with one eg electron. Among the rare earth manganites, only orthorhombic manganites with octahedral Mn3+ ions exhibit good catalytic activity, but hexagonal manganites are poor catalysts. Interestingly, not only the perovskite rare earth cobaltites but also solid solutions of Co3+ in cubic rare earth sesquioxides exhibit catalytic activity comparable to LaCoO3, the Co3+ ion in all these oxides also being in the IS t2g5eg1 state.

  12. Oxidative state and oxidative metabolism in the brain of rats with adjuvant-induced arthritis.

    Science.gov (United States)

    Wendt, Mariana Marques Nogueira; de Sá-Nakanishi, Anacharis Babeto; de Castro Ghizoni, Cristiane Vizioli; Bersani Amado, Ciomar Aparecida; Peralta, Rosane Marina; Bracht, Adelar; Comar, Jurandir Fernando

    2015-06-01

    The purpose of the present study was to evaluate the oxidative status of the brain of arthritic rats, based mainly on the observation that arthritis induces a pronounced oxidative stress in the liver of arthritis rats and that morphological alterations have been reported to occur in patients with rheumatoid arthritis. Rats with adjuvant-induced arthritis were used. These animals presented higher levels of reactive oxygen species (ROS) in the total brain homogenate (25% higher) and in the mitochondria (+55%) when compared to healthy rats. The nitrite plus nitrate contents, nitric oxide (NO) markers, were also increased in both mitochondria (+27%) and cytosol (+14%). Arthritic rats also presented higher levels of protein carbonyl groups in the total homogenate (+43%), mitochondria (+69%) and cytosol (+145%). Arthritis caused a diminution of oxygen consumption in isolated brain mitochondria only when ascorbate was the electron donor. The disease diminished the mitochondrial cytochrome c oxidase activity by 55%, but increased the transmembrane potential by 16%. The pro-oxidant enzyme xanthine oxidase was 150%, 110% and 283% higher, respectively, in the brain homogenate, mitochondria and cytosol of arthritic animals. The same occurred with the calcium-independent NO-synthase activity that was higher in the brain homogenate (90%) and cytosol (122%) of arthritic rats. The catalase activity, on the other hand, was diminished by arthritis in all cellular fractions (between 30 and 40%). It is apparent that the brain of rats with adjuvant-induced arthritis presents a pronounced oxidative stress and a significant injury to lipids and proteins, a situation that possibly contributes to the brain symptoms of the arthritis disease.

  13. Nitric oxide mitigates arsenic-induced oxidative stress and genotoxicity in Vicia faba L.

    Science.gov (United States)

    Shukla, Pratiksha; Singh, A K

    2015-09-01

    The protective effects of nitric oxide (NO) against arsenic (As)-induced structural disturbances in Vicia faba have been investigated. As treatment (0.25, 0.50, and 1 mM) resulted in a declined growth of V. faba seedlings. Arsenic treatment stimulates the activity of SOD and CAT while the activities of APX and GST content were decreased. The oxidative stress markers such as superoxide radical, hydrogen peroxide and malondialdehyde (lipid peroxidation) contents were enhanced by As. Overall results revealed that significant accumulation of As suppressed growth, photosynthesis, antioxidant enzymes (SOD, CAT, APX, and GST activity), mitotic index, and induction of different chromosomal abnormalities, hence led to oxidative stress. The concentration of SNP (0.02 mM) was very effective in counteracting the adverse effect of As toxicity. These abnormalities use partially or fully reversed by a simultaneous application of As and NO donor and sodium nitroprusside and has an ameliorating effect against As-induced oxidative stress and genotoxicity in V. faba roots.

  14. Nitric oxide in liver fibrosis: The role of inducible nitric oxide synthase.

    Science.gov (United States)

    Iwakiri, Yasuko

    2015-12-01

    The inducible form of nitric oxide synthase (iNOS) is expressed in hepatic cells in pathological conditions. Its induction is involved in the development of liver fibrosis, and thus iNOS could be a therapeutic target for liver fibrosis. This review summarizes the role of iNOS in liver fibrosis, focusing on 1) iNOS biology, 2) iNOS-expressing liver cells, 3) iNOS-related therapeutic strategies, and 4) future directions.

  15. Effects of Kombucha on oxidative stress induced nephrotoxicity in rats

    Directory of Open Access Journals (Sweden)

    Gharib Ola

    2009-11-01

    Full Text Available Abstract Background Trichloroethylene (TCE may induce oxidative stress which generates free radicals and alters antioxidants or oxygen-free radical scavenging enzymes. Methods Twenty male albino rats were divided into four groups: (1 the control group treated with vehicle, (2 Kombucha (KT-treated group, (3 TCE-treated group and (4 KT/TCE-treated group. Kidney lipid peroxidation, glutathione content, nitric oxide (NO and total blood free radical concentrations were evaluated. Serum urea, creatinine level, gamma-glutamyl transferase (GGT and lactate dehydrogenase (LDH activities were also measured. Results TCE administration increased the malondiahyde (MDA and NO contents in kidney, urea and creatinine concentrations in serum, total free radical level in blood and GGT and LDH activities in serum, whereas it decreased the glutathione (GSH level in kidney homogenate. KT administration significantly improved lipid peroxidation and oxidative stress induced by TCE. Conclusion The present study indicates that Kombucha may repair damage caused by environmental pollutants such as TCE and may be beneficial to patient suffering from renal impairment.

  16. Nitric oxide ameliorates zinc oxide nanoparticles-induced phytotoxicity in rice seedlings.

    Science.gov (United States)

    Chen, Juan; Liu, Xiang; Wang, Chao; Yin, Shan-Shan; Li, Xiu-Ling; Hu, Wen-Jun; Simon, Martin; Shen, Zhi-Jun; Xiao, Qiang; Chu, Cheng-Cai; Peng, Xin-Xiang; Zheng, Hai-Lei

    2015-10-30

    Nitric oxide (NO) has been found to function in enhancing plant tolerance to various environmental stresses. However, role of NO in relieving zinc oxide nanoparticles (ZnO NPs)-induced phytotoxicity remains unknown. Here, sodium nitroprusside (SNP, a NO donor) was used to investigate the possible roles and the regulatory mechanisms of NO in counteracting ZnO NPs toxicity in rice seedlings. Our results showed that 10 μM SNP significantly inhibited the appearance of ZnO NP toxicity symptoms. SNP addition significantly reduced Zn accumulation, reactive oxygen species production and lipid peroxidation caused by ZnO NPs. The protective role of SNP in reducing ZnO NPs-induced oxidative damage is closely related to NO-mediated antioxidant system. A decrease in superoxide dismutase activity, as well as an increase in reduced glutathione content and peroxidase, catalase and ascorbate peroxidase activity was observed under SNP and ZnO NPs combined treatments, compared to ZnO NPs treatment alone. The relative transcript abundance of corresponding antioxidant genes exhibited a similar change. The role of NO in enhancing ZnO NPs tolerance was further confirmed by genetic analysis using a NO excess mutant (noe1) and an OsNOA1-silenced plant (noa1) of rice. Together, this study provides the first evidence indicating that NO functions in ameliorating ZnO NPs-induced phytotoxicity.

  17. Assessment of Eccentric Exercise-Induced Oxidative Stress Using Oxidation-Reduction Potential Markers

    Directory of Open Access Journals (Sweden)

    Dimitrios Stagos

    2015-01-01

    Full Text Available The aim of the present study was to investigate the use of static (sORP and capacity ORP (cORP oxidation-reduction potential markers as measured by the RedoxSYS Diagnostic System in plasma, for assessing eccentric exercise-induced oxidative stress. Nineteen volunteers performed eccentric exercise with the knee extensors. Blood was collected before, immediately after exercise, and 24, 48, and 72 h after exercise. Moreover, common redox biomarkers were measured, which were protein carbonyls, thiobarbituric acid-reactive substances, total antioxidant capacity in plasma, and catalase activity and glutathione levels in erythrocytes. When the participants were examined as one group, there were not significant differences in any marker after exercise. However, in 11 participants there was a high increase in cORP after exercise, while in 8 participants there was a high decrease. Thus, the participants were divided in low cORP group exhibiting significant decrease in cORP after exercise and in high cORP group exhibiting significant increase. Moreover, only in the low cORP group there was a significant increase in lipid peroxidation after exercise suggesting induction of oxidative stress. The results suggested that high decreases in cORP values after exercise may indicate induction of oxidative stress by eccentric exercise, while high increases in cORP values after exercise may indicate no existence of oxidative stress.

  18. Assessment of eccentric exercise-induced oxidative stress using oxidation-reduction potential markers.

    Science.gov (United States)

    Stagos, Dimitrios; Goutzourelas, Nikolaos; Ntontou, Amalia-Maria; Kafantaris, Ioannis; Deli, Chariklia K; Poulios, Athanasios; Jamurtas, Athanasios Z; Bar-Or, David; Kouretas, Dimitrios

    2015-01-01

    The aim of the present study was to investigate the use of static (sORP) and capacity ORP (cORP) oxidation-reduction potential markers as measured by the RedoxSYS Diagnostic System in plasma, for assessing eccentric exercise-induced oxidative stress. Nineteen volunteers performed eccentric exercise with the knee extensors. Blood was collected before, immediately after exercise, and 24, 48, and 72 h after exercise. Moreover, common redox biomarkers were measured, which were protein carbonyls, thiobarbituric acid-reactive substances, total antioxidant capacity in plasma, and catalase activity and glutathione levels in erythrocytes. When the participants were examined as one group, there were not significant differences in any marker after exercise. However, in 11 participants there was a high increase in cORP after exercise, while in 8 participants there was a high decrease. Thus, the participants were divided in low cORP group exhibiting significant decrease in cORP after exercise and in high cORP group exhibiting significant increase. Moreover, only in the low cORP group there was a significant increase in lipid peroxidation after exercise suggesting induction of oxidative stress. The results suggested that high decreases in cORP values after exercise may indicate induction of oxidative stress by eccentric exercise, while high increases in cORP values after exercise may indicate no existence of oxidative stress.

  19. Nitric oxide-induced signalling in rat lacrimal acinar cells

    DEFF Research Database (Denmark)

    Looms, Dagnia Karen; Tritsaris, K.; Dissing, S.

    2002-01-01

    The aim of the present study was to investigate the physiological role of nitric oxide (NO) in mediating secretory processes in rat lacrimal acinar cells. In addition, we wanted to determine whether the acinar cells possess endogenous nitric oxide synthase (NOS) activity by measuring NO productio...... not by itself causing fast transient increases in [Ca2+]i. In addition, we suggest that endogenously produced NO activated by ß-adrenergic receptor stimulation, plays an important role in signalling to the surrounding tissue.......The aim of the present study was to investigate the physiological role of nitric oxide (NO) in mediating secretory processes in rat lacrimal acinar cells. In addition, we wanted to determine whether the acinar cells possess endogenous nitric oxide synthase (NOS) activity by measuring NO production......-adrenergic stimulation and not by a rise in [Ca2+]i alone.   We show that in rat lacrimal acinar cells, NO and cGMP induce Ca2+ release from intracellular stores via G kinase activation. However, the changes in [Ca2+]i are relatively small, suggesting that this pathway plays a modulatory role in Ca2+ signalling, thus...

  20. Bee products prevent agrichemical-induced oxidative damage in fish.

    Directory of Open Access Journals (Sweden)

    Daiane Ferreira

    Full Text Available In southern South America and other parts of the world, aquaculture is an activity that complements agriculture. Small amounts of agrichemicals can reach aquaculture ponds, which results in numerous problems caused by oxidative stress in non-target organisms. Substances that can prevent or reverse agrichemical-induced oxidative damage may be used to combat these effects. This study includes four experiments. In each experiment, 96 mixed-sex, 6-month-old Rhamdia quelen (118±15 g were distributed into eight experimental groups: a control group that was not exposed to contaminated water, three groups that were exposed to various concentrations of bee products, three groups that were exposed to various concentrations of bee products plus tebuconazole (TEB; Folicur 200 CE™ and a group that was exposed to 0.88 mg L(-1 of TEB alone (corresponding to 16.6% of the 96-h LC50. We show that waterborne bee products, including royal jelly (RJ, honey (H, bee pollen (BP and propolis (P, reversed the oxidative damage caused by exposure to TEB. These effects were likely caused by the high polyphenol contents of these bee-derived compounds. The most likely mechanism of action for the protective effects of bee products against tissue oxidation and the resultant damage is that the enzymatic activities of superoxide dismutase (SOD, catalase (CAT and glutathione-S-transferase (GST are increased.

  1. Carbofuran-induced oxidative stress in mammalian brain.

    Science.gov (United States)

    Rai, Devendra K; Sharma, Bechan

    2007-09-01

    Chronic exposure to carbofuran, a carbamate pesticide, via oral administration has been reported to generate reactive oxygen species (ROS) in rat brain. However, information regarding the effect of short-term intraperitoneal (i.p.) carbofuran intoxication on oxidative stress is lacking. In the present study, the effect of carbofuran on oxidative indices in brain of Wistar rats has been determined by exposing the animals to three subacute concentrations (0.2, 0.4 and 0.8 mg/kg body weight) equivalent to 10, 20, and 40%, respectively, of its LD50 (i.p.) for 24 h. Rat liver has been used as a positive control. The results demonstrated that carbofuran treatment at the 3 concentrations tested caused significant increase in lipid peroxidation (LPO) by 12.50, 34.38, and 59.38%, respectively. The increased oxidative stress at same pesticide concentrations significantly induced activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase in rat brain; the impact on catalase being more marked only at high-pesticide doses (0.4 and 0.8 mg/kg body weight). Carbofuran also caused reduction in protein content of rat tissues tested. Rat brain was more severely affected by carbofuran than liver. The results clearly demonstrated that i.p. administration of carbofuran accelerated oxidative stress in rat brain in a dose-dependent manner.

  2. Tyrosol attenuates ischemia-reperfusion-induced kidney injury via inhibition of inducible nitric oxide synthase.

    Science.gov (United States)

    Wang, Pengqi; Zhu, Qingjun; Wu, Nan; Siow, Yaw L; Aukema, Harold; O, Karmin

    2013-04-17

    Tyrosol is a natural phenolic antioxidant compound. Oxidative stress represents one of the important mechanisms underlying ischemia-reperfusion-induced kidney injury. The aim of this study was to investigate the effect of tyrosol against ischemia-reperfusion-induced acute kidney injury. The left kidney of Sprague-Dawley rats was subjected to 45 min of ischemia followed by reperfusion for 6 h. Ischemia-reperfusion caused an increase in peroxynitrite formation and lipid peroxidation. The level of nitric oxide (NO) metabolites and the mRNA of inducible nitric oxide synthase (iNOS) were elevated in ischemia-reperfused kidneys. Administration of tyrosol (100 mg/kg body weight) to rats prior to the induction of ischemia significantly reduced peroxynitrite formation, lipid peroxidation, and the level of NO metabolites. Tyrosol administration also attenuated ischemia-reperfusion-induced NF-κB activation and iNOS expression. Such a treatment improved kidney function. Results suggest that tyrosol may have a protective effect against acute kidney injury through inhibition of iNOS-mediated oxidative stress.

  3. Salsolinol, a catechol neurotoxin, induces oxidative modification of cytochrome c

    Directory of Open Access Journals (Sweden)

    Jung Hoon Kang

    2013-02-01

    Full Text Available Methyl-6,7-dihydroxy-1,2,3,4-tetrahydroisoquinoline (salsolinol,an endogenous neurotoxin, is known to perform a role in thepathogenesis of Parkinson’s disease (PD. In this study, weevaluated oxidative modification of cytochrome c occurring afterincubation with salsolinol. When cytochrome c was incubatedwith salsolinol, protein aggregation increased in a dosedependentmanner. The formation of carbonyl compounds andthe release of iron were obtained in salsolinol- treated cytochromec. Salsolinol also led to the release of iron fromcytochrome c. Reactive oxygen species (ROS scavengers andiron specific chelator inhibited the salsolinol-mediated cytochromec modification and carbonyl compound formation. It issuggested that oxidative damage of cytochrome c by salsolinolmight induce the increase of iron content in cells, subsequentlyleading to the deleterious condition which was observed. Thismechanism may, in part, provide an explanation for thedeterioration of organs under neurodegenerative disorders suchas PD. [BMB Reports 2013; 46(2: 119-123

  4. Neutron induced degradation in nitrided pyrogenic field oxide MOS capacitors

    CERN Document Server

    Vaidya, S J; Shaikh, A M; Chandorkar, A N

    2002-01-01

    Neutron induced oxide charge trapping and generation of interface states in MOS capacitors with pyrogenic and nitrided pyrogenic field oxides have been studied. In order to assess the damage due to neutrons alone, it is necessary to account for the damage produced by the accompanying gamma rays from neutron radiation. This is done by measuring the intensity of gamma radiation accompanying neutrons at different neutron fluences at the irradiation position. MOS capacitor structures were subjected to neutron radiation in a swimming pool type of reactor. Other samples from the same batch were then subjected to an equivalent dose of gamma radiation from a Co sup 6 sup 0 source. The difference in the damage observed was used to characterize the damage caused by neutrons. It is observed that neutrons, though uncharged, are capable of causing ionization damage. This damage is found to be significant when the radiation is performed under biased conditions. Nitridation in different ambients is found to improve the radi...

  5. Radiation induced defects and thermoluminescence mechanism in aluminum oxide

    Energy Technology Data Exchange (ETDEWEB)

    Atobe, K.; Kobayashi, T.; Awata, T. [Naruto Univ. of Education, Tokushima (Japan); Okada, M. [Kyoto Univ., Kumatori, Osaka (Japan). Research Reactor Inst; Nakagawa, M. [Kagawa Univ., Faculty of Education, Takamatsu, Kagawa (Japan)

    2001-01-01

    The thermoluminescence of the irradiated aluminum oxides were measured to study the radiation induced defects and their behaviors. Neutron and {gamma}-ray irradiation were performed for a shingle crystal of the high purity aluminum oxide. The thermoluminescence glow curve and its activation energy were measured. The spectroscopy measurement on the thermoluminescence and the absorption are also carried out. The observed 430 and 340 nm peaks are discussed relating to the F{sup +} and F centers, respectively. Activation state of the F center transits to 3P state through 1P state by emitting phonons. Trapped electron on 3P state emits phonon of 2.9 eV (430 nm) during transition to the ground state. The above reaction can be written by the equation. F{sup +} + e {yields} (F){sup *} {yields} F + h{nu}(2.9 eV, 470 nm). (Katsuta, H.)

  6. Impaired mitochondrial fat oxidation induces adaptive remodeling of muscle metabolism.

    Science.gov (United States)

    Wicks, Shawna E; Vandanmagsar, Bolormaa; Haynie, Kimberly R; Fuller, Scott E; Warfel, Jaycob D; Stephens, Jacqueline M; Wang, Miao; Han, Xianlin; Zhang, Jingying; Noland, Robert C; Mynatt, Randall L

    2015-06-23

    The correlations between intramyocellular lipid (IMCL), decreased fatty acid oxidation (FAO), and insulin resistance have led to the hypothesis that impaired FAO causes accumulation of lipotoxic intermediates that inhibit muscle insulin signaling. Using a skeletal muscle-specific carnitine palmitoyltransferase-1 KO model, we show that prolonged and severe mitochondrial FAO inhibition results in increased carbohydrate utilization, along with reduced physical activity; increased circulating nonesterified fatty acids; and increased IMCLs, diacylglycerols, and ceramides. Perhaps more importantly, inhibition of mitochondrial FAO also initiates a local, adaptive response in muscle that invokes mitochondrial biogenesis, compensatory peroxisomal fat oxidation, and amino acid catabolism. Loss of its major fuel source (lipid) induces an energy deprivation response in muscle coordinated by signaling through AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) to maintain energy supply for locomotion and survival. At the whole-body level, these adaptations result in resistance to obesity.

  7. INSULIN INDUCES NITRIC OXIDE PRODUCTION IN BOVINEAORTIC ENDOTHELIAL CELLS

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    Objective To examine the effects of insulin on cell proliferation, nitric oxide (NO) release and nitric oxide synthase (NOS) gene expression in bovine aortic endothelial cells ( BAEC ) . Methods The mi togenesis was assessed by MTT method; the products of NO in the culture media, by Griess reaction; and the levels of NOS mRNA in BAEC , by RT/PCR tech nique. Results BAEC were not responsive to the growth-promoting effects of insulin. Stimulation with insulin resulted a dose-dependent rise of NO in the culture supernatants 2h later, with a maximum at 12~24h and a decline at 24h. This rise was inhibited by an inhibitor of NOS (L-NAME). NOS mRNA increased slightly in BAEC without statistical significance. Conelu sion The study suggested that the insulin-induced NO release might be caused directly by NOS activation.

  8. Quinolinic acid induces oxidative stress in rat brain synaptosomes.

    Science.gov (United States)

    Santamaría, A; Galván-Arzate, S; Lisý, V; Ali, S F; Duhart, H M; Osorio-Rico, L; Ríos, C; St'astný, F

    2001-03-26

    The oxidative action of quinolinic acid (QUIN), and the protective effects of glutathione (GSH), and 2-amino-5-phosphonovaleric acid (APV), were tested in rat brain synaptosomes, Reactive oxygen species (ROS) formation was quantified after the exposure of synaptosomes to increasing concentrations of QUIN (25-500 microM). The potency of QUIN to induce lipid peroxidation (LP) was tested as a regional index of thiobarbituric acid-reactive substances (TBARS) production, and the antioxidant actions of both GSH (50 microM) and APV (250 microM) on QUIN-induced LP were evaluated in synaptosomes prepared from different brain regions. QUIN induced concentration-dependent increases in ROS formation and TBARS in all regions analyzed, but increased production of fluorescent peroxidized lipids only in the striatum and the hippocampus, whereas both GSH and APV decreased this index. These results suggest that the excitotoxic action of QUIN involves regional selectivity in the oxidative status of brain synaptosomes, and may be prevented by substances exhibiting antagonism at the NMDA receptor.

  9. Role of Oxidative Damage in Radiation-Induced Bone Loss

    Science.gov (United States)

    Schreurs, Ann-Sofie; Alwood, Joshua S.; Limoli, Charles L.; Globus, Ruth K.

    2014-01-01

    During prolonged spaceflight, astronauts are exposed to both microgravity and space radiation, and are at risk for increased skeletal fragility due to bone loss. Evidence from rodent experiments demonstrates that both microgravity and ionizing radiation can cause bone loss due to increased bone-resorbing osteoclasts and decreased bone-forming osteoblasts, although the underlying molecular mechanisms for these changes are not fully understood. We hypothesized that excess reactive oxidative species (ROS), produced by conditions that simulate spaceflight, alter the tight balance between osteoclast and osteoblast activities, leading to accelerated skeletal remodeling and culminating in bone loss. To test this, we used the MCAT mouse model; these transgenic mice over-express the human catalase gene targeted to mitochondria, the major organelle contributing free radicals. Catalase is an anti-oxidant that converts reactive species, hydrogen peroxide into water and oxygen. This animal model was selected as it displays extended lifespan, reduced cardiovascular disease and reduced central nervous system radio-sensitivity, consistent with elevated anti-oxidant activity conferred by the transgene. We reasoned that mice overexpressing catalase in mitochondria of osteoblast and osteoclast lineage cells would be protected from the bone loss caused by simulated spaceflight. Over-expression of human catalase localized to mitochondria caused various skeletal phenotypic changes compared to WT mice; this includes greater bone length, decreased cortical bone area and moment of inertia, and indications of altered microarchitecture. These findings indicate mitochondrial ROS are important for normal bone-remodeling and skeletal integrity. Catalase over-expression did not fully protect skeletal tissue from structural decrements caused by simulated spaceflight; however there was significant protection in terms of cellular oxidative damage (MDA levels) to the skeletal tissue. Furthermore, we

  10. Expression and activity of inducible nitric oxide synthase and endothelial nitric oxide synthase correlate with ethanol-induced liver injury

    Institute of Scientific and Technical Information of China (English)

    Guang-Jin Yuan; Xiao-Rong Zhou; Zuo-Jiong Gong; Pin Zhang; Xiao-Mei Sun; Shi-Hua Zheng

    2006-01-01

    AIM: To study the expression and activity of inducible nitric oxide synthase (iNOS) and endothelial nitric oxide synthase (eNOS) in rats with ethanol-induced liver injury and their relation with liver damage, activation of nuclear factor-KB (NF-кB) and tumor necrosis factor-α (TNF-α)expression in the liver.METHODS: Female Sprague-Dawley rats were given fish oil (0.5 mL) along with ethanol or isocaloric dextrose daily via gastrogavage for 4 or 6 wk. Liver injury was assessed using serum alanine aminotransferase (ALT)activity and pathological analysis. Liver malondialdehyde (MDA), nitric oxide contents, iNOS and eNOS activity were determined. NF-KB p65, iNOS, eNOS and TNF-αprotein or mRNA expression in the liver were detected by immunohistochemistry or reverse transcriptase-polymerase chain reaction (RT-PCR).RESULTS: Chronic ethanol gavage for 4 wk caused steatosis, inflammation and necrosis in the liver, and elevated serum ALT activity. Prolonged ethanol administration (6 wk) enhanced the liver damage. These responses were accompanied with increased lipid peroxidation, NO contents, iNOS activity and reduced eNOS activity. NF-кB p65, iNOS and TNF-α protein or mRNA expression were markedly induced after chronic ethanol gavage, whereas eNOS mRNA expression remained unchanged. The enhanced iNOS activity and expression were positively correlated with the liver damage, especially the necro-inflammation, activation of NF-кB, and TNF-α mRNA expression.CONCLUSION: iNOS expression and activity are induced in the liver after chronic ethanol exposure in rats, which are correlated with the liver damage, especially the necro-inflammation, activation of NF-KB and TNF-αexpression. eNOS activity is reduced, but its mRNA expression is not affected.

  11. Autecology of an arsenite chemolithotroph: sulfide constraints on function and distribution in a geothermal spring.

    Science.gov (United States)

    D'Imperio, Seth; Lehr, Corinne R; Breary, Michele; McDermott, Timothy R

    2007-11-01

    Previous studies in an acid-sulfate-chloride spring in Yellowstone National Park found that microbial arsenite [As(III)] oxidation is absent in regions of the spring outflow channel where H(2)S exceeds approximately 5 microM and served as a backdrop for continued efforts in the present study. Ex situ assays with microbial mat samples demonstrated immediate As(III) oxidation activity when H(2)S was absent or at low concentrations, suggesting the presence of As(III) oxidase enzymes that could be reactivated if H(2)S is removed. Cultivation experiments initiated with mat samples taken from along the H(2)S gradient in the outflow channel resulted in the isolation of an As(III)-oxidizing chemolithotroph from the low-H(2)S region of the gradient. The isolate was phylogenetically related to Acidicaldus and was characterized in vitro for spring-relevant properties, which were then compared to its distribution pattern in the spring as determined by denaturing gradient gel electrophoresis and quantitative PCR. While neither temperature nor oxygen requirements appeared to be related to the occurrence of this organism within the outflow channel, H(2)S concentration appeared to be an important constraint. This was verified by in vitro pure-culture modeling and kinetic experiments, which suggested that H(2)S inhibition of As(III) oxidation is uncompetitive in nature. In summary, the studies reported herein illustrate that H(2)S is a potent inhibitor of As(III) oxidation and will influence the niche opportunities and population distribution of As(III) chemolithotrophs.

  12. Inducible repair of oxidative DNA damage in Escherichia coli.

    Science.gov (United States)

    Demple, B; Halbrook, J

    Hydrogen peroxide is lethal to many cell types, including the bacterium Escherichia coli. Peroxides yield transient radical species that can damage DNA and cause mutations. Such partially reduced oxygen species are occasionally released during cellular respiration and are generated by lethal and mutagenic ionizing radiation. Because cells live in an environment where the threat of oxidative DNA damage is continual, cellular mechanisms may have evolved to avoid and repair this damage. Enzymes are known which evidently perform these functions. We report here that resistance to hydrogen peroxide toxicity can be induced in E. coli, that this novel induction is specific and occurs, in part, at the level of DNA repair.

  13. Inorganic polyphosphate suppresses lipopolysaccharide-induced inducible nitric oxide synthase (iNOS expression in macrophages.

    Directory of Open Access Journals (Sweden)

    Kana Harada

    Full Text Available In response to infection, macrophages produce a series of inflammatory mediators, including nitric oxide (NO, to eliminate pathogens. The production of these molecules is tightly regulated via various mechanisms, as excessive responses are often detrimental to host tissues. Here, we report that inorganic polyphosphate [poly(P], a linear polymer of orthophosphate ubiquitously found in mammalian cells, suppresses inducible nitric oxide synthase (iNOS expression induced by lipopolysaccharide (LPS, a cell wall component of Gram-negative bacteria, in mouse peritoneal macrophages. Poly(P with longer chains is more potent than those with shorter chains in suppressing LPS-induced iNOS expression. In addition, poly(P decreased LPS-induced NO release. Moreover, poly(P suppressed iNOS mRNA expression induced by LPS stimulation, thereby indicating that poly(P reduces LPS-induced iNOS expression by down-regulation at the mRNA level. In contrast, poly(P did not affect the LPS-induced release of TNF, another inflammatory mediator. Poly(P may serve as a regulatory factor of innate immunity by modulating iNOS expression in macrophages.

  14. Oxidative stress in NSC-741909-induced apoptosis of cancer cells

    Directory of Open Access Journals (Sweden)

    Huang Peng

    2010-04-01

    Full Text Available Abstract Background NSC-741909 is a novel anticancer agent that can effectively suppress the growth of several cell lines derived from lung, colon, breast, ovarian, and kidney cancers. We recently showed that NSC-741909-induced antitumor activity is associated with sustained Jun N-terminal kinase (JNK activation, resulting from suppression of JNK dephosphorylation associated with decreased protein levels of MAPK phosphatase-1. However, the mechanisms of NSC-741909-induced antitumor activity remain unclear. Because JNK is frequently activated by oxidative stress in cells, we hypothesized that reactive oxygen species (ROS may be involved in the suppression of JNK dephosphorylation and the cytotoxicity of NSC-741909. Methods The generation of ROS was measured by using the cell-permeable nonfluorescent compound H2DCF-DA and flow cytometry analysis. Cell viability was determined by sulforhodamine B assay. Western blot analysis, immunofluorescent staining and flow cytometry assays were used to determine apoptosis and molecular changes induced by NSC-741909. Results Treatment with NSC-741909 induced robust ROS generation and marked MAPK phosphatase-1 and -7 clustering in NSC-741909-sensitive, but not resistant cell lines, in a dose- and time-dependent manner. The generation of ROS was detectable as early as 30 min and ROS levels were as high as 6- to 8-fold above basal levels after treatment. Moreover, the NSC-741909-induced ROS generation could be blocked by pretreatment with antioxidants, such as nordihydroguaiaretic acid, aesculetin, baicalein, and caffeic acid, which in turn, inhibited the NSC-741909-induced JNK activation and apoptosis. Conclusion Our results demonstrate that the increased ROS production was associated with NSC-741909-induced antitumor activity and that ROS generation and subsequent JNK activation is one of the primary mechanisms of NSC-741909-mediated antitumor cell activity.

  15. Lipid oxidation in human low-density lipoprotein induced by metmyoglobin/H2O2

    DEFF Research Database (Denmark)

    Witting, P K; Willhite, C A; Davies, Michael Jonathan

    1999-01-01

    Metmyoglobin (metMb) and H(2)O(2) can oxidize low-density lipoprotein (LDL) in vitro, and oxidized LDL may be atherogenic. The role of alpha-tocopherol (alpha-TOH) in LDL oxidation by peroxidases such as metMb is unclear. Herein, we show that during metMb/H(2)O(2)-induced oxidation of native LDL...

  16. Manganese-induced oxidative stress in two ontogenetic stages of chamomile and amelioration by nitric oxide.

    Science.gov (United States)

    Kováčik, Jozef; Babula, Petr; Hedbavny, Josef; Švec, Pavel

    2014-02-01

    Impact of manganese (Mn(2+)) excess (100, 500 and 1000 μM over 7 days) on two ontogenetic stages (7-week-old plants and 7-day-old seedlings) of Matricaria chamomilla was compared. Mn excess depressed growth of seedlings (but not germination) and stimulated oxidative stress (ROS and lipid peroxidation) in both plants and seedlings. Growth inhibition could be evoked by higher Mn uptake and higher translocation factor in seedlings than in plants. Total thiols staining revealed elevation in almost all treatments. In 7-week-old plants, activity of peroxidases increased slightly and rather decreased under high Mn doses. Superoxide rather than hydrogen peroxide contributed to visualized ROS presence. Fluorescence of nitric oxide (NO) showed stimulation in plants but decrease in seedlings. Impact of exogenous nitric oxide donor (sodium nitroprusside/SNP) was therefore tested and results showed amelioration of 1000 μM Mn-induced oxidative stress in seedlings (decrease in H2O2 and increase in NO content while antioxidative enzyme activities were variably affected) concomitantly with depleted Mn accumulation. It is concluded that NO participates in tolerance to Mn excess but negative effects of the highest SNP dose were also observed. Extensive fluorescence microscopy is also explanatively discussed.

  17. A new arthritis therapy with oxidative burst inducers.

    Directory of Open Access Journals (Sweden)

    Malin Hultqvist

    2006-09-01

    Full Text Available BACKGROUND: Despite recent successes with biological agents as therapy for autoimmune inflammatory diseases such as rheumatoid arthritis (RA, many patients fail to respond adequately to these treatments, making a continued search for new therapies extremely important. Recently, the prevailing hypothesis that reactive oxygen species (ROS promote inflammation was challenged when polymorphisms in Ncf1, that decrease oxidative burst, were shown to increase disease severity in mouse and rat arthritis models. Based on these findings we developed a new therapy for arthritis using oxidative burst-inducing substances. METHODS AND FINDINGS: Treatment of rats with phytol (3,7,11,15-tetramethyl-2-hexadecene-1-ol increased oxidative burst in vivo and thereby corrected the effect of the genetic polymorphism in arthritis-prone Ncf1(DA rats. Importantly, phytol treatment also decreased the autoimmune response and ameliorated both the acute and chronic phases of arthritis. When compared to standard therapies for RA, anti-tumour necrosis factor-alpha and methotrexate, phytol showed equally good or better therapeutic properties. Finally, phytol mediated its effect within hours of administration and involved modulation of T cell activation, as injection prevented adoptive transfer of disease with arthritogenic T cells. CONCLUSIONS: Treatment of arthritis with ROS-promoting substances such as phytol targets a newly discovered pathway leading to autoimmune inflammatory disease and introduces a novel class of therapeutics for treatment of RA and possibly other chronic inflammatory diseases.

  18. Aniline Induces Oxidative Stress and Apoptosis of Primary Cultured Hepatocytes

    Directory of Open Access Journals (Sweden)

    Yue Wang

    2016-11-01

    Full Text Available The toxicity and carcinogenicity of aniline in humans and animals have been well documented. However, the molecular mechanism involved in aniline-induced liver toxicity and carcinogenesis remains unclear. In our research, primary cultured hepatocytes were exposed to aniline (0, 1.25, 2.50, 5.0 and 10.0 μg/mL for 24 h in the presence or absence of N-acetyl-l-cysteine (NAC. Levels of reactive oxygen species (ROS, malondialdehyde (MDA, and glutathione (GSH, activities of superoxide dismutase (SOD and catalase (CAT, mitochondrial membrane potential, DNA damage, cell viability, and apoptosis were detected. Levels of ROS and MDA were significantly increased and levels of GSH and CAT, activity of SOD, and mitochondrial membrane potential in hepatocytes were significantly decreased by aniline compared with the negative control group. The tail moment and DNA content of the tail in exposed groups were significantly higher than those in the negative control group. Cell viability was reduced and apoptotic death was induced by aniline in a concentration-dependent manner. The phenomena of ROS generation, oxidative damage, loss of mitochondrial membrane potential, DNA damage and apoptosis could be prevented if ROS inhibitor NAC was added. ROS generation is involved in the loss of mitochondrial membrane potential and DNA injury, which may play a role in aniline-induced apoptosis in hepatocytes. Our study provides insight into the mechanism of aniline-induced toxicity and apoptosis of hepatocytes.

  19. Live-cell Imaging Approaches for the Investigation of Xenobiotic-Induced Oxidant Stress

    Science.gov (United States)

    BACKGROUND: Oxidant stress is arguably a universal feature in toxicology. Research studies on the role of oxidant stress induced by xenobiotic exposures have typically relied on the identification of damaged biomolecules using a variety of conventional biochemical and molecular t...

  20. Live-cell Imaging Approaches for the Investigation of Xenobiotic-Induced Oxidant Stress

    Science.gov (United States)

    BACKGROUND: Oxidant stress is arguably a universal feature in toxicology. Research studies on the role of oxidant stress induced by xenobiotic exposures have typically relied on the identification of damaged biomolecules using a variety of conventional biochemical and molecular t...

  1. Production of Nitric Oxide and Expression of Inducible Nitric Oxide Synthase in Ovarian Cystic Tumors

    Directory of Open Access Journals (Sweden)

    Rosekeila Simões Nomelini

    2008-01-01

    Full Text Available Tumor sections from nonneoplastic (n=15, benign (n=28, and malignant ovarian tumors (n=20 were obtained from 63 women. Immunohistochemistry of the tumor sections demonstrated that inducible nitric oxide synthase (iNOS expression was increased in ovarian cancer samples compared to nonneoplastic or benign tumor samples. Using the Griess method, nitric oxide (NO metabolite levels were also found to be elevated in malignant tumor samples compared to benign tumor samples (P80 μM were more frequent than NO levels <80 μM, and iNOS expression in well-differentiated carcinomas was greater than in moderately/poorly differentiated carcinomas (P<.05. These data suggest an important role for NO in ovarian carcinogenesis.

  2. Uranium induces oxidative stress in lung epithelial cells

    Energy Technology Data Exchange (ETDEWEB)

    Periyakaruppan, Adaikkappan; Kumar, Felix; Sarkar, Shubhashish; Sharma, Chidananda S.; Ramesh, Govindarajan T. [Texas Southern University, Molecular Neurotoxicology Laboratory/Proteomics Core, Department of Biology, Houston, TX (United States)

    2007-06-15

    Uranium compounds are widely used in the nuclear fuel cycle, antitank weapons, tank armor, and also as a pigment to color ceramics and glass. Effective management of waste uranium compounds is necessary to prevent exposure to avoid adverse health effects on the population. Health risks associated with uranium exposure includes kidney disease and respiratory disorders. In addition, several published results have shown uranium or depleted uranium causes DNA damage, mutagenicity, cancer and neurological defects. In the current study, uranium toxicity was evaluated in rat lung epithelial cells. The study shows uranium induces significant oxidative stress in rat lung epithelial cells followed by concomitant decrease in the antioxidant potential of the cells. Treatment with uranium to rat lung epithelial cells also decreased cell proliferation after 72 h in culture. The decrease in cell proliferation was attributed to loss of total glutathione and superoxide dismutase in the presence of uranium. Thus the results indicate the ineffectiveness of antioxidant system's response to the oxidative stress induced by uranium in the cells. (orig.)

  3. Nitric oxide protects carbon assimilation process of watermelon from boron-induced oxidative injury.

    Science.gov (United States)

    Farag, Mohamed; Najeeb, Ullah; Yang, Jinghua; Hu, Zhongyuan; Fang, Zhang Ming

    2017-02-01

    Nitric oxide (NO) mediates plant response to a variety of abiotic stresses; however, limited information is available on its effect on boron (B)-stressed watermelon plants. The present study investigates the mechanism through which NO protects watermelon seedlings from B deficiency and toxicity stresses. Five days old watermelon seedlings were exposed to B (0, 0.5 and 10 mg L(-1)) alone or with 75 μmole of NO donor sodium nitroprusside (SNP) for 30 days. Both low and high B concentrations in the media altered nutrient accumulation and impaired various physiological processes of watermelon seedlings, leading to a significant reduction in biomass production. The plants exposed to B deficient or toxic concentrations had 66 and 69% lower shoot dry weight, respectively compared with optimum B levels. B toxicity-induced growth inhibition of watermelon seedlings was associated with high B translocation to shoot tissues, which caused lipid membrane peroxidation (12% increase) and chlorophyll destruction (25% reduction). In contrast, B deficiency accelerated generation of reactive oxygen species (ROS), specifically OH(-1) and induced cellular oxidative injury. Exogenously applied SNP promoted leaf chlorophyll, photosynthesis and consequently biomass production in B-stressed watermelon seedlings by reducing B accumulation, lipid membrane peroxidation and ROS generation. It also activated antioxidant enzymes such as SOD, POD and APX, and protected the seedlings from ROS-induced cellular burst.

  4. The basic chemistry of exercise-induced DNA oxidation: oxidative damage, redox signalling and their interplay

    Directory of Open Access Journals (Sweden)

    James Nathan Cobley

    2015-06-01

    Full Text Available Acute exercise increases reactive oxygen and nitrogen species generation. This phenomenon is associated with two major outcomes: (1 redox signalling and (2 macromolecule damage. Mechanistic knowledge of how exercise-induced redox signalling and macromolecule damage are interlinked is limited. This review focuses on the interplay between exercise-induced redox signalling and DNA damage, using hydroxyl radical (·OH and hydrogen peroxide (H2O2 as exemplars. It is postulated that the biological fate of H2O2 links the two processes and thus represents a bifurcation point between redox signalling and damage. Indeed, H2O2 can participate in two electron signalling reactions but its diffusion and chemical properties permit DNA oxidation following reaction with transition metals and ·OH generation. It is also considered that the sensing of DNA oxidation by repair proteins constitutes a non-canonical redox signalling mechanism. Further layers of interaction are provided by the redox regulation of DNA repair proteins and their capacity to modulate intracellular H2O2 levels. Overall, exercise-induced redox signalling and DNA damage may be interlinked to a greater extent than was previously thought but this requires further investigation.

  5. Regulation of prostaglandin generation in carrageenan-induced pleurisy by inducible nitric oxide synthase in knockout mice.

    NARCIS (Netherlands)

    Rossi, A.; Cuzzocrea, S.; Mazzon, E.; Serraino, I.; Sarro, A. de; Dugo, L.; Felice, M.R.; Loo, F.A.J. van de; Rosa, M. Di; Musci, G.; Caputi, A.P.; Sautebin, L.

    2003-01-01

    In the present study, by comparing the responses in wild-type mice (iNOSWT) and mice lacking (iNOSKO) the inducible (or type 2) nitric oxide synthase (iNOS), we investigated the correlation between endogenous nitric oxide (NO) and prostaglandin (PG) generation in carrageenan-induced pleurisy. The

  6. Regulation of prostaglandin generation in carrageenan-induced pleurisy by inducible nitric oxide synthase in knockout mice.

    NARCIS (Netherlands)

    Rossi, A.; Cuzzocrea, S.; Mazzon, E.; Serraino, I.; Sarro, A. de; Dugo, L.; Felice, M.R.; Loo, F.A.J. van de; Rosa, M. Di; Musci, G.; Caputi, A.P.; Sautebin, L.

    2003-01-01

    In the present study, by comparing the responses in wild-type mice (iNOSWT) and mice lacking (iNOSKO) the inducible (or type 2) nitric oxide synthase (iNOS), we investigated the correlation between endogenous nitric oxide (NO) and prostaglandin (PG) generation in carrageenan-induced pleurisy. The in

  7. Oxidized DNA induces an adaptive response in human fibroblasts

    Energy Technology Data Exchange (ETDEWEB)

    Kostyuk, Svetlana V., E-mail: svet.kostyuk@gmail.com [Research Centre for Medical Genetics, Russian Academy of Medical Sciences, Moscow (Russian Federation); Tabakov, Viacheslav J.; Chestkov, Valerij V.; Konkova, Marina S.; Glebova, Kristina V.; Baydakova, Galina V.; Ershova, Elizaveta S.; Izhevskaya, Vera L. [Research Centre for Medical Genetics, Russian Academy of Medical Sciences, Moscow (Russian Federation); Baranova, Ancha, E-mail: abaranov@gmu.edu [Research Centre for Medical Genetics, Russian Academy of Medical Sciences, Moscow (Russian Federation); Center for the Study of Chronic Metabolic Diseases, School of System Biology, George Mason University, Fairfax, VA 22030 (United States); Veiko, Natalia N. [Research Centre for Medical Genetics, Russian Academy of Medical Sciences, Moscow (Russian Federation)

    2013-07-15

    Highlights: • We describe the effects of gDNAOX on human fibroblasts cultivated in serum withdrawal conditions. • gDNAOX evokes an adaptive response in human fibroblasts. • gDNAOX increases the survival rates in serum starving cell populations. • gDNAOX enhances the survival rates in cell populations irradiated at 1.2 Gy dose. • gDNAOX up-regulates NRF2 and inhibits NF-kappaB-signaling. - Abstract: Cell-free DNA (cfDNA) released from dying cells contains a substantial proportion of oxidized nucleotides, thus, forming cfDNA{sup OX}. The levels of cfDNA{sup OX} are increased in the serum of patients with chronic diseases. Oxidation of DNA turns it into a stress signal. The samples of genomic DNA (gDNA) oxidized by H{sub 2}O{sub 2}in vitro (gDNA{sup OX}) induce effects similar to that of DNA released from damaged cells. Here we describe the effects of gDNA{sup OX} on human fibroblasts cultivated in the stressful conditions of serum withdrawal. In these cells, gDNA{sup OX} evokes an adaptive response that leads to an increase in the rates of survival in serum starving cell populations as well as in populations irradiated at the dose of 1.2 Gy. These effects are not seen in control populations of fibroblasts treated with non-modified gDNA. In particular, the exposure to gDNA{sup OX} leads to a decrease in the expression of the proliferation marker Ki-67 and an increase in levels of PSNA, a decrease in the proportion of subG1- and G2/M cells, a decrease in proportion of cells with double strand breaks (DSBs). Both gDNA{sup OX} and gDNA suppress the expression of DNA sensors TLR9 and AIM2 and up-regulate nuclear factor-erythroid 2 p45-related factor 2 (NRF2), while only gDNA{sup OX} inhibits NF-κB signaling. gDNA{sup OX} is a model for oxidized cfDNA{sup OX} that is released from the dying tumor cells and being carried to the distant organs. The systemic effects of oxidized DNA have to be taken into account when treating tumors. In particular, the damaged DNA

  8. The protective effects of cerium oxide nanoparticles against hepatic oxidative damage induced by monocrotaline

    Directory of Open Access Journals (Sweden)

    Kamal A Amin

    2011-01-01

    Full Text Available Kamal A Amin1, Mohamed S Hassan2, El-Said T Awad3, Khalid S Hashem11Department of Biochemistry, 2Department of Internal Medicine, Faculty of Veterinary Medicine, Beni-Suef University, Beni-Suef, Egypt; 3Department of Biochemistry, Faculty of Veterinary Medicine, Cairo University, Cairo, EgyptObjective: The objective of the present study was to determine the ability of cerium oxide (CeO2 nanoparticles to protect against monocrotaline (MCT-induced hepatotoxicity in a rat model.Method: Twenty male Sprague Dawley rats were arbitrarily assigned to four groups: control (received saline, CeO2 (given 0.0001 nmol/kg intraperitoneally [IP], MCT (given 10 mg/kg body weight IP as a single dose, and MCT + CeO2 (received CeO2 both before and after MCT. Electron microscopic imaging of the rat livers was carried out, and hepatic total glutathione (GSH, glutathione reductase (GR, glutathione peroxidase (GPX, glutathione S-transferase (GST, superoxide dismutase (SOD, and catalase (CAT enzymatic activities were quantified.Results: Results showed a significant MCT-induced decrease in total hepatic GSH, GPX, GR, and GST normalized to control values with concurrent CeO2 administration. In addition, MCT produced significant increases in hepatic CAT and SOD activities, which also ameliorated with CeO2.Conclusions: These results indicate that CeO2 acts as a putative novel and effective hepatoprotective agent against MCT-induced hepatotoxicity.Keywords: monocrotaline, ceruim oxide nanoparticle, hepatotoxicity, oxidative stress

  9. Effect of methanolic extract of Asparagus racemosus Willd. on lipopolysaccharide induced-oxidative stress in rats.

    Science.gov (United States)

    Ahmad, Mohammad Parwez; Hussain, Arshad; Siddiqui, Hefazat Hussain; Wahab, Shadma; Adak, Manoranjan

    2015-03-01

    Lipopolysaccharide (LPS) induced oxidative stress and impairment of normal physiological function generally categorized by increased anxiety and reduced mobility. Therefore, the present study was to find out the effect Methanolic extract of Asparagus racemosus (MEAR ) in lipopolysaccharide (LPS)-induced oxidative stress in rats . LPS-induced oxidative stress in rats was measured by locomotor activity by photoactometer test, anxiety with elevated plus maze test and also studied the oxidative stress markers, nitric oxide and cytokines. The obtained data shows that LPS markedly exhausted (pAsparagus racemosus Willd. is a functionally newer type of cerebroprotective agent.

  10. Prolonged inorganic arsenite exposure suppresses insulin-stimulated AKT S473 phosphorylation and glucose uptake in 3T3-L1 adipocytes: Involvement of the adaptive antioxidant response

    Energy Technology Data Exchange (ETDEWEB)

    Xue, Peng [The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 (United States); School of Public Health, China Medical University, Shenyang 110001 (China); Hou, Yongyong; Zhang, Qiang; Woods, Courtney G.; Yarborough, Kathy; Liu, Huiyu [The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 (United States); Sun, Guifan [School of Public Health, China Medical University, Shenyang 110001 (China); Andersen, Melvin E. [The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 (United States); Pi, Jingbo, E-mail: jpi@thehamner.org [The Hamner Institutes for Health Sciences, Research Triangle Park, NC 27709 (United States)

    2011-04-08

    Highlights: {yields} In 3T3-L1 adipocytes iAs{sup 3+} decreases insulin-stimulated glucose uptake. {yields} iAs{sup 3+} attenuates insulin-induced phosphorylation of AKT S473. {yields} iAs{sup 3+} activates the cellular adaptive oxidative stress response. {yields} iAs{sup 3+} impairs insulin-stimulated ROS signaling. {yields} iAs{sup 3+} decreases expression of adipogenic genes and GLUT4. -- Abstract: There is growing evidence that chronic exposure of humans to inorganic arsenic, a potent environmental oxidative stressor, is associated with the incidence of type 2 diabetes (T2D). One critical feature of T2D is insulin resistance in peripheral tissues, especially in mature adipocytes, the hallmark of which is decreased insulin-stimulated glucose uptake (ISGU). Despite the deleterious effects of reactive oxygen species (ROS), they have been recognized as a second messenger serving an intracellular signaling role for insulin action. Nuclear factor erythroid 2-related factor 2 (NRF2) is a central transcription factor regulating cellular adaptive response to oxidative stress. This study proposes that in response to arsenic exposure, the NRF2-mediated adaptive induction of endogenous antioxidant enzymes blunts insulin-stimulated ROS signaling and thus impairs ISGU. Exposure of differentiated 3T3-L1 cells to low-level (up to 2 {mu}M) inorganic arsenite (iAs{sup 3+}) led to decreased ISGU in a dose- and time-dependent manner. Concomitant to the impairment of ISGU, iAs{sup 3+} exposure significantly attenuated insulin-stimulated intracellular ROS accumulation and AKT S473 phosphorylation, which could be attributed to the activation of NRF2 and induction of a battery of endogenous antioxidant enzymes. In addition, prolonged iAs{sup 3+} exposure of 3T3-L1 adipocytes resulted in significant induction of inflammatory response genes and decreased expression of adipogenic genes and glucose transporter type 4 (GLUT4), suggesting chronic inflammation and reduction in GLUT4

  11. Strain-induced phenomenon in complex oxide thin films

    Science.gov (United States)

    Haislmaier, Ryan

    Complex oxide materials wield an immense spectrum of functional properties such as ferroelectricity, ferromagnetism, magnetoelectricity, optoelectricity, optomechanical, magnetoresistance, superconductivity, etc. The rich coupling between charge, spin, strain, and orbital degrees of freedom makes this material class extremely desirable and relevant for next generation electronic devices and technologies which are trending towards nanoscale dimensions. Development of complex oxide thin film materials is essential for realizing their integration into nanoscale electronic devices, where theoretically predicted multifunctional capabilities of oxides could add tremendous value. Employing thin film growth strategies such as epitaxial strain and heterostructure interface engineering can greatly enhance and even unlock novel material properties in complex oxides, which will be the main focus of this work. However, physically incorporating oxide materials into devices remains a challenge. While advancements in molecular beam epitaxy (MBE) of thin film oxide materials has led to the ability to grow oxide materials with atomic layer precision, there are still major limitations such as controlling stoichiometric compositions during growth as well as creating abrupt interfaces in multi-component layered oxide structures. The work done in this thesis addresses ways to overcome these limitations in order to harness intrinsic material phenomena. The development of adsorption-controlled stoichiometric growth windows of CaTiO3 and SrTiO3 thin film materials grown by hybrid MBE where Ti is supplied using metal-organic titanium tetraisopropoxide material is thoroughly outlined. These growth windows enable superior epitaxial strain-induced ferroelectric and dielectric properties to be accessed as demonstrated by chemical, structural, electrical, and optical characterization techniques. For tensile strained CaTiO3 and compressive strained SrTiO 3 films, the critical effects of

  12. APOPTOSIS GENE EXPRESSION IN HUMAN EPDERMAL KERATINOCYTES TREATED WITH SODIUM ARSENITE USING REAL TIME PCR ARRAY

    Science.gov (United States)

    Arsenic exposure via contaminated drinking water is a great public health concern worldwide. Chronic arsenic exposure has been associated with human skin, lung and bladder cancer and other chronic effects. We have previous reported that sodium arsenite stimulated cell proliferati...

  13. COMPARATIVE GENOTOXIC RESPONSES TO ARSENITE IN GUINEA PIG, MOUSE, RAT AND HUMAN LYMPHOCYTES

    Science.gov (United States)

    Comparative genotoxic responses to arsenite in guinea pig, mouse, rat and human lymphocytes.Inorganic arsenic is a known human carcinogen causing skin, lung, and bladder cancer following chronic exposures. Yet, long-term laboratory animal carcinogenicity studies have ...

  14. Synergistic effect of radon and sodium arsenite on DNA damage in HBE cells.

    Science.gov (United States)

    Liu, Xing; Sun, Bin; Wang, Xiaojuan; Nie, Jihua; Chen, Zhihai; An, Yan; Tong, Jian

    2016-01-01

    Human epidemiological studies showed that radon and arsenic exposures are major risk factors for lung cancer in Yunnan tin miners. However, biological evidence for this phenomenon is absent. In this study, HBE cells were exposed to different concentrations of sodium arsenite, different radon exposure times, or a combination of these two factors. The results showed a synergistic effect of radon and sodium arsenite in cell cytotoxicity as determined by cell viability. Elevated intracellular ROS levels and increased DNA damage indexed by comet assay and γ-H2AX were detected. Moreover, DNA HR repair in terms of Rad51 declined when the cells were exposed to both radon and sodium arsenite. The synergistic effect of radon and sodium arsenite in HBE cells may be attributed to the enhanced DSBs and inhibited HR pathway upon co-exposure.

  15. Oxidative stress induced by zearalenone in porcine granulosa cells and its rescue by curcumin in vitro

    National Research Council Canada - National Science Library

    Qin, Xunsi; Cao, Mingjun; Lai, Fangnong; Yang, Fan; Ge, Wei; Zhang, Xifeng; Cheng, Shunfeng; Sun, Xiaofeng; Qin, Guoqing; Shen, Wei; Li, Lan

    2015-01-01

    ... it. Ongoing studies provide remarkable evidence that oxidative stress is involved in reproductive toxicity induced by various stimuli, such as environmental toxicants and food toxicity. Zearalenone (ZEA...

  16. Nitric oxide synthase is induced in sporulation of Physarum polycephalum

    Science.gov (United States)

    Golderer, Georg; Werner, Ernst R.; Leitner, Stefan; Gröbner, Peter; Werner-Felmayer, Gabriele

    2001-01-01

    The myxomycete Physarum polycephalum expresses a calcium-independent nitric oxide (NO) synthase (NOS) resembling the inducible NOS isoenzyme in mammals. We have now cloned and sequenced this, the first nonanimal NOS to be identified, showing that it shares Physarum macroplasmodia during the 5-day starvation period needed to induce sporulation competence. Induction of both NOS and sporulation competence were inhibited by glucose, a growth signal and known repressor of sporulation, and by l-N6–(1-iminoethyl)-lysine (NIL), an inhibitor of inducible NOS. Sporulation, which is triggered after the starvation period by light exposure, was also prevented by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), an inhibitor of NO-sensitive guanylate cyclase. In addition, also expression of lig1, a sporulation-specific gene, was strongly attenuated by NIL or ODQ. 8-Bromo-cGMP, added 2 h before the light exposure, restored the capacity of NIL-treated macroplasmodia to express lig1 and to sporulate. This indicates that the second messenger used for NO signaling in sporulation of Physarum is cGMP and links this signaling pathway to expression of lig1. PMID:11358872

  17. Redox proteomics changes in the fungal pathogen Trichosporon asahii on arsenic exposure: identification of protein responses to metal-induced oxidative stress in an environmentally-sampled isolate.

    Directory of Open Access Journals (Sweden)

    Sidra Ilyas

    Full Text Available Trichosporon asahii is a yeast pathogen implicated in opportunistic infections. Cultures of an isolate collected from industrial wastewater were exposed for 2 days to 100 mg/L sodium arsenite (NaAsO2 and cadmium (CdCl2. Both metals reduced glutathione transferase (GST activity but had no effect on superoxide dismutase or catalase. NaAsO2 exposure increased glutathione reductase activity while CdCl2 had no effect. Protein thiols were labeled with 5-iodoacetamido fluorescein followed by one dimensional electrophoresis which revealed extensive protein thiol oxidation in response to CdCl2 treatment but thiol reduction in response to NaAsO2. Two dimensional electrophoresis analyses showed that the intensity of some protein spots was enhanced on treatment as judged by SameSpots image analysis software. In addition, some spots showed decreased IAF fluorescence suggesting thiol oxidation. Selected spots were excised and tryptic digested for identification by MALDI-TOF/TOF MS. Twenty unique T. asahii proteins were identified of which the following proteins were up-regulated in response to NaAsO2: 3-isopropylmalate dehydrogenase, phospholipase B, alanine-glyoxylate aminotransferase, ATP synthase alpha chain, 20S proteasome beta-type subunit Pre3p and the hypothetical proteins A1Q1_08001, A1Q2_03020, A1Q1_06950, A1Q1_06913. In addition, the following showed decreased thiol-associated fluorescence consistent with thiol oxidation; aconitase; aldehyde reductase I; phosphoglycerate kinase; translation elongation factor 2; heat shock protein 70 and hypothetical protein A1Q2_04745. Some proteins showed both increase in abundance coupled with decrease in IAF fluorescence; 3-hydroxyisobutyryl-CoA hydrolase; homoserine dehydrogenase Hom6 and hypothetical proteins A1Q2_03020 and A1Q1_00754. Targets implicated in redox response included 10 unique metabolic enzymes, heat shock proteins, a component of the 20S proteasome and translation elongation factor 2. These data

  18. A Comparison of the Effects of Neuronal Nitric Oxide Synthase and Inducible Nitric Oxide Synthase Inhibition on Cartilage Damage

    Directory of Open Access Journals (Sweden)

    Nevzat Selim Gokay

    2016-01-01

    Full Text Available The objective of this study was to investigate the effects of selective inducible nitric oxide synthase and neuronal nitric oxide synthase inhibitors on cartilage regeneration. The study involved 27 Wistar rats that were divided into five groups. On Day 1, both knees of 3 rats were resected and placed in a formalin solution as a control group. The remaining 24 rats were separated into 4 groups, and their right knees were surgically damaged. Depending on the groups, the rats were injected with intra-articular normal saline solution, neuronal nitric oxide synthase inhibitor 7-nitroindazole (50 mg/kg, inducible nitric oxide synthase inhibitor amino-guanidine (30 mg/kg, or nitric oxide precursor L-arginine (200 mg/kg. After 21 days, the right and left knees of the rats were resected and placed in formalin solution. The samples were histopathologically examined by a blinded evaluator and scored on 8 parameters. Although selective neuronal nitric oxide synthase inhibition exhibited significant (P=0.044 positive effects on cartilage regeneration following cartilage damage, it was determined that inducible nitric oxide synthase inhibition had no statistically significant effect on cartilage regeneration. It was observed that the nitric oxide synthase activation triggered advanced arthrosis symptoms, such as osteophyte formation. The fact that selective neuronal nitric oxide synthase inhibitors were observed to have mitigating effects on the severity of the damage may, in the future, influence the development of new agents to be used in the treatment of cartilage disorders.

  19. Evidence for toxicity differences between inorganic arsenite and thioarsenicals in human bladder cancer cells.

    Science.gov (United States)

    Naranmandura, Hua; Ogra, Yasumitsu; Iwata, Katsuya; Lee, Jane; Suzuki, Kazuo T; Weinfeld, Michael; Le, X Chris

    2009-07-15

    Arsenic toxicity is dependent on its chemical species. In humans, the bladder is one of the primary target organs for arsenic-induced carcinogenicity. However, little is known about the mechanisms underlying arsenic-induced carcinogenicity, and what arsenic species are responsible for this carcinogenicity. The present study aimed at comparing the toxic effect of DMMTA(V) with that of inorganic arsenite (iAs(III)) on cell viability, uptake efficiency and production of reactive oxygen species (ROS) toward human bladder cancer EJ-1 cells. The results were compared with those of a previous study using human epidermoid carcinoma A431 cells. Although iAs(III) was known to be toxic to most cells, here we show that iAs(III) (LC(50)=112 microM) was much less cytotoxic than DMMTA(V) (LC(50)=16.7 microM) in human bladder EJ-1 cells. Interestingly, pentavalent sulfur-containing DMMTA(V) generated a high level of intracellular ROS in EJ-1 cells. However, this was not observed in the cells exposed to trivalent inorganic iAs(III) at their respective LC(50) dose. Furthermore, the presence of N-acetyl-cysteine completely inhibited the cytotoxicity of DMMTA(V) but not iAs(III), suggesting that production of ROS was the main cause of cell death from exposure to DMMTA(V), but not iAs(III). Because the cellular uptake of iAs(III) is mediated by aquaporin proteins, and because the resistance of cells to arsenite can be influenced by lower arsenic uptake due to lower expression of aquaporin proteins (AQP 3, 7 and 9), the expression of several members of the aquaporin family was also examined. In human bladder EJ-1 cells, mRNA/proteins of AQP3, 7 and 9 were not detected by reverse transcription polymerase chain reaction (RT-PCR)/western blotting. In A431 cells, only mRNA and protein of AQP3 were detected. The large difference in toxicity between the two cell lines could be related to their differences in uptake of arsenic species.

  20. Role of inducible nitric oxide synthase pathway on methotrexate-induced intestinal mucositis in rodents

    Directory of Open Access Journals (Sweden)

    Siqueira Francisco JWS

    2011-08-01

    Full Text Available Abstract Background Methotrexate treatment has been associated to intestinal epithelial damage. Studies have suggested an important role of nitric oxide in such injury. The aim of this study was to investigate the role of nitric oxide (NO, specifically iNOS on the pathogenesis of methotrexate (MTX-induced intestinal mucositis. Methods Intestinal mucositis was carried out by three subcutaneous MTX injections (2.5 mg/kg in Wistar rats and in inducible nitric oxide synthase knock-out (iNOS-/- and wild-type (iNOS+/+ mice. Rats were treated intraperitoneally with the NOS inhibitors aminoguanidine (AG; 10 mg/Kg or L-NAME (20 mg/Kg, one hour before MTX injection and daily until sacrifice, on the fifth day. The jejunum was harvested to investigate the expression of Ki67, iNOS and nitrotyrosine by immunohistochemistry and cell death by TUNEL. The neutrophil activity by myeloperoxidase (MPO assay was performed in the three small intestine segments. Results AG and L-NAME significantly reduced villus and crypt damages, inflammatory alterations, cell death, MPO activity, and nitrotyrosine immunostaining due to MTX challenge. The treatment with AG, but not L-NAME, prevented the inhibitory effect of MTX on cell proliferation. MTX induced increased expression of iNOS detected by immunohistochemistry. MTX did not cause significant inflammation in the iNOS-/- mice. Conclusion These results suggest an important role of NO, via activation of iNOS, in the pathogenesis of intestinal mucositis.

  1. Oxidative stress and nitric oxide in rats with alcohol-induced acute pancreatitis

    Institute of Scientific and Technical Information of China (English)

    Gülnur Andican; Remisa Gelisgen; Gülden Burcak; Ethem Unal; Osman Baran Tortum; Tayfun Karahasanoglu

    2005-01-01

    AIM: Oxygen free radical mediated tissue damage is well established in pathogenesis of acute pancreatitis (AP).Whether nitric oxide (NO) plays a deleterious or a protective role is unknown. In alcohol-induced AP, we studied NO, lipooxidative damage and glutathione in pancreas, lung and circulation.METHODS: AP was induced in rats (n = 25) by injection of ethyl alcohol into the common biliary duct. A sham laparatomy was performed in controls (n = 15). After 24 h the animals were killed, blood and tissue sampling were done.RESULTS: Histopathologic evidence confirmed the development of AP. Marked changes were observed in the pulmonary tissue. Compared with controls, the AP group displayed higher values for NO metabolites in pancreas and lungs, and thiobarbituric acid reactive substances in circulation. Glutathione was lower in pancreas and in circulation. Glutathione and NO were positively correlated in pancreas and lungs of controls but negatively correlated in circulation of experimental group. In the experimental group, plasma thiobarbituric acid reactive substances were negatively correlated with pancreas thiobarbituric acid reactive substances but positively correlated with pancreas NO.CONCLUSION: NO increases in both pancreas and lungs in AP and NO contributes to the pathogenesis of AP under oxidative stress.

  2. Development of a biosorbent for arsenite: structural modeling based on X-ray spectroscopy.

    Science.gov (United States)

    Teixeira, Monica Cristina; Ciminelli, Virginia S T

    2005-02-01

    This work describes a biological route for direct sorption of aqueous As(III) species, which are the most toxic and mobile arsenic species found in soils. Based upon the biochemical mechanisms that explain arsenic toxicity, we propose that a waste biomass with a high fibrous protein content obtained from chicken feathers can be used for selective As(III) adsorption. Prior to adsorption, the disulfide bridges present in the biomass are reduced by thioglycolate. Our investigations demonstrated that As(III) is specifically adsorbed on the biomass and, contrary to the behavior observed with inorganic sorbents, the lower is the pH the more effective is the removal. Arsenic uptake reaches values of up to 270 micromol As(III)/g of biomass. Analyses by synchrotron light techniques, such as XANES, demonstrated that arsenic is adsorbed in its trivalent state, an advantage over conventional techniques for As uptake, which usually require a previous oxidation stage. EXAFS analyses showed that each As atom is directly bound to three S atoms with an estimated distance of 2.26 A. The uptake mechanism is explained in terms of the structural similarities between the As(III)-biomass complex structure and that of arsenite ions and Ars-Operon system encoded proteins and phytochelatins. The biological route presented here offers the perspective of a direct removal of arsenic in its reduced form.

  3. Electrochemical determination of arsenite in neutral media on reusable gold nanostructured films.

    Science.gov (United States)

    Du, Ying; Zhao, Wei; Xu, Jing-Juan; Chen, Hong-Yuan

    2009-07-15

    We report a simple and novel method of stirring-only-driven accumulation and electrochemical determination of arsenite (As(III)) with both of the oxidation and reduction peaks associated with As(0)/As(III) using a gold nanofilm electrode in neutral solution. Under stirring, a large amount of As(III) was deposited on the modified electrode and the electrochemical response was greatly amplified. The accumulated As(III) on the electrode showed well-defined redox couple in 0.1M blank phosphate buffer solution (pH 7.0), which could be used for the measurement of As(III). Under optimal conditions, As(III) could be detected in the range from 0.20 to 375 ppb with a detection limit of 0.04 ppb. In particular, with the use of the reduction peak of As(III) the modified electrode exhibits excellent performance for As(III) determination even in the presence of abundant Cu(II). The regeneration of the electrodes is facile with good reproducibility. The electrochemical system was applied to analyze As(III) in lake water, As(III) spiked tap water and drinking water.

  4. Transporters of arsenite in rice and their role in arsenic accumulation in rice grain.

    Science.gov (United States)

    Ma, Jian Feng; Yamaji, Naoki; Mitani, Namiki; Xu, Xiao-Yan; Su, Yu-Hong; McGrath, Steve P; Zhao, Fang-Jie

    2008-07-22

    Arsenic poisoning affects millions of people worldwide. Human arsenic intake from rice consumption can be substantial because rice is particularly efficient in assimilating arsenic from paddy soils, although the mechanism has not been elucidated. Here we report that two different types of transporters mediate transport of arsenite, the predominant form of arsenic in paddy soil, from the external medium to the xylem. Transporters belonging to the NIP subfamily of aquaporins in rice are permeable to arsenite but not to arsenate. Mutation in OsNIP2;1 (Lsi1, a silicon influx transporter) significantly decreases arsenite uptake. Furthermore, in the rice mutants defective in the silicon efflux transporter Lsi2, arsenite transport to the xylem and accumulation in shoots and grain decreased greatly. Mutation in Lsi2 had a much greater impact on arsenic accumulation in shoots and grain in field-grown rice than Lsi1. Arsenite transport in rice roots therefore shares the same highly efficient pathway as silicon, which explains why rice is efficient in arsenic accumulation. Our results provide insight into the uptake mechanism of arsenite in rice and strategies for reducing arsenic accumulation in grain for enhanced food safety.

  5. Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats

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    B.H. Bakkal

    2013-09-01

    Full Text Available Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg. Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage.

  6. Effect of ozone oxidative preconditioning in preventing early radiation-induced lung injury in rats

    Energy Technology Data Exchange (ETDEWEB)

    Bakkal, B.H. [Department of Radiation Oncology, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Gultekin, F.A. [Department of General Surgery, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Guven, B. [Department of Biochemistry, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Turkcu, U.O. [Mugla School of Health Sciences, Mugla Sitki Kocman University, Mugla (Turkey); Bektas, S. [Department of Pathology, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey); Can, M. [Department of Biochemistry, School of Medicine, Bulent Ecevit University, Kozlu, Zonguldak (Turkey)

    2013-09-27

    Ionizing radiation causes its biological effects mainly through oxidative damage induced by reactive oxygen species. Previous studies showed that ozone oxidative preconditioning attenuated pathophysiological events mediated by reactive oxygen species. As inhalation of ozone induces lung injury, the aim of this study was to examine whether ozone oxidative preconditioning potentiates or attenuates the effects of irradiation on the lung. Rats were subjected to total body irradiation, with or without treatment with ozone oxidative preconditioning (0.72 mg/kg). Serum proinflammatory cytokine levels, oxidative damage markers, and histopathological analysis were compared at 6 and 72 h after total body irradiation. Irradiation significantly increased lung malondialdehyde levels as an end-product of lipoperoxidation. Irradiation also significantly decreased lung superoxide dismutase activity, which is an indicator of the generation of oxidative stress and an early protective response to oxidative damage. Ozone oxidative preconditioning plus irradiation significantly decreased malondialdehyde levels and increased the activity of superoxide dismutase, which might indicate protection of the lung from radiation-induced lung injury. Serum tumor necrosis factor alpha and interleukin-1 beta levels, which increased significantly following total body irradiation, were decreased with ozone oxidative preconditioning. Moreover, ozone oxidative preconditioning was able to ameliorate radiation-induced lung injury assessed by histopathological evaluation. In conclusion, ozone oxidative preconditioning, repeated low-dose intraperitoneal administration of ozone, did not exacerbate radiation-induced lung injury, and, on the contrary, it provided protection against radiation-induced lung damage.

  7. Nitric Oxide Reduces Hydrogen Peroxide Accumulation Involved in Water Stress-induced Subcellular Anti-oxidant Defense in Maize Plants

    Institute of Scientific and Technical Information of China (English)

    Jianrong Sang; Mingyi Jiang; Fan Lin; Shucheng Xu; Aying Zhang; Mingpu Tan

    2008-01-01

    Nitric oxide (NO) Is a bioactive molecule involved in many biological events, and has been reported as pro-oxidant as well as anti-oxidant in plants. In the present study, the sources of NO production under water stress, the role of NO in water stress-induced hydrogen peroxide (H2O2) accumulation and subcellular activities of anti-oxidant enzymes in leaves of maize (Zea mays L.) plants were investigated. Water stress Induced defense increases in the generation of NO In maize mesphyll cells and the activity of nitric oxide synthase (NOS) in the cytosolic and microsomal fractions of maize leaves. Water stress-induced defense increases in the production of NO were blocked by pretreatments with Inhibitors of NOS and nitrate reductase (NR), suggesting that NO is produced from NOS and NR in leaves of maize plants exposed to water stress. Water stress also induced increases in the activities of the chloroplastic and cytosolic anti-oxidant enzymes superoxide dismutase (SOD), ascorbate peroxidass (APX), and glutathione reductase (GR), and the increases in the activities of anti-oxidant enzymes were reduced by pretreatments with inhibitors of NOS and NR. Exogenous NO increases the activities of water stress-induced subcellular anti-oxidant enzymes, which decreases accumulation of H2O2. Our results suggest that NOS and NR are involved in water strese-induced NO production and NOS is the major source of NO. The potential ability of NO to scavenge H2O2 is, at least in part, due to the induction of a subcellular anti-oxidant defense.

  8. Nitrous oxide-induced hypothermia in the rat

    Energy Technology Data Exchange (ETDEWEB)

    Quock, R.M.; Panek, R.W.; Kouchich, F.J.; Rosenthal, M.A.

    1987-08-10

    Exposure of rats to high levels of nitrous oxide (N2O) in oxygen reduced body temperature in a concentration-related manner. The hypothermia was partly reversed by pretreatment with naloxone but not naltrexone. But in rats rendered tolerant to morphine by pellet implantation, exposure to 75% N2O/25% O2 evoked a marked hypothermia similar to that observed in morphine-naive animals. In another experiment, the hypothermic effect of chloral hydrate was also sensitive to antagonism by pretreatment with naloxone but not naltrexone. These observations lead the authors to suspect that N2O-induced hypothermia in rats is possibly not mediated by opiate receptors. The thermotropic activity of N2O may result from some non-opioid action of N2O. Its selective antagonism by naloxone (but not naltrexone) may be due to a unique non-opioid analeptic action of naloxone. 32 references, 4 figures.

  9. Graphene Oxide Nanoribbons Induce Autophagic Vacuoles in Neuroblastoma Cell Lines

    Directory of Open Access Journals (Sweden)

    Emanuela Mari

    2016-11-01

    Full Text Available Since graphene nanoparticles are attracting increasing interest in relation to medical applications, it is important to understand their potential effects on humans. In the present study, we prepared graphene oxide (GO nanoribbons by oxidative unzipping of single-wall carbon nanotubes (SWCNTs and analyzed their toxicity in two human neuroblastoma cell lines. Neuroblastoma is the most common solid neoplasia in children. The hallmark of these tumors is the high number of different clinical variables, ranging from highly metastatic, rapid progression and resistance to therapy to spontaneous regression or change into benign ganglioneuromas. Patients with neuroblastoma are grouped into different risk groups that are characterized by different prognosis and different clinical behavior. Relapse and mortality in high risk patients is very high in spite of new advances in chemotherapy. Cell lines, obtained from neuroblastomas have different genotypic and phenotypic features. The cell lines SK-N-BE(2 and SH-SY5Y have different genetic mutations and tumorigenicity. Cells were exposed to low doses of GO for different times in order to investigate whether GO was a good vehicle for biological molecules delivering individualized therapy. Cytotoxicity in both cell lines was studied by measuring cellular oxidative stress (ROS, mitochondria membrane potential, expression of lysosomial proteins and cell growth. GO uptake and cytoplasmic distribution of particles were studied by Transmission Electron Microscopy (TEM for up to 72 h. The results show that GO at low concentrations increased ROS production and induced autophagy in both neuroblastoma cell lines within a few hours of exposure, events that, however, are not followed by growth arrest or death. For this reason, we suggest that the GO nanoparticle can be used for therapeutic delivery to the brain tissue with minimal effects on healthy cells.

  10. Cerebral ischemia—induced neuronal apoptosis mediated by nitric oxide

    Institute of Scientific and Technical Information of China (English)

    NomuY

    2002-01-01

    To elucidate the cellular and molecular mechanism of cerebral ischemia-induced neuronal apoptosis mediated by nitric oxide (NO) in the brain,we investigated:(1)cell death in hippocampal CA1 neurons of rats after a rransient four vessel occlusion (4VO)/reperfusion and (2) apoptosis induced by NOC18(NO releaser) using SHSY5Y cells,a human neuroblastoma cell line.We found that 4VO caused expression of inducible type of NO synthase (iNOS) in glial cells and neuronal apoptosis in CA1 region of rats.Next we examined in vitro apoptotic effects of NOC18 on SHSY5Y cells and suggest that NO decrease mitochondrial membrane potential,release cytochrome C from mitochondria,activates caspase-3,degrade inhibitor of caspase-activated DNase(Icad),and activated DNase translocate into nucleus and induce DNA fragmentation.Thus we conclude that the excess amount of NO produced by glial iNOS at cerebral ischemia could be involved in neuronal apoptosis in CA1 region.Regarding NO action on neurons,we further obtained that NO propects neuronal apoptosis in PC12 cells perhaps by nitrosylation of caspase,subsequent reduction of proteolytic activity.Taken together,we suggest that NO seem to exert dual effects(toxic and beneficial) on neuronal apoptosis,the one (toxic);apoptosis-induction throuth the decrease in mitochondrial membrane potentials and cytochrome C release and the othe (beneficial);protection against apoptosis through the inhibition of caspase activity.

  11. CIRRHOSIS INDUCES APOPTOSIS IN RENAL TISSUE THROUGH INTRACELLULAR OXIDATIVE STRESS

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    Keli Cristina Simões da SILVEIRA

    2015-03-01

    Full Text Available Background Renal failure is a frequent and serious complication in patients with decompensated cirrhosis. Objectives We aimed to evaluate the renal oxidative stress, cell damage and impaired cell function in animal model of cirrhosis. Methods Secondary biliary cirrhosis was induced in rats by ligation of the common bile duct. We measured TBARS, ROS and mitochondrial membrane potential in kidney as markers of oxidative stress, and activities of the antioxidant enzymes. Relative cell viability was determined by trypan blue dye-exclusion assay. Annexin V-PE was used with a vital dye, 7-AAD, to distinguish apoptotic from necrotic cells and comet assay was used for determined DNA integrity in single cells. Results In bile duct ligation animals there was significant increase in the kidney lipoperoxidation and an increase of the level of intracellular ROS. There was too an increase in the activity of all antioxidant enzymes evaluated in the kidney. The percentage viability was above 90% in the control group and in bile duct ligation was 64.66% and the dominant cell death type was apoptosis. DNA damage was observed in the bile duct ligation. There was a decreased in the mitochondrial membrane potential from 71.40% ± 6.35% to 34.48% ± 11.40% in bile duct ligation. Conclusions These results indicate that intracellular increase of ROS cause damage in the DNA and apoptosis getting worse the renal function in cirrhosis.

  12. Liposomal Antioxidants for Protection against Oxidant-Induced Damage

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    Zacharias E. Suntres

    2011-01-01

    Full Text Available Reactive oxygen species (ROS, including superoxide anion, hydrogen peroxide, and hydroxyl radical, can be formed as normal products of aerobic metabolism and can be produced at elevated rates under pathophysiological conditions. Overproduction and/or insufficient removal of ROS result in significant damage to cell structure and functions. In vitro studies showed that antioxidants, when applied directly and at relatively high concentrations to cellular systems, are effective in conferring protection against the damaging actions of ROS, but results from animal and human studies showed that several antioxidants provide only modest benefit and even possible harm. Antioxidants have yet to be rendered into reliable and safe therapies because of their poor solubility, inability to cross membrane barriers, extensive first-pass metabolism, and rapid clearance from cells. There is considerable interest towards the development of drug-delivery systems that would result in the selective delivery of antioxidants to tissues in sufficient concentrations to ameliorate oxidant-induced tissue injuries. Liposomes are biocompatible, biodegradable, and nontoxic artificial phospholipid vesicles that offer the possibility of carrying hydrophilic, hydrophobic, and amphiphilic molecules. This paper focus on the use of liposomes for the delivery of antioxidants in the prevention or treatment of pathological conditions related to oxidative stress.

  13. Strain-induced topological quantum phase transition in phosphorene oxide

    Science.gov (United States)

    Kang, Seoung-Hun; Park, Jejune; Woo, Sungjong; Kwon, Young-Kyun

    Using ab initio density functional theory, we investigate the structural stability and electronic properties of phosphorene oxides (POx) with different oxygen compositions x. A variety of configurations are modeled and optimized geometrically to search for the equilibrium structure for each x value. Our electronic structure calculations on the equilibrium configuration obtained for each x reveal that the band gap tends to increase with the oxygen composition of x 0.5. We further explore the strain effect on the electronic structure of the fully oxidized phosphorene, PO, with x = 1. At a particular strain without spin-orbit coupling (SOC) is observed a band gap closure near the Γ point in the k space. We further find the strain in tandem with SOC induces an interesting band inversion with a reopened very small band gap (5 meV), and thus gives rise to a topological quantum phase transition from a normal insulator to a topological insulator. Such a topological phase transition is confirmed by the wave function analysis and the band topology identified by the Z2 invariant calculation.

  14. Transparent conducting oxide induced by liquid electrolyte gating

    Science.gov (United States)

    ViolBarbosa, Carlos; Karel, Julie; Kiss, Janos; Gordan, Ovidiu-dorin; Altendorf, Simone G.; Utsumi, Yuki; Samant, Mahesh G.; Wu, Yu-Han; Tsuei, Ku-Ding; Felser, Claudia; Parkin, Stuart S. P.

    2016-10-01

    Optically transparent conducting materials are essential in modern technology. These materials are used as electrodes in displays, photovoltaic cells, and touchscreens; they are also used in energy-conserving windows to reflect the infrared spectrum. The most ubiquitous transparent conducting material is tin-doped indium oxide (ITO), a wide-gap oxide whose conductivity is ascribed to n-type chemical doping. Recently, it has been shown that ionic liquid gating can induce a reversible, nonvolatile metallic phase in initially insulating films of WO3. Here, we use hard X-ray photoelectron spectroscopy and spectroscopic ellipsometry to show that the metallic phase produced by the electrolyte gating does not result from a significant change in the bandgap but rather originates from new in-gap states. These states produce strong absorption below ˜1 eV, outside the visible spectrum, consistent with the formation of a narrow electronic conduction band. Thus WO3 is metallic but remains colorless, unlike other methods to realize tunable electrical conductivity in this material. Core-level photoemission spectra show that the gating reversibly modifies the atomic coordination of W and O atoms without a substantial change of the stoichiometry; we propose a simple model relating these structural changes to the modifications in the electronic structure. Thus we show that ionic liquid gating can tune the conductivity over orders of magnitude while maintaining transparency in the visible range, suggesting the use of ionic liquid gating for many applications.

  15. Nitric Oxide Signaling in Hypergravity-Induced Neuronal Plasticity

    Science.gov (United States)

    Holstein, Gay R.

    2003-01-01

    The goal of this research project was to identify the neurons and circuits in the vestibular nuclei and nucleus prepositus hypoglossi that utilize nitric oxide (NO) for intercellular signaling during gravity-induced plasticity. This objective was pursued using histochemical and immunocytochemical approaches to localize NO-producing neurons and characterize the fine morphology of the cells in ground-based studies of normal rats, rats adapted to hypergravity, and rats adapted to hypergravity and then re-adapted to the 1G environment. NO-producing neurons were identified and studied using four methodologies: i) immunocytochemistry employing polyclonal antibodies directed against neuronal nitric oxide synthase (nNOS), to provide an indication of the capacity of a cell for NO production; ii) immunocytochemistry employing a monoclonal antibody directed against L-citrulline, to provide an indirect index of the enzyme's activity; iii) histochemistry based on the NADPH-diaphorase reaction, for fuI1 cytological visualization of neurons; and iv) double immunofluorescence to co-localize nNOS and L-citrulline in individual vestibular nuclei (VN) and neurons.

  16. Urea-induced oxidative damage in Elodea densa leaves.

    Science.gov (United States)

    Maleva, Maria; Borisova, Galina; Chukina, Nadezda; Prasad, M N V

    2015-09-01

    Urea being a fertilizer is expected to be less toxic to plants. However, it was found that urea at 100 mg L(-1) caused the oxidative stress in Elodea leaves due to the formation of reactive oxygen species (ROS) and lipid peroxidation that are known to stimulate antioxidant pathway. Urea at a concentration of 500 and 1000 mg L(-1) decreased low-molecular-weight antioxidants. In this case, the antioxidant status of plants was supported by the activity of antioxidant enzymes such as superoxide dismutase and guaiacol peroxidase. A significant increase in the soluble proteins and -SH groups was observed with high concentrations of urea (30-60 % of control). Thus, the increased activity of antioxidant enzymes, low-molecular-weight antioxidants, and induced soluble protein thiols are implicated in plant resistance to oxidative stress imposed by urea. We found that guaiacol peroxidase plays an important role in the removal of the peroxide in Elodea leaves exposed to 1000 mg L(-1)of urea.

  17. Mechanism of inducible nitric oxide synthase exclusion from mycobacterial phagosomes.

    Directory of Open Access Journals (Sweden)

    Alexander S Davis

    2007-12-01

    Full Text Available Mycobacterium tuberculosis is sensitive to nitric oxide generated by inducible nitric oxide synthase (iNOS. Consequently, to ensure its survival in macrophages, M. tuberculosis inhibits iNOS recruitment to its phagosome by an unknown mechanism. Here we report the mechanism underlying this process, whereby mycobacteria affect the scaffolding protein EBP50, which normally binds to iNOS and links it to the actin cytoskeleton. Phagosomes harboring live mycobacteria showed reduced capacity to retain EBP50, consistent with lower iNOS recruitment. EBP50 was found on purified phagosomes, and its expression increased upon macrophage activation, paralleling expression changes seen with iNOS. Overexpression of EBP50 increased while EBP50 knockdown decreased iNOS recruitment to phagosomes. Knockdown of EBP50 enhanced mycobacterial survival in activated macrophages. We tested another actin organizer, coronin-1, implicated in mycobacterium-macrophage interaction for contribution to iNOS exclusion. A knockdown of coronin-1 resulted in increased iNOS recruitment to model latex bead phagosomes but did not increase iNOS recruitment to phagosomes with live mycobacteria and did not affect mycobacterial survival. Our findings are consistent with a model for the block in iNOS association with mycobacterial phagosomes as a mechanism dependent primarily on reduced EBP50 recruitment.

  18. Oats supplementation prevents alcohol-induced gut leakiness in rats by preventing alcohol-induced oxidative tissue damage.

    Science.gov (United States)

    Tang, Yueming; Forsyth, Christopher B; Banan, Ali; Fields, Jeremy Z; Keshavarzian, Ali

    2009-06-01

    We reported previously that oats supplementation prevents gut leakiness and alcoholic steatohepatitis (ASH) in our rat model of alcoholic liver disease. Because oxidative stress is implicated in the pathogenesis of both alcohol-induced gut leakiness and ASH, and because oats have antioxidant properties, we tested the hypothesis that oats protect by preventing alcohol-induced oxidative damage to the intestine. Male Sprague-Dawley rats were gavaged for 12 weeks with alcohol (starting dose of 1 g/kg increasing to 6 g/kg/day over the first 2 weeks) or dextrose, with or without oats supplementation (10 g/kg/day). Oxidative stress and injury were assessed by measuring colonic mucosal inducible nitric-oxide synthase (iNOS) (by immunohistochemistry), nitric oxide (colorimetric assay), and protein carbonylation and nitrotyrosination (immunoblotting). Colonic barrier integrity was determined by assessing the integrity of the actin cytoskeleton (immunohistochemistry) and the integrity of tight junctions (electron microscopy). Oats supplementation prevented alcohol-induced up-regulation of iNOS, nitric oxide overproduction in the colonic mucosa, and increases in protein carbonyl and nitrotyrosine levels. This protection was associated with prevention of ethanol (EtOH)-induced disorganization of the actin cytoskeleton and disruption of tight junctions. We conclude that oats supplementation attenuates EtOH-induced disruption of intestinal barrier integrity, at least in part, by inhibiting EtOH-induced increases in oxidative stress and oxidative tissue damage. This inhibition prevents alcohol-induced disruption of the cytoskeleton and tight junctions. This study suggests that oats may be a useful therapeutic agent--a nutraceutical--for the prevention of alcohol-induced oxidative stress and organ dysfunction.

  19. Vitiligo: How do oxidative stress-induced autoantigens trigger autoimmunity?

    Science.gov (United States)

    Xie, Heng; Zhou, Fubo; Liu, Ling; Zhu, Guannan; Li, Qiang; Li, Chunying; Gao, Tianwen

    2016-01-01

    Vitiligo is a common depigmentation disorder characterized by a loss of functional melanocytes and melanin from epidermis, in which the autoantigens and subsequent autoimmunity caused by oxidative stress play significant roles according to hypotheses. Various factors lead to reactive oxygen species (ROS) overproduction in the melanocytes of vitiligo: the exogenous and endogenous stimuli that cause ROS production, low levels of enzymatic and non-enzymatic antioxidants, disturbed antioxidant pathways and polymorphisms of ROS-associated genes. These factors synergistically contribute to the accumulation of ROS in melanocytes, finally leading to melanocyte damage and the production of autoantigens through the following ways: apoptosis, accumulation of misfolded peptides and cytokines induced by endoplasmic reticulum stress as well as the sustained unfolded protein response, and an 'eat me' signal for phagocytic cells triggered by calreticulin. Subsequently, autoantigens presentation and dendritic cells maturation occurred mediated by the release of antigen-containing exosomes, adenosine triphosphate and melanosomal autophagy. With the involvement of inducible heat shock protein 70, cellular immunity targeting autoantigens takes the essential place in the destruction of melanocytes, which eventually results in vitiligo. Several treatments, such as narrow band ultraviolet, quercetin and α-melanophore-stimulating hormone, are reported to be able to lower ROS thereby achieving repigmentation in vitiligo. In therapies targeting autoimmunity, restore of regulatory T cells is absorbing attention, in which narrow band ultraviolet also plays a role.

  20. Lycopene Protects the Diabetic Rat Kidney Against Oxidative Stress-mediated Oxidative Damage Induced by Furan

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    Dilek Pandir

    2016-01-01

    Full Text Available Furan is a food and environmental contaminant and a potent carcinogen in animals. Lycopene is one dietary carotenoid found in fruits such as tomato, watermelon and grapefruit. The present study was designed to explore the protective effect of lycopene against furan-induced oxidative damage in streptozotocin (STZ-induced diabetic rat kidney. At the end of the experimental period (28 days, we found that lycopene markedly decreased the malondialdehide (MDA levels in the kidney, urea, uric acid and creatinine levels in the serum of furan-treated rats. The increase of histopathology in the kidney of furan-treated rats were effectively suppressed by lycopene. Furthermore, lycopene markedly restored superoxide dismutase (SOD, catalase (CAT, glutathione peroxidase (GPx and glutathione-S-transferase (GST activities in the kidney of furan-treated rats. In conclusion, these results suggested that lycopene could protect the rat kidney against furan-induced injury by improving renal function, attenuating histopathologic changes, reducing MDA production and renewing the activities of antioxidant enzymes.

  1. Arsenite activates NFκB through induction of C-reactive protein

    Energy Technology Data Exchange (ETDEWEB)

    Druwe, Ingrid L.; Sollome, James J.; Sanchez-Soria, Pablo; Hardwick, Rhiannon N.; Camenisch, Todd D.; Vaillancourt, Richard R., E-mail: vaillancourt@pharmacy.arizona.edu

    2012-06-15

    C-reactive protein (CRP) is an acute phase protein in humans. Elevated levels of CRP are produced in response to inflammatory cytokines and are associated with atherosclerosis, hypertension, cardiovascular disease and insulin resistance. Exposure to inorganic arsenic, a common environmental toxicant, also produces cardiovascular disorders, namely atherosclerosis and is associated with insulin-resistance. Inorganic arsenic has been shown to contribute to cardiac toxicities through production of reactive oxygen species (ROS) that result in the activation of NFκB. In this study we show that exposure of the hepatic cell line, HepG2, to environmentally relevant levels of arsenite (0.13 to 2 μM) results in elevated CRP expression and secretion. ROS analysis of the samples showed that a minimal amount of ROS are produced by HepG2 cells in response to these concentrations of arsenic. In addition, treatment of FvB mice with 100 ppb sodium arsenite in the drinking water for 6 months starting at weaning age resulted in dramatically higher levels of CRP in both the liver and inner medullary region of the kidney. Further, mouse Inner Medullary Collecting Duct cells (mIMCD-4), a mouse kidney cell line, were stimulated with 10 ng/ml CRP which resulted in activation of NFκB. Pretreatment with 10 nM Y27632, a known Rho-kinase inhibitor, prior to CRP exposure attenuated NFκB activation. These data suggest that arsenic causes the expression and secretion of CRP and that CRP activates NFκB through activation of the Rho-kinase pathway, thereby providing a novel pathway by which arsenic can contribute to metabolic syndrome and cardiovascular disease. -- Highlights: ► Exposure to arsenic can induce the expression and secretion of CRP. ► Mice treated with NaAsO{sub 2} showed higher levels of CRP in both the liver and kidney. ► mIMCD-3 were stimulated with CRP which resulted in activation of NFκB. ► CRP activates NFκB through activation of the Rho-kinase pathway. ► Data

  2. Interleukin 1 beta induces diabetes and fever in normal rats by nitric oxide via induction of different nitric oxide synthases

    DEFF Research Database (Denmark)

    Reimers, J I; Bjerre, U; Mandrup-Poulsen, T

    1994-01-01

    Substantial in vitro evidence suggests that nitric oxide may be a major mediator of interleukin 1 (IL-1) induced pancreatic beta-cell inhibition and destruction in the initial events leading to insulin-dependent diabetes mellitus. Using NG-nitro-L-arginine methyl ester, an inhibitor of both......, glucagon, corticosterone and leukocyte- and differential-counts in normal rats injected once daily for 5 days with interleukin 1 beta (IL-1 beta) (0.8 microgram/rat = 4.0 micrograms/kg). Inhibition of both the constitutive and the inducible forms of nitric oxide synthase prevented IL-1 beta-induced fever...

  3. Arsenite-loaded nanoparticles inhibit PARP-1 to overcome multidrug resistance in hepatocellular carcinoma cells

    Science.gov (United States)

    Liu, Hanyu; Zhang, Zongjun; Chi, Xiaoqin; Zhao, Zhenghuan; Huang, Dengtong; Jin, Jianbin; Gao, Jinhao

    2016-08-01

    Hepatocellular carcinoma (HCC) is one of the highest incidences in cancers; however, traditional chemotherapy often suffers from low efficiency caused by drug resistance. Herein, we report an arsenite-loaded dual-drug (doxorubicin and arsenic trioxide, i.e., DOX and ATO) nanomedicine system (FeAsOx@SiO2-DOX, Combo NP) with significant drug synergy and pH-triggered drug release for effective treatment of DOX resistant HCC cells (HuH-7/ADM). This nano-formulation Combo NP exhibits the synergistic effect of DNA damage by DOX along with DNA repair interference by ATO, which results in unprecedented killing efficiency on DOX resistant cancer cells. More importantly, we explored the possible mechanism is that the activity of PARP-1 is inhibited by ATO during the treatment of Combo NP, which finally induces apoptosis of HuH-7/ADM cells by poly (ADP-ribosyl) ation suppression and DNA lesions accumulation. This study provides a smart drug delivery strategy to develop a novel synergistic combination therapy for effectively overcome drug- resistant cancer cells.

  4. Protective effects of phyllanthus emblica leaf extract on sodium arsenite-mediated adverse effects in mice.

    Science.gov (United States)

    Sayed, Sadia; Ahsan, Nazmul; Kato, Masashi; Ohgami, Nobutaka; Rashid, Abdur; Akhand, Anwarul Azim

    2015-02-01

    Groundwater contamination of arsenic is the major cause of a serious health hazard in Bangladesh. No specific treatment is yet available to manage the large number of individuals exposed to arsenic. In this study, we evaluated the protective effects of Phyllanthus emblica (Indian gooseberry or Amla) leaf extract (PLE) on arsenic-mediated toxicity in experimental mice. Male Swiss albino mice were divided into three different groups (n=6/group). 'Control' mice received arsenic free water together with normal feed. Mice in the remaining two groups designated 'SA' and 'SA+PLE' were exposed to sodium arsenite (SA, 10 µg/g body weight/day) through drinking water in addition to receiving normal feed and PLE-supplemented feed, respectively. The weight gain of SA-exposed mice was decreased compared with the controls; however, this decrease in body weight gain was prevented when the feed was supplemented with PLE. A secondary effect of arsenic was enlargement of the liver, kidney and spleen of SA-group mice. Deposition of arsenic in those organs was demonstrated by ICP-MS. When PLE was supplemented in the feed the enlargement of the organs was minimized; however, the deposition of arsenic was not significantly reduced. These results indicated that PLE may not block arsenic deposition in tissue directly but rather may play a protective role to reduce arsenic-induced toxicity. Therefore, co-administration of PLE in arsenic-exposed animals might have a future therapeutic application for protecting against arsenic-mediated toxicity.

  5. Adsorption kinetics and isotherms of arsenite and arsenate on hematite nanoparticles and aggregates.

    Science.gov (United States)

    Dickson, Dionne; Liu, Guangliang; Cai, Yong

    2017-01-15

    Iron (Fe) nanoparticles, e.g., zerovalent iron (ZVI) and iron oxide nanoparticles (IONP), have been used for remediation and environmental management of arsenic (As) contamination. These Fe nanoparticles, although originally nanosized, tend to form aggregates, in particular in the environment. The interactions of As with both nanoparticles and micron-sized aggregates should be considered when these Fe nanomaterials are used for mitigation of As issue. The objective of this study was to compare the adsorption kinetics and isotherm of arsenite (As(III)) and arsenate (As(V)) on bare hematite nanoparticles and aggregates and how this affects the fate of arsenic in the environment. The adsorption kinetic process was investigated with regards to the aggregation of the nanoparticles and the type of sorbed species. Kinetic data were best described by a pseudo second-order model. Both As species had similar rate constants, ranging from 3.82 to 6.45 × 10(-4) g/(μg·h), as rapid adsorption occurred within the first 8 h regardless of particle size. However, hematite nanoparticles and aggregates showed a higher affinity to adsorb larger amounts of As(V) (4122 ± 62.79 μg/g) than As(III) (2899 ± 71.09 μg/g) at equilibrium. We were able to show that aggregation and sedimentation of hematite nanoparticles occurs during the adsorption process and this might cause the immobilization and reduced bioavailability of arsenic. Isotherm studies were described by the Freundlich model and it confirmed that hematite nanoparticles have a significantly higher adsorption capacity for both As(V) and As(III) than hematite aggregates. This information is useful and can assist in predicting arsenic adsorption behavior and assessing the role of iron oxide nanoparticles in the biogeochemical cycling of arsenic.

  6. Physico chemical studies on the composition of complex arsenites of metals Part IV: conductometric and potentiometric studies on the composition of cadmium arsenite

    Directory of Open Access Journals (Sweden)

    M. S. Bhadraver

    1962-07-01

    Full Text Available The formation and precipitation of cadmium arsenite has been studied by conductometric and potentiometric titrations between cadmium nitrate and sodium arsenite (meta at different concentrations with either of the substances used as the reagent in titration. In the case of direct titrations (cadmium nitrate added to sodium arsenite in the conductivity cell, one distinct break in the curves is observed corresponding to the formation of the Cd (AsO/sub 2//sub 2/ where the molecular ratio is 2:1. The direct and reverse potentiometric titrations curves give one maxima in dE/dV at point corresponding to the formation of the complex Cd (AsO/sub/2/sub/2 where the molecular ratio of reactants Cd:AsO/sub/2 is 1:2. The composition has been arrived at by comparing the calculated values with observed values by conductometric and potentiometric titrations. The composition of cadmium arsenite arrived at both by conductometry and potentiometry is best representative as Cd(AsO/sub/2/sub/2

  7. Acidosis induces reprogramming of cellular metabolism to mitigate oxidative stress

    Science.gov (United States)

    2013-01-01

    Background A variety of oncogenic and environmental factors alter tumor metabolism to serve the distinct cellular biosynthetic and bioenergetic needs present during oncogenesis. Extracellular acidosis is a common microenvironmental stress in solid tumors, but little is known about its metabolic influence, particularly when present in the absence of hypoxia. In order to characterize the extent of tumor cell metabolic adaptations to acidosis, we employed stable isotope tracers to examine how acidosis impacts glucose, glutamine, and palmitate metabolism in breast cancer cells exposed to extracellular acidosis. Results Acidosis increased both glutaminolysis and fatty acid β-oxidation, which contribute metabolic intermediates to drive the tricarboxylic acid cycle (TCA cycle) and ATP generation. Acidosis also led to a decoupling of glutaminolysis and novel glutathione (GSH) synthesis by repressing GCLC/GCLM expression. We further found that acidosis redirects glucose away from lactate production and towards the oxidative branch of the pentose phosphate pathway (PPP). These changes all serve to increase nicotinamide adenine dinucleotide phosphate (NADPH) production and counter the increase in reactive oxygen species (ROS) present under acidosis. The reduced novel GSH synthesis under acidosis may explain the increased demand for NADPH to recycle existing pools of GSH. Interestingly, acidosis also disconnected novel ribose synthesis from the oxidative PPP, seemingly to reroute PPP metabolites to the TCA cycle. Finally, we found that acidosis activates p53, which contributes to both the enhanced PPP and increased glutaminolysis, at least in part, through the induction of G6PD and GLS2 genes. Conclusions Acidosis alters the cellular metabolism of several major metabolites, which induces a significant degree of metabolic inflexibility. Cells exposed to acidosis largely rely upon mitochondrial metabolism for energy generation to the extent that metabolic intermediates are

  8. Aloin Protects Skin Fibroblasts from Heat Stress-Induced Oxidative Stress Damage by Regulating the Oxidative Defense System.

    Directory of Open Access Journals (Sweden)

    Fu-Wei Liu

    Full Text Available Oxidative stress is commonly involved in the pathogenesis of skin damage induced by environmental factors, such as heat stress. Skin fibroblasts are responsible for the connective tissue regeneration and the skin recovery from injury. Aloin, a bioactive compound in Aloe vera, has been reported to have various pharmacological activities, such as anti-inflammatory effects. The aim of this study was to investigate the protective effect of aloin against heat stress-mediated oxidative stress in human skin fibroblast Hs68 cells. Hs68 cells were first incubated at 43°C for 30 min to mimic heat stress. The study was further examined if aloin has any effect on heat stress-induced oxidative stress. We found that aloin protected Hs68 cells against heat stress-induced damage, as assessed by 3-(4,5-dimethylthiazol-2-yl-2,5-diphenyltetrazolium bromide and lactate dehydrogenase assay. Aloin protected Hs68 cells by regulating reactive oxygen species production and increasing the levels of glutathione, cytosolic and mitochondrial superoxide dismutase. Aloin also prevented the elevation of thiobarbituric acid reactive substances and the reduction of 8-OH-dG induced by heat stress. These results indicated that aloin protected human skin fibroblasts from heat stress-induced oxidative stress damage by regulating the oxidative defense system.

  9. Adaptation of a methanogenic consortium to arsenite inhibition.

    Science.gov (United States)

    Rodriguez-Freire, Lucia; Moore, Sarah E; Sierra-Alvarez, Reyes; Field, James A

    2015-12-01

    Arsenic (As) is a ubiquitous metalloid known for its adverse effects to human health. Microorganisms are also impacted by As toxicity, including methanogenic archaea, which can affect the performance of process in which biological activity is required (i.e. stabilization of activated sludge in wastewater treatment plants). The novel ability of a mixed methanogenic granular sludge consortium to adapt to the inhibitory effect of arsenic (As) was investigated by exposing the culture to approximately 0.92 mM of As(III) for 160 d in an arsenate (As(V)) reducing bioreactor using ethanol as the electron donor. The results of shaken batch bioassays indicated that the original, unexposed sludge was severely inhibited by arsenite (As(III)) as evidenced by the low 50% inhibition concentrations (IC50) determined, i.e., 19 and 90 μM for acetoclastic- and hydrogenotrophic methanogenesis, respectively. The tolerance of the acetoclastic and hydrogenotrophic methanogens in the sludge to As(III) increased 47-fold (IC50 = 910 μM) and 12-fold (IC50= 1100 μM), respectively, upon long-term exposure to As. In conclusion, the methanogenic community in the granular sludge demonstrated a considerable ability to adapt to the severe inhibitory effects of As after a prolonged exposure period.

  10. Selenite modulates the level of phenolics and nutrient element to alleviate the toxicity of arsenite in rice (Oryza sativa L.).

    Science.gov (United States)

    Chauhan, Reshu; Awasthi, Surabhi; Tripathi, Preeti; Mishra, Seema; Dwivedi, Sanjay; Niranjan, Abhishek; Mallick, Shekhar; Tripathi, Pratibha; Pande, Veena; Tripathi, Rudra Deo

    2017-04-01

    Arsenic (As) contamination of paddy rice is a serious threat all over the world particularly in South East Asia. Selenium (Se) plays important role in protection of plants against various abiotic stresses including heavy metals. Moreover, arsenite (AsIII) and selenite (SeIV) can be biologically antagonistic due to similar electronic configuration and sharing the common transporter for their uptake in plant. In the present study, the response of oxidative stress, phenolic compounds and nutrient elements was analyzed to investigate Se mediated As tolerance in rice seedlings during AsIII and SeIV exposure in hydroponics. Selenite (25µM) significantly decreased As accumulation in plant than As (25µM) alone treated plants. Level of oxidative stress related parameters viz., reactive oxygen species (ROS), lipid peroxidation, electrical conductivity, nitric oxide and pro-oxidant enzyme (NADPH oxidase), were in the order of As>As+Se>control>Se. Selenium ameliorated As phytotoxicity by increased level of phenolic compounds particularly gallic acid, protocatechuic acid, ferulic acid and rutin and thiol metabolism related enzymes viz., serine acetyl transferase (SAT) and cysteine synthase (CS). Selenium supplementation enhanced the uptake of nutrient elements viz., Fe, Mn, Co, Cu, Zn, Mo, and improved plant growth. The results concluded that Se addition in As contaminated environment might be an important strategy to reduce As uptake and associated phytotoxicity in rice plant by modulation of phenolic compounds and increased uptake of nutrient elements.

  11. Protective effects of thymoquinone against apoptosis and oxidative stress by arsenic in rat kidney.

    Science.gov (United States)

    Sener, Umit; Uygur, Ramazan; Aktas, Cevat; Uygur, Emine; Erboga, Mustafa; Balkas, Gulseren; Caglar, Veli; Kumral, Bahadir; Gurel, Ahmet; Erdogan, Hasan

    2016-01-01

    We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

  12. Combined administration of taurine and monoisoamyl DMSA protects arsenic induced oxidative injury in rats.

    Science.gov (United States)

    Flora, Swaran J S; Chouhan, Swapnila; Kannan, Gurusamy M; Mittal, Megha; Swarnkar, Harimohan

    2008-01-01

    Arsenic is a naturally occurring element that is ubiquitously present in the environment. High concentration of naturally occurring arsenic in drinking water is a major health problem in different parts of the world. Despite arsenic being a health hazard and a well documented carcinogen, no safe, effective and specific preventive or therapeutic measures are available. Among various recent strategies adopted, administration of an antioxidant has been reported to be the most effective. The present study was designed to evaluate the therapeutic efficacy of monoisoamyl dimercaptosuccinic acid (MiADMSA), administered either individually or in combination with taurine post chronic arsenic exposure in rats. Arsenic exposed male rats (25 ppm, sodium arsenite in drinking water for 24 weeks) were treated with taurine (100 mg/kg, i.p., once daily), monoisoamyl dimercaptosuccinic acid (MiADMSA) (50 mg/kg, oral, once daily) either individually or in combination for 5 consecutive days. Biochemical variables indicative of oxidative stress along-with arsenic concentration in blood, liver and kidney were measured. Arsenic exposure significantly reduced blood delta-aminolevulinic acid dehydratase (ALAD) activity, a key enzyme involved in the heme biosynthesis and enhanced zinc protoporphyrin (ZPP) level. Clinical hematological variables like white blood cells (WBC), mean cell hemoglobin (MCH), and mean cell hemoglobin concentration (MCHC) showed significant decrease with a significant elevation in platelet (PLT) count. These changes were accompanied by significant decrease in superoxide dismutase (SOD) activity and increased catalase activity. Arsenic exposure caused a significant decrease in hepatic and renal glutathione (GSH) level and an increase in oxidized glutathione (GSSG). These biochemical changes were correlated with an increased uptake of arsenic in blood, liver and kidney. Administration of taurine significantly reduced hepatic oxidative stress however co

  13. Combined Administration of Taurine and Monoisoamyl Dmsa Protects Arsenic Induced Oxidative Injury in Rats

    Directory of Open Access Journals (Sweden)

    Swaran J. S. Flora

    2008-01-01

    Full Text Available Arsenic is a naturally occurring element that is ubiquitously present in the environment. High concentration of naturally occurring arsenic in drinking water is a major health problem in different parts of the world. Despite arsenic being a health hazard and a well documented carcinogen, no safe, effective and specific preventive or therapeutic measures are available. Among various recent strategies adopted, administration of an antioxidant has been reported to be the most effective. The present study was designed to evaluate the therapeutic efficacy of monoisoamyl dimercaptosuccinic acid (MiADMSA, administered either individually or in combination with taurine post chronic arsenic exposure in rats. Arsenic exposed male rats (25 ppm, sodium arsenite in drinking water for 24 weeks were treated with taurine (100 mg/kg, i.p., once daily, monoisoamyl dimercaptosuccinic acid (MiADMSA (50 mg/kg, oral, once daily either individually or in combination for 5 consecutive days. Biochemical variables indicative of oxidative stress along-with arsenic concentration in blood, liver and kidney were measured. Arsenic exposure significantly reduced blood δ-aminolevulinic acid dehydratase (ALAD activity, a key enzyme involved in the heme biosynthesis and enhanced zinc protoporphyrin (ZPP level. Clinical hematological variables like white blood cells (WBC, mean cell hemoglobin (MCH, and mean cell hemoglobin concentration (MCHC showed significant decrease with a significant elevation in platelet (PLT count. These changes were accompanied by significant decrease in superoxide dismutase (SOD activity and increased catalase activity. Arsenic exposure caused a significant decrease in hepatic and renal glutathione (GSH level and an increase in oxidized glutathione (GSSG. These biochemical changes were correlated with an increased uptake of arsenic in blood, liver and kidney. Administration of taurine significantly reduced hepatic oxidative stress however co

  14. Platinum-induced structural collapse in layered oxide polycrystalline films

    Energy Technology Data Exchange (ETDEWEB)

    Wang, Jianlin; Liu, Changhui [CAS Key Laboratory of Materials for Energy Conversion, Department of Materials Science and Engineering, University of Science and Technology of China, Hefei 230026 (China); Huang, Haoliang [CAS Key Laboratory of Materials for Energy Conversion, Department of Materials Science and Engineering, University of Science and Technology of China, Hefei 230026 (China); Synergetic Innovation Center of Quantum Information and Quantum Physics, University of Science and Technology of China, Hefei 230026 (China); Fu, Zhengping; Peng, Ranran, E-mail: pengrr@ustc.edu.cn, E-mail: yllu@ustc.edu.cn [CAS Key Laboratory of Materials for Energy Conversion, Department of Materials Science and Engineering, University of Science and Technology of China, Hefei 230026 (China); Synergetic Innovation Center of Quantum Information and Quantum Physics, University of Science and Technology of China, Hefei 230026 (China); Hefei National Laboratory for Physical Sciences at the Microscale, University of Science and Technology of China, Hefei 230026 (China); Zhai, Xiaofang [Synergetic Innovation Center of Quantum Information and Quantum Physics, University of Science and Technology of China, Hefei 230026 (China); Hefei National Laboratory for Physical Sciences at the Microscale, University of Science and Technology of China, Hefei 230026 (China); Lu, Yalin, E-mail: pengrr@ustc.edu.cn, E-mail: yllu@ustc.edu.cn [CAS Key Laboratory of Materials for Energy Conversion, Department of Materials Science and Engineering, University of Science and Technology of China, Hefei 230026 (China); Synergetic Innovation Center of Quantum Information and Quantum Physics, University of Science and Technology of China, Hefei 230026 (China); Hefei National Laboratory for Physical Sciences at the Microscale, University of Science and Technology of China, Hefei 230026 (China); Laser and Optics Research Center, Department of Physics, United States Air Force Academy, Colorado 80840 (United States)

    2015-03-30

    Effect of a platinum bottom electrode on the SrBi{sub 5}Fe{sub 1−x}Co{sub x}Ti{sub 4}O{sub 18} layered oxide polycrystalline films was systematically studied. The doped cobalt ions react with the platinum to form a secondary phase of PtCoO{sub 2}, which has a typical Delafossite structure with a weak antiferromagnetism and an exceptionally high in-plane electrical conductivity. Formation of PtCoO{sub 2} at the interface partially consumes the cobalt dopant and leads to the structural collapsing from 5 to 4 layers, which was confirmed by X-ray diffraction and high resolution transmission electron microscopy measurements. Considering the weak magnetic contribution from PtCoO{sub 2}, the observed ferromagnetism should be intrinsic of the Aurivillius compounds. Ferroelectric properties were also indicated by the piezoresponse force microscopy. In this work, the platinum induced secondary phase at the interface was observed, which has a strong impact on Aurivillius structural configuration and thus the ferromagnetic and ferroelectric properties.

  15. Resveratrol protects mouse oocytes from methylglyoxal-induced oxidative damage.

    Science.gov (United States)

    Liu, Yu; He, Xiao-Qin; Huang, Xin; Ding, Lu; Xu, Lin; Shen, Yu-Ting; Zhang, Fei; Zhu, Mao-Bi; Xu, Bai-Hui; Qi, Zhong-Quan; Wang, Hai-Long

    2013-01-01

    Methylglyoxal, a reactive dicarbonyl compound, is mainly formed from glycolysis. Methylglyoxal can lead to the dysfunction of mitochondria, the depletion of cellular anti-oxidation enzymes and the formation of advanced glycation ends. Previous studies showed that the accumulation of methylglyoxal and advanced glycation ends can impair the oocyte maturation and reduce the oocyte quality in aged and diabetic females. In this study, we showed that resveratrol, a kind of phytoalexin found in the skin of grapes, red wine and other botanical extracts, can alleviate the adverse effects caused by methylglyoxal, such as inhibition of oocyte maturation and disruption of spindle assembly. Besides, methylglyoxal-treated oocytes displayed more DNA double strands breaks and this can also be decreased by treatment of resveratrol. Further investigation of these processes revealed that methylglyoxal may affect the oocyte quality by resulting in excessive reactive oxygen species production, aberrant mitochondrial distribution and high level lipid peroxidation, and resveratrol can block these cytotoxic changes. Collectively, our results showed that resveratrol can protect the oocytes from methylglyoxal-induced cytotoxicity and this was mainly through the correction of the abnormity of cellular reactive oxygen species metabolism.

  16. Inducible nitric oxide synthase is expressed in synovial fluid granulocytes.

    Science.gov (United States)

    Cedergren, J; Forslund, T; Sundqvist, T; Skogh, T

    2002-10-01

    The objective of the study was to evaluate the NO-producing potential of synovial fluid (SF) cells. SF from 15 patients with arthritis was compared with blood from the same individuals and with blood from 10 healthy controls. Cellular expression of inducible nitric oxide synthase (iNOS) was analysed by flow cytometry. High-performance liquid chromatography was used to measure l-arginine and l-citrulline. Nitrite and nitrate were measured colourimetrically utilizing the Griess' reaction. Compared to whole blood granulocytes in patients with chronic arthritis, a prominent iNOS expression was observed in SF granulocytes (P < 0.001). A slight, but statistically significant, increase in iNOS expression was also recorded in lymphocytes and monocytes from SF. l-arginine was elevated in SF compared to serum (257 +/- 78 versus 176 +/- 65 micro mol/l, P = 0.008), whereas a slight increase in l-citrulline (33 +/- 11 versus 26 +/- 9 micro mol/l), did not reach statistical significance. Great variations but no significant differences were observed comparing serum and SF levels of nitrite and nitrate, respectively, although the sum of nitrite and nitrate tended to be elevated in SF (19.2 +/- 20.7 versus 8.6 +/- 6.5 micro mol/l, P = 0.054). Synovial fluid leucocytes, in particular granulocytes, express iNOS and may thus contribute to intra-articular NO production in arthritis.

  17. Responsiveness of entomopathogenic fungi to menadione-induced oxidative stress.

    Science.gov (United States)

    Azevedo, Rosana F F; Souza, Roberta K F; Braga, Gilberto U L; Rangel, Drauzio E N

    2014-12-01

    Entomopathogenic fungi are predisposed to ROS induced by heat and UV-A radiation when outside the insect host. When inside the host, they are subject to phagocytic cells that generate ROS to eliminate invading pathogens. The oxidative stress tolerance of the entomopathogenic fungi Aschersonia aleyrodis (ARSEF 430 and 10276), Aschersonia placenta (ARSEF 7637), Beauveria bassiana (ARSEF 252), Isaria fumosorosea (ARSEF 3889), Lecanicillium aphanocladii (ARSEF 6433), Metarhizium acridum (ARSEF 324), Metarhizium anisopliae (ARSEF 5749), Metarhizium brunneum (ARSEF 1187 and ARSEF 5626), Metarhizium robertsii (ARSEF 2575), Tolypocladium cylindrosporum (ARSEF 3392), Tolypocladium inflatum (ARSEF 4877), and Simplicillium lanosoniveum (ARSEF 6430 and ARSEF 6651) was studied based on conidial germination on a medium supplemented with menadione. Conidial germination was evaluated 24 h after inoculation on potato dextrose agar (PDA) (control) or PDA supplemented with menadione. The two Aschersonia species (ARSEF 430, 7637, and 10276) were the most susceptible fungi, followed by the two Tolypocladium species (ARSEF 3392 and 4877) and the M. acridum (ARSEF 324). Metarhizium brunneum (ARSEF 5626) and M. anisopliae (ARSEF 5749) were the most tolerant isolates with MIC 0.28 mM. All fungal isolates, except ARSEF 5626 and ARSEF 5749, were not able to germinate at 0.20 mM.

  18. A Comparative Study on Rat Intestinal Epithelial Cells and Resident Gut Bacteria (ii) Effect of Arsenite

    Institute of Scientific and Technical Information of China (English)

    2006-01-01

    In order to use facultative gut bacteria as an alternate to animals for the initial gastrointestinal toxicity screening of heavy metals, a comparative study on rat intestinal epithelial cells and resident gut bacteria was undertaken.Methods in vitro growth rate of four gut bacteria, dehydrogenase (DHA) and esterase (EA) activity test, intestinal epithelial and bacterial cell membrane enzymes and in situ effect of arsenite were analysed. Results Growth profile of mixed resident population of gut bacteria and pure isolates of Escherichia coli, Pseudomonas sp., Lactobacillus sp., and Staphylococcus sp.revealed an arsenite (2-20 ppm) concentration-dependent inhibition. The viability pattern of epithelial cells also showed similar changes. DHA and EA tests revealed significant inhibition (40%-72%) with arsenite exposure of 5 and 10 ppm in isolated gut bacteria and epithelial cells. Decrease in membrane alkaline phosphatase and Ca2+-Mg2+-ATPase activities was in the range of 33%-55% in four bacteria at the arsenite exposure of 10 ppm, whereas it was 60%-65% in intestinal epithelial villus cells. in situ incubation of arsenite using intestinal loops also showed more or less similar changes in membrane enzymes of resident gut bacterial population and epithelial cells. Conclusion The results indicate that facultative gut bacteria can be used as suitable in vitro model for the preliminary screening of arsenical gastrointestinal cytotoxic effects.

  19. Improved Photo-Induced Stability in Amorphous Metal-Oxide Based TFTs for Transparent Displays.

    Science.gov (United States)

    Koo, Sang-Mo; Ha, Tae-Jun

    2015-10-01

    In this paper, we investigate the origin of photo-induced instability in amorphous metal-oxide based thin-film transistors (oxide-TFTs) by exploring threshold voltage (Vth) shift in transfer characteristics. The combination of photo irradiation and prolonged gate bias stress enhanced the shift in Vth in amorphous hafnium-indium-zinc-oxide (a-HfIZO) TFTs. Such results stem from the extended trapped charges at the localized defect states related to oxygen vacancy which play a role in a screening effect on the electric field induced by gate voltage. We also demonstrate the chemically clean interface in oxide-TFTs by employing oxygen annealing which reduces the density of trap states, thereby resulting in improved photo-induced stability. We believe that this work stimulates the research society of transparent electronics by providing a promising approach to suppress photo-induced instability in metal-oxide TFTs.

  20. Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway.

    Science.gov (United States)

    Zhu, Yao; Zhang, Ya-Jie; Liu, Wei-Wei; Shi, Ai-Wu; Gu, Ning

    2016-08-09

    Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Salidroside (SAL), one of the main effective constituents of Rhodiola rosea, has been reported to suppress oxidative stress-induced cardiomyocyte injury and necrosis by promoting transcription of nuclear factor E2-related factor 2 (Nrf2)-regulated genes such as heme oxygenase-1 (HO-1) and NAD(P)H dehydrogenase (quinone1) (NQO1). However, it has not been indicated whether SAL might ameliorate endothelial injury induced by oxidative stress. Here, our study demonstrated that SAL might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway. The results of our study indicated that SAL decreased the levels of intercellular reactive oxygen species (ROS) and malondialdehyde (MDA), and improved the activities of superoxide dismutase (SOD) and catalase (CAT), resulting in protective effects against oxidative stress-induced cell damage in HUVECs. It suppressed oxidative stress damage by inducing Nrf2 nuclear translocation and activating the expression of Nrf2-regulated antioxidant enzyme genes such as HO-1 and NQO1 in HUVECs. Knockdown of Nrf2 with siRNA abolished the cytoprotective effects against oxidative stress, decreased the expression of Nrf2, HO-1, and NQO1, and inhibited the nucleus translocation of Nrf2 in HUVECs. This study is the first to demonstrate that SAL suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.

  1. Salidroside Suppresses HUVECs Cell Injury Induced by Oxidative Stress through Activating the Nrf2 Signaling Pathway

    Directory of Open Access Journals (Sweden)

    Yao Zhu

    2016-08-01

    Full Text Available Oxidative stress plays an important role in the pathogenesis of cardiovascular diseases. Salidroside (SAL, one of the main effective constituents of Rhodiola rosea, has been reported to suppress oxidative stress-induced cardiomyocyte injury and necrosis by promoting transcription of nuclear factor E2-related factor 2 (Nrf2-regulated genes such as heme oxygenase-1 (HO-1 and NAD(PH dehydrogenase (quinone1 (NQO1. However, it has not been indicated whether SAL might ameliorate endothelial injury induced by oxidative stress. Here, our study demonstrated that SAL might suppress HUVEC cell injury induced by oxidative stress through activating the Nrf2 signaling pathway. The results of our study indicated that SAL decreased the levels of intercellular reactive oxygen species (ROS and malondialdehyde (MDA, and improved the activities of superoxide dismutase (SOD and catalase (CAT, resulting in protective effects against oxidative stress-induced cell damage in HUVECs. It suppressed oxidative stress damage by inducing Nrf2 nuclear translocation and activating the expression of Nrf2-regulated antioxidant enzyme genes such as HO-1 and NQO1 in HUVECs. Knockdown of Nrf2 with siRNA abolished the cytoprotective effects against oxidative stress, decreased the expression of Nrf2, HO-1, and NQO1, and inhibited the nucleus translocation of Nrf2 in HUVECs. This study is the first to demonstrate that SAL suppresses HUVECs cell injury induced by oxidative stress through activating the Nrf2 signaling pathway.

  2. Anti-oxidative effects of curcumin on immobilization-induced oxidative stress in rat brain, liver and kidney.

    Science.gov (United States)

    Samarghandian, Saeed; Azimi-Nezhad, Mohsen; Farkhondeh, Tahereh; Samini, Fariborz

    2017-03-01

    Restraint stress has been indicated to induce oxidative damage in tissues. Several investigations have reported that curcumin (CUR) may have a protective effect against oxidative stress. The present study was designed to investigate the protective effects of CUR on restraint stress induced oxidative stress damage in the brain, liver and kidneys. For chronic restraint stress, rats were kept in the restrainers for 1h every day, for 21 consecutive days. The animals received systemic administrations of CUR daily for 21days. In order to evaluate the changes of the oxidative stress parameters following restraint stress, the levels of malondialdehyde (MDA), reduced glutathione (GSH), as well as antioxidant enzyme activities superoxide dismutase (SOD) glutathione peroxidase (GPx), glutathione reductase (GR) and catalase (CAT) were measured in the brain, liver and kidney of rats after the end of restraint stress. The restraint stress significantly increased MDA level, but decreased the level of GSH and activists of SOD, GPx, GR, and CAT the brain, liver and kidney of rats in comparison to the normal rats (Poxidative stress and lipid peroxidation, prevented apoptosis, and increased antioxidant defense mechanism activity in the tissues versus the control group (Pstress-induced oxidative damage in the brain, liver and kidney of rats and propose that CUR may be useful agents against oxidative stress in the tissues.

  3. Effects of resveratrol on hydrogen peroxide-induced oxidative stress in embryonic neural stem cells

    Institute of Scientific and Technical Information of China (English)

    Sibel Konyalioglu; Guliz Armagan; Ayfer Yalcin; Cigdem Atalayin; Taner Dagci

    2013-01-01

    Resveratrol, a natural phenolic compound, has been shown to prevent cardiovascular diseases and cancer and exhibit neuroprotective effects. In this study, we examined the neuroprotective and antioxidant effects of resveratrol against hydrogen peroxide in embryonic neural stem cells. Hydrogen peroxide treatment alone increased catalase and glutathione peroxidase activities but did not change superoxide dismutase levels compared with hydrogen peroxide + resveratrol treatment. Nitric oxide synthase activity and concomitant nitric oxide levels increased in response to hydrogen peroxide treatment. Conversely, resveratrol treatment decreased nitric oxide synthase activity and nitric oxide levels. Resveratrol also attenuated hydrogen peroxide-induced nuclear or mitochondrial DNA damage. We propose that resveratrol may be a promising agent for protecting embryonic neural stem cells because of its potential to decrease oxidative stress by inducing higher activity of antioxidant enzymes, decreasing nitric oxide production and nitric oxide synthase activity, and alleviating both nuclear and mitochondrial DNA damage.

  4. Inducible nitric oxide synthase and guinea-pig ileitis induced by adjuvant

    Directory of Open Access Journals (Sweden)

    N. D. Seago

    1995-01-01

    Full Text Available We sought to establish a model of inflammatory bowel disease by augmenting the activity of the local immune system with Freund's complete adjuvant, and to determine if inducible nitric oxide synthase (iNOS expression and peroxynitrite formation accompanied the inflammatory condition. In anaesthetized guinea-pigs, a loop of distal ileum received intraluminal 50% ethanol followed by Freund's complete adjuvant. Control animals were sham operated. When the animals were killed 7 or 14 days later, loop lavage fluid was examined for nitrite and PGE2 levels; mucosal levels of granulocyte and macrophages were estimated by myeloperoxidase (MPO and N-acetyl-D-glucosaminidase (NAG activity, respectively. Cellular localization if iNOS and peroxynitrite formation were determined by immunohistochemistry with polyclonal antibodies directed against peptide epitopes of mouse iNOS and nitrotyrosine, respectfully. Adjuvant administration resulted in a persistent ileitis, featuring gut thickening, crypt hyperplasia, villus tip swelling and disruption, and cellular infiltration. Lavage levels of PGE2 and nitrite were markedly elevated by adjuvant treatment. Immunoreactive iNOS and nitrotyrosine bordered on detectability in normal animals but were markedly evident with adjuvant treatment at day 7 and particularly day 14. Immunohistochemistry suggested that enteric neurons and epithelia were major sites of iNOS activity and peroxynitrite formation. We conclude that local administration of adjuvant establishes a chronic ileitis. Inducible nitric oxide synthase may contribute to the inflammatory process.

  5. Oxidative DNA damage is a preliminary step during rat tongue carcinogenesis induced by 4-nitroquinoline 1-oxide.

    Science.gov (United States)

    Miranda, Sandra Regina; Noguti, Juliana; Carvalho, Juliana Gonçalves; Oshima, Celina Tijuko Fujiyama; Ribeiro, Daniel Araki

    2011-04-01

    The aim of this study was to investigate oxidative DNA damage during 4-nitroquinoline 1-oxide (4NQO)-induced rat tongue carcinogenesis. For this purpose, male Wistar rats were distributed into three groups of 10 animals each and treated with 50 ppm 4NQO solution through their drinking water for 4, 12, and 20 weeks. Ten animals were used as negative control. The alkaline Comet assay modified with lesion-specific enzymes was used to detect single and double strand breaks, labile sites (SBs), and oxidised purines and pyrimidines. Although no histopathological abnormalities were induced in the epithelium after 4 weeks of carcinogen exposure, oxidative DNA damage was detected in the 'normal' oral epithelium. In pre-neoplastic lesions and squamous cell carcinomas induced after 12 and 20 weeks following carcinogen exposure, respectively, oxidative DNA damage was also increased (P < 0.05) when compared to negative control. In conclusion, our results suggest that oxidative DNA damage is an early event during multistep carcinogenesis assay induced by 4NQO. This kind of approach should be considered to persons with high risk of oral cancer, such as in smokers or alcohol consumers.

  6. Involvement of inositol biosynthesis and nitric oxide in the mediation of UV-B induced oxidative stress

    Directory of Open Access Journals (Sweden)

    Dmytro I Lytvyn

    2016-04-01

    Full Text Available The involvement of NO-signaling in ultraviolet B (UV-B induced oxidative stress in plants is an open question. Inositol biosynthesis contributes to numerous cellular functions, including the regulation of plants tolerance to stress. This work reveals the involvement of inositol-3-phosphate synthase 1 (IPS1, a key enzyme for biosynthesis of myo-inositol and its derivatives, in the response to NO-dependent oxidative stress in Arabidopsis. Homozygous mutants deficient for IPS1 (atips1 and wild-type plants were transformed with a reduction-oxidation-sensitive green fluorescent protein 2 (grx1-rogfp2 and used for the dynamic measurement of UV-B-induced and SNP (sodium nitroprusside-mediated oxidative stresses by confocal microscopy. atips1 mutants displayed greater tissue-specific resistance to the action of UV-B than the wild type. SNP can act both as an oxidant or repairer depending on the applied concentration, but mutant plants were more tolerant than the wild type to nitrosative effects of high concentration of SNP. Additionally, pretreatment with low concentrations of SNP (10, 100 μM before UV-B irradiation resulted in a tissue-specific protective effect that was enhanced in atips1. We conclude that the interplay between nitric oxide and inositol signaling can be involved in the mediation of UV-B-initiated oxidative stress in the plant cell.

  7. Anti-oxidative effects of Phellinus linteus and red ginseng extracts on oxidative stress-induced DNA damage.

    Science.gov (United States)

    Park, Byung-Jae; Lim, Yeong-Seok; Lee, Hee-Jung; Eum, Won Sik; Park, Jinseu; Han, Kyu Hyung; Choi, Soo Young; Lee, Kil Soo

    2009-08-31

    Anti-oxidative effect of Phellinus linteus (P. linteus) and red ginseng extracts on DNA damage induced by reactive oxygen species (ROS) were investigated in this study. P. linteus (PLE) and red ginseng extracts (RGE) inhibited the breaking of E. coli ColE1 plasmid DNA strands as well as nuclear DNA of rat hepatocytes damaged by oxidative stress. In addition, a reaction mixture of PLE and RGE showed synergistic inhibitory effect against DNA damage. These results suggest that PLE and RGE have a cellular defensive effect against DNA damage induced by ROS.

  8. Arsenite as an electron donor for anoxygenic photosynthesis: Description of three strains of Ectothiorhodospria from Mono Lake, California, and Big Soda Lake, Nevada

    Science.gov (United States)

    McCann, Shelley; Boren, Alison; Hernandez-Maldonado, Jaime; Stoneburner, Brendon; Saltikov, Chad W; Stolz, John F.; Oremland, Ronald S.

    2017-01-01

    Three novel strains of photosynthetic bacteria from the family Ectothiorhodospiraceae were isolated from soda lakes of the Great Basin Desert, USA by employing arsenite (As(III)) as the sole electron donor in the enrichment/isolation process. Strain PHS-1 was previously isolated from a hot spring in Mono Lake, while strain MLW-1 was obtained from Mono Lake sediment, and strain BSL-9 was isolated from Big Soda Lake. Strains PHS-1, MLW-1, and BSL-9 were all capable of As(III)-dependent growth via anoxygenic photosynthesis and contained homologs of arxA, but displayed different phenotypes. Comparisons were made with three related species: Ectothiorhodospira shaposhnikovii DSM 2111, Ectothiorhodospira shaposhnikovii DSM 243T, and Halorhodospira halophila DSM 244. All three type cultures oxidized arsenite to arsenate but did not grow with As(III) as the sole electron donor. DNA–DNA hybridization indicated that strain PHS-1 belongs to the same species as Ect. shaposhnikovii DSM 2111 (81.1% sequence similarity), distinct from Ect. shaposhnikovii DSM 243T (58.1% sequence similarity). These results suggest that the capacity for light-driven As(III) oxidation is a common phenomenon among purple photosynthetic bacteria in soda lakes. However, the use of As(III) as a sole electron donor to sustain growth via anoxygenic photosynthesis is confined to novel isolates that were screened for by this selective cultivation criterion.

  9. Beneficial Effects of Nitric Oxide Induced Mild Oxidative Stress on Post-Thawed Bull Semen Quality

    Directory of Open Access Journals (Sweden)

    Mohsen Sharafi

    2015-07-01

    Full Text Available Background: Cryopreservation of semen requires optimized conditions to minimize the harmful effects of various stresses. The main approach for protection of sperm against stress is based on the use of antioxidants and cryoprotectants, which are described as defensive methods. Recently, the application of controlled mild stressors has been described for activation of a temporary response in oocyte, embryo and somatic cells. In this study a sub-lethal oxidative stress induced by precise concentrations of nitric oxide (NO has been evaluated for sperm during cryopreservation. Materials and Methods: In this experimental study, we used different concentrations of NO [0 μM (NO-0, 0.01 μM (NO-0.01, 0.1 μM (NO-0.1, 1 μM (NO-1, 10 μM (NO-10 and 100 μM (NO-100] during cryopreservation of bull semen. Their effects on post-thawed sperm quality that included motility and velocity parameters, plasma membrane functionality, acrosome integrity, apoptosis status, mitochondrial activity and lipid peroxidation after freezing-thawing were investigated. Results: Exposure of sperm before freezing to NO-1 significantly increased total motility (88.4 ± 2.8%, progressive motility (50.4 ± 3.2% and average path velocity (VAP, 53.8 ± 3.1 μm/s compared to other extenders. In addition, NO-1 significantly increased plasma membrane functionality (89.3 ± 2.9% compared to NO-0 (75.3 ± 2.9%, NO-0.01 (78.3 ± 2.9%, NO-0.1 (76.4 ± 2.9%, NO-10 (64 ± 2.9% and NO-100 (42 ± 2.9%. Sperm exposed to NO-1 produced the highest percentage of viable (85.6 ± 2.3% and the lowest percentage of apoptotic (10.8 ± 2.4% spermatozoa compared to the other extenders. Also, NO-100 resulted in a higher percentage of dead spermatozoa (27.1 ± 2.7% compared to the other extenders. In terms of mitochondrial activity, there was no significant difference among NO-0 (53.4 ± 3.2, NO-0.01 (52.1 ± 3.2, NO-0.1 (50.8 ± 3.2 and NO-1 (53.1 ± 3.2. For acrosome integrity, no significant different

  10. Oxidative stress induces itch via activation of transient receptor potential subtype ankyrin 1 in mice

    Institute of Scientific and Technical Information of China (English)

    Tong Liu; Ru-Rong Ji

    2012-01-01

    Objective To investigate the role of oxidative stress in itch-indicative scratching behavior in mice,and furthermore,to define the cellular and molecular mechanisms underlying oxidative stress-mediated itch.Methods Scratching behavior was induced by intradermal injection of the oxidants hydrogen peroxide (H2O2) or tert-butylhydroperoxide (tBHP) into the nape of the neck in mice.The mice were observed for 30 min.Results Intradermal H2O2 (0.03%-1%) or tBHP (1-30 μmol) elicited robust scratching behavior,displaying an inverted U-shaped dose-response curve.Naloxone,an opioid receptor antagonist,but not morphine,largely suppressed the oxidant-induced scratching.Chlorpheniramine,a histamine H 1 receptor antagonist,blocked histamine-but not oxidant-induced scratching,indicating the involvement of a histamine-independent mechanism in oxidant-evoked itch.Further,resiniferatoxin treatment abolished oxidant-induced scratching,suggesting an essential role of C-fibers.Notably,blockade of transient receptor potential subtype ankyrin 1 (TRPA1) with the selective TRPA1 antagonist HC-030031,or genetic deletion of Trpal but not Trpvl (subfamily V,member 1) resulted in a profound reduction in H2O2-evoked scratching.Finally,systemic administration of the antioxidant Nacety1-L-cysteine or trolox (a water-soluble vitamin E analog) attenuated scratching induced by the oxidants.Conclusion Oxidative stress by different oxidants induces profound scratching behavior,which is largely histamine-and TRPV1-independent but TRPA1-dependent.Antioxidants and TRPA1 antagonists may be used to treat human itch conditions associated with oxidative stress.

  11. Melatonin inhibits snake venom and antivenom induced oxidative stress and augments treatment efficacy.

    Science.gov (United States)

    Sharma, Rachana D; Katkar, Gajanan D; Sundaram, Mahalingam S; Swethakumar, Basavarajaiah; Girish, Kesturu S; Kemparaju, Kempaiah

    2017-05-01

    Snakebite is a neglected health hazard. Its patho-physiology has largely been focused on systemic and local toxicities; whereas, venom and antivenom induced oxidative stress has long been ignored. Antivenom therapy although neutralizes venom lethality and saves many lives, remains ineffective against oxidative stress. This prompted us to complement antivenom with an antioxidant molecule melatonin that would protect against oxidative stress and increase the efficacy of the existing snakebite therapy. Here we show that D. russelli and E. carinatus venoms induce strong oxidative stress that persists even after antivenom administration in mice model. Additionally, antivenoms also induce oxidative stress. Polyvalent antivenom induce more oxidative stress than monovalent antivenom. Strikingly, antivenom and melatonin together not only inhibit venom and antivenom induced oxidative stress but also significantly reduce the neutralizing antivenom dose. This study provides a therapeutic potential for enhancing the existing snakebite therapy. The combined treatment of antivenom+melatonin would prevent the upsurge of oxidative stress as well as minimize the antivenom load. Thus the investigation offers immense scope for physicians and toxinologists to reinvestigate, design new strategies and think beyond the conventional mode of antivenom therapy.

  12. Correlation between oxidative stress and alteration of intracellular calcium handling in isoproterenol-induced myocardial infarction.

    Science.gov (United States)

    Díaz-Muñoz, Mauricio; Alvarez-Pérez, Marco Antonio; Yáñez, Lucía; Vidrio, Susana; Martínez, Lidia; Rosas, Gisele; Yáñez, Mario; Ramírez, Sotero; de Sánchez, Victoria Chagoya

    2006-09-01

    Myocardial Ca(2+) overload and oxidative stress are well documented effects associated to isoproterenol (ISO)-induced myocardial necrosis, but information correlating these two issues is scarce. Using an ISO-induced myocardial infarction model, 3 stages of myocardial damage were defined: pre-infarction (0-12 h), infarction (12-24 h) and post-infarction (24-96 h). Alterations in Ca(2+) homeostasis and oxidative stress were studied in mitochondria, sarcoplasmic reticulum and plasmalemma by measuring the Ca(2+) content, the activity of Ca(2+) handling proteins, and by quantifying TBARs, nitric oxide (NO) and oxidative protein damage (changes in carbonyl and thiol groups). Free radicals generated system, antioxidant enzymes and oxidative stress (GSH/GSSG ratio) were also monitored at different times of ISO-induced cardiotoxicity. The Ca(2+) overload induced by ISO was counterbalanced by a diminution in the ryanodine receptor activity and the Na(+)-Ca(+2) exchanger as well as by the increase in both calcium ATPases activities (vanadate- and thapsigargine-sensitive) and mitochondrial Ca(2+) uptake during pre-infarction and infarction stages. Pro-oxidative reactions and antioxidant defences during the 3 stages of cardiotoxicity were observed, with maximal oxidative stress during the infarction. Significant correlations were found among pro-oxidative reactions with plasmalemma and sarcoplasmic reticulum Ca(2+) ATPases, and ryanodine receptor activities at the onset and development of ISO-induced infarction. These findings could be helpful in the design of antioxidant therapies in this pathology.

  13. Laser induced densification of cerium gadolinium oxide: Application to single-chamber solid oxide fuel cells

    Energy Technology Data Exchange (ETDEWEB)

    Mariño, Mariana [École Nationale Supérieure des Mines, SPIN-EMSE, CNRS: UMR 5307, LGF, F-42023 Saint-Étienne (France); Rieu, Mathilde, E-mail: rieu@emse.fr [École Nationale Supérieure des Mines, SPIN-EMSE, CNRS: UMR 5307, LGF, F-42023 Saint-Étienne (France); Viricelle, Jean-Paul [École Nationale Supérieure des Mines, SPIN-EMSE, CNRS: UMR 5307, LGF, F-42023 Saint-Étienne (France); Garrelie, Florence [Université Jean Monnet, Laboratoire Hubert Curien, CNRS: UMR 5516, 42000 Saint-Etienne (France)

    2016-06-30

    Graphical abstract: - Highlights: • CGO surface densifications were induced by UV and IR laser irradiations. • Grain growth or densified cracked surfaces were observed by SEM. • UV laser treatments allow a decrease of gas permeation through electrolyte layer. • Electrical conductivity of the electrolyte was modified by laser treatments. • Grain growth of electrolyte induced by UV laser improved cell performances. - Abstract: In single-chamber solid oxide fuel cells (SC-SOFC), anode and cathode are placed in a gas chamber where they are exposed to a fuel/air mixture. Similarly to conventional dual-chamber SOFC, the anode and the cathode are separated by an electrolyte. However, as in the SC-SOFC configuration the electrolyte does not play tightness role between compartments, this one can be a porous layer. Nevertheless, it is necessary to have a diffusion barrier to prevent the transportation of hydrogen produced locally at the anode to the cathode that reduces fuel cell performances. This study aims to obtain directly a diffusion barrier through the surface densification of the electrolyte Ce{sub 0.9}Gd{sub 0.1}O{sub 1.95} (CGO) by a laser treatment. KrF excimer laser and Yb fiber laser irradiations were used at different fluences and number of pulses to modify the density of the electrolyte coating. Microstructural characterizations confirmed the modifications on the surface of the electrolyte for appropriate experimental conditions showing either grain growth or densified but cracked surfaces. Gas permeation and electrical conductivities of the modified electrolyte were evaluated. Finally SC-SOFC performances were improved for the cells presenting grain growth at the electrolyte surface.

  14. Graphene produced by radiation-induced reduction of graphene oxide

    OpenAIRE

    Kumar, Prashant; K. S. Subrahmanyam; Rao, C. N. R.

    2010-01-01

    Effect of irradiation on graphene oxide by sunlight, UV light and KrF excimer laser has been investigated in detail. Both sunlight and ultraviolet light reduce graphene oxide well after prolonged irradiation, but laser irradiation produces graphene with negligible oxygen functionalities within a short time. Laser irradiation is also useful for one-step synthesis of metal particle decorated graphene. Laser irradiation of graphene oxide appears to be an efficient procedure for large-scale synth...

  15. Graphene produced by radiation-induced reduction of graphene oxide

    OpenAIRE

    Kumar, Prashant; Subrahmanyam, K. S.; Rao, C. N. R.

    2010-01-01

    Effect of irradiation on graphene oxide by sunlight, UV light and KrF excimer laser has been investigated in detail. Both sunlight and ultraviolet light reduce graphene oxide well after prolonged irradiation, but laser irradiation produces graphene with negligible oxygen functionalities within a short time. Laser irradiation is also useful for one-step synthesis of metal particle decorated graphene. Laser irradiation of graphene oxide appears to be an efficient procedure for large-scale synth...

  16. In vitro effect of sodium arsenite on Echinococcus granulosus protoscoleces.

    Science.gov (United States)

    Xing, Guoqiang; Wang, Bo; Lei, Ying; Liu, Chunli; Wang, Zhuo; Shi, Hongjuan; Yang, Rentan; Qin, Wenjuan; Jiang, Yufeng; Lv, Hailong

    2016-06-01

    Cystic echinococcosis (CE) caused by the metacestodes of Echinococcus granulosus is an important cosmopolitan zoonosis. Surgery is the main treatment option for CE. Meanwhile, chemotherapy is used as an significant adjunct to surgery. However, the benzimidazole carbamate group and the existing scolicidal agents may not be as effective as hoped. In this study, we aimed to explore the in vitro effect of sodium arsenite (NaAsO2) on Echinococcus granulosus protoscoleces, the causative agents of CE. Protoscoleces of E. granulosus were incubated in vitro with 4, 8, 12, 16, and 20μM NaAsO2. Viability and changes in morphology were investigated by 0.1% eosin staining. The ultrastructural alterations were observed by scanning electron microscopy (SEM) and transmission electron microscopy (TEM). Additionally, caspase-3 activity was measured by colorimetric assay. Obvious protoscolicidal effect was seen with NaAsO2 at concentrations of 16μM and 20μM. Protoscolex mortality was 83.24% (16μM) and 100% (20μM) after 6 days post-incubation. SEM showed that the primary site of drug damage was the tegument of the protoscoleces. TEM analysis demonstrated that the internal tissues were severely affected and revealed an increase in the number of lipid droplets and vacuoles after treatment with 16μM NaAsO2. Meanwhile, the caspase-3 activity significantly increased in protoscoleces after 24h of NaAsO2 incubation compared to the untreated controls. Our study demonstrated the clear in vitro scolicidal effect of NaAsO2 against E. granulosus protoscoleces. However, the in vivo efficacy, specific mechanism, and any possible side effects of NaAsO2 remain to be investigated.

  17. [Effectiveness of arsenite adsorption by ferric and alum water treatment residuals with different grain sizes].

    Science.gov (United States)

    Lin, Lu; Xu, Jia-Rui; Wu, Hao; Wang, Chang-Hui; Pei, Yuan-Sheng

    2013-07-01

    Effectiveness of arsenite adsorption by ferric and alum water treatment residuals (FARs) with different grain sizes was studied. The results indicated that the content of active Fe and Al, the specific surface area and pore volume in FARs with different grain sizes were in the range of 523.72-1 861.72 mmol x kg(-1), 28.15-265.59 m2 x g(-1) and 0.03-0.09 cm3 x g(-1), respectively. The contents of organic matter, fulvic acid, humic acid and humin were in the range of 46.97-91.58 mg x kg(-1), 0.02-32.27 mg x kg(-1), 22.27-34.09 mg x kg(-1) and 10.76-34.22 mg x kg(-1), respectively. Results of SEM and XRD analysis further demonstrated that FARs with different grain sizes were amorphousness. Batch experiments suggested that both the pseudo-first-order and pseudo-second-order equations could well describe the kinetics adsorption processes of arsenite by FARs. Moreover, the contents of arsenite absorbed by FARs increased with the increase of arsenite concentrations. The theoretical saturated adsorption capacities calculated from Langmuir isotherm model were in the range of 6.72-21.79 mg x g(-1). Interestingly, pH showed little effect on the arsenite adsorption capability of FARs. The capability of FARs had a close relationship with their physicochemical properties. Correlation analysis showed that the active Fe and Al contents and pore volume had major effects on the arsenite adsorption capability of FARs.

  18. Dissecting structural and electronic effects in inducible nitric oxide synthase.

    Science.gov (United States)

    Hannibal, Luciana; Page, Richard C; Haque, Mohammad Mahfuzul; Bolisetty, Karthik; Yu, Zhihao; Misra, Saurav; Stuehr, Dennis J

    2015-04-01

    Nitric oxide synthases (NOSs) are haem-thiolate enzymes that catalyse the conversion of L-arginine (L-Arg) into NO and citrulline. Inducible NOS (iNOS) is responsible for delivery of NO in response to stressors during inflammation. The catalytic performance of iNOS is proposed to rely mainly on the haem midpoint potential and the ability of the substrate L-Arg to provide a hydrogen bond for oxygen activation (O-O scission). We present a study of native iNOS compared with iNOS-mesohaem, and investigate the formation of a low-spin ferric haem-aquo or -hydroxo species (P) in iNOS mutant W188H substituted with mesohaem. iNOS-mesohaem and W188H-mesohaem were stable and dimeric, and presented substrate-binding affinities comparable to those of their native counterparts. Single turnover reactions catalysed by iNOSoxy with L-Arg (first reaction step) or N-hydroxy-L-arginine (second reaction step) showed that mesohaem substitution triggered higher rates of Fe(II)O₂ conversion and altered other key kinetic parameters. We elucidated the first crystal structure of a NOS substituted with mesohaem and found essentially identical features compared with the structure of iNOS carrying native haem. This facilitated the dissection of structural and electronic effects. Mesohaem substitution substantially reduced the build-up of species P in W188H iNOS during catalysis, thus increasing its proficiency towards NO synthesis. The marked structural similarities of iNOSoxy containing native haem or mesohaem indicate that the kinetic behaviour observed in mesohaem-substituted iNOS is most heavily influenced by electronic effects rather than structural alterations.

  19. Inducible nitric oxide synthase haplotype associated with migraine and aura.

    Science.gov (United States)

    de O S Mansur, Thiago; Gonçalves, Flavia M; Martins-Oliveira, Alisson; Speciali, Jose G; Dach, Fabiola; Lacchini, Riccardo; Tanus-Santos, Jose E

    2012-05-01

    Migraine is a complex neurological disorder with a clear neurogenic inflammatory component apparently including enhanced nitric oxide (NO) formation. Excessive NO amounts possibly contributing to migraine are derived from increased expression and activity of inducible NO synthase (iNOS). We tested the hypothesis that two functional, clinically relevant iNOS genetic polymorphisms (C(-1026)A-rs2779249 and G2087A-rs2297518) are associated with migraine with or without aura. We studied 142 healthy women without migraine (control group) and 200 women with migraine divided into two groups: 148 with migraine without aura (MWA) and 52 with aura (MA). Genotypes were determined by real-time polymerase chain reaction using the Taqman(®) allele discrimination assays. The PHASE 2.1 software was used to estimate the haplotypes. The A allele for the G2087A polymorphism was more commonly found in the MA group than in the MWA group (28 vs. 18%; P 0.05). The haplotype combining both A alleles for the two polymorphisms was more commonly found in the MA group than in the control group or in the MWA group (19 vs. 10 or 8%; P = 0.0245 or 0.0027, respectively). Our findings indicate that the G2087A and the C(-1026)A polymorphism in the iNOS gene affect the susceptibility to migraine with aura when their effects are combined within haplotypes, whereas the G2087A affects the susceptibility to aura in migraine patients. These finding may have therapeutic implications when examining the effects of selective iNOS inhibitors.

  20. DNA damage and oxidative stress induced by acetylsalicylic acid in Daphnia magna.

    Science.gov (United States)

    Gómez-Oliván, Leobardo Manuel; Galar-Martínez, Marcela; Islas-Flores, Hariz; García-Medina, Sandra; SanJuan-Reyes, Nely

    2014-08-01

    Acetylsalicylic acid is a nonsteroidal anti-inflammatory widely used due to its low cost and high effectiveness. This compound has been found in water bodies worldwide and is toxic to aquatic organisms; nevertheless its capacity to induce oxidative stress in bioindicators like Daphnia magna remains unknown. This study aimed to evaluate toxicity in D. magna induced by acetylsalicylic acid in water, using oxidative stress and DNA damage biomarkers. An acute toxicity test was conducted in order to determine the median lethal concentration (48-h LC50) and the concentrations to be used in the subsequent subacute toxicity test in which the following biomarkers were evaluated: lipid peroxidation, oxidized protein content, activity of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, and level of DNA damage. Lipid peroxidation level and oxidized protein content were significantly increased (pacetylsalicylic acid induces oxidative stress and DNA damage in D. magna.

  1. Caryocar brasiliense camb protects against genomic and oxidative damage in urethane-induced lung carcinogenesis

    Science.gov (United States)

    Colombo, N.B.R.; Rangel, M.P.; Martins, V.; Hage, M.; Gelain, D.P.; Barbeiro, D.F.; Grisolia, C.K.; Parra, E.R.; Capelozzi, V.L.

    2015-01-01

    The antioxidant effects of Caryocar brasiliense Camb, commonly known as the pequi fruit, have not been evaluated to determine their protective effects against oxidative damage in lung carcinogenesis. In the present study, we evaluated the role of pequi fruit against urethane-induced DNA damage and oxidative stress in forty 8-12 week old male BALB/C mice. An in vivo comet assay was performed to assess DNA damage in lung tissues and changes in lipid peroxidation and redox cycle antioxidants were monitored for oxidative stress. Prior supplementation with pequi oil or its extract (15 µL, 60 days) significantly reduced urethane-induced oxidative stress. A protective effect against DNA damage was associated with the modulation of lipid peroxidation and low protein and gene expression of nitric oxide synthase. These findings suggest that the intake of pequi fruit might protect against in vivo genotoxicity and oxidative stress. PMID:26200231

  2. Caryocar brasiliense camb protects against genomic and oxidative damage in urethane-induced lung carcinogenesis

    Directory of Open Access Journals (Sweden)

    N.B.R. Colombo

    2015-01-01

    Full Text Available The antioxidant effects of Caryocar brasiliense Camb, commonly known as the pequi fruit, have not been evaluated to determine their protective effects against oxidative damage in lung carcinogenesis. In the present study, we evaluated the role of pequi fruit against urethane-induced DNA damage and oxidative stress in forty 8-12 week old male BALB/C mice. An in vivo comet assay was performed to assess DNA damage in lung tissues and changes in lipid peroxidation and redox cycle antioxidants were monitored for oxidative stress. Prior supplementation with pequi oil or its extract (15 µL, 60 days significantly reduced urethane-induced oxidative stress. A protective effect against DNA damage was associated with the modulation of lipid peroxidation and low protein and gene expression of nitric oxide synthase. These findings suggest that the intake of pequi fruit might protect against in vivo genotoxicity and oxidative stress.

  3. The role of nitric oxide and oxidative stress in intestinal damage induced by selenium deficiency in chickens.

    Science.gov (United States)

    Yu, Jiao; Yao, Haidong; Gao, Xuejiao; Zhang, Ziwei; Wang, Jiu-Feng; Xu, Shi-Wen

    2015-02-01

    Nitric oxide (NO) is an essential messenger molecule and is associated with inflammation and oxidative stress. Although NO has important biological functions in mammals, its role in the mechanism that occurs after intestinal injuries in chickens remains unknown. The objective of the present study was to investigate the real role of NO and oxidative stress in the intestinal injuries of chickens induced by selenium (Se) deficiency. A total 150 chickens were randomly divided into the following two groups: a low-Se group (L group, fed a Se-deficient diet containing 0.020 mg/kg Se) and a control group (C group, fed a commercial diet containing 0.2 mg/kg Se). The activities and mRNA levels of glutathione peroxidase (GSH-Px), the production of glutathione (GSH) and NO, and the protein and mRNA levels of inducible nitric oxide synthase (iNOS) were examined in the intestinal tissues (duodenum, jejunum, and rectum) at 15, 25, 35, 45, and 55 days. Methane dicarboxylic aldehyde (MDA) levels were also detected by assay kits. Then, the morphologies of the tissues were observed under the microscope after hematoxylin and eosin staining (H&E staining). The results showed that Se deficiency induced higher inflammatory damage and MDA levels (P chickens and that low levels of GSH-Px and high contents of NO may exert a major role in the injury of the intestinal tract induced by Se deficiency.

  4. Crocin reduced acrylamide-induced neurotoxicity in Wistar rat through inhibition of oxidative stress

    Directory of Open Access Journals (Sweden)

    Soghra Mehri

    2015-09-01

    Conclusion: The administration of crocin markedly improved behavioral and histopathological damages in Wistar rats exposed to ACR. Reduction of oxidative stress can be considered as an important mechanism of neuroprotective effects of crocin against ACR-induced toxicity.

  5. Mitochondrial calcium uniporter protein MCU is involved in oxidative stress-induced cell death.

    Science.gov (United States)

    Liao, Yajin; Hao, Yumin; Chen, Hong; He, Qing; Yuan, Zengqiang; Cheng, Jinbo

    2015-06-01

    Mitochondrial calcium uniporter (MCU) is a conserved Ca(2+) transporter at mitochondrial in eukaryotic cells. However, the role of MCU protein in oxidative stress-induced cell death remains unclear. Here, we showed that ectopically expressed MCU is mitochondrial localized in both HeLa and primary cerebellar granule neurons (CGNs). Knockdown of endogenous MCU decreases mitochondrial Ca(2+) uptake following histamine stimulation and attenuates cell death induced by oxidative stress in both HeLa cells and CGNs. We also found MCU interacts with VDAC1 and mediates VDAC1 overexpression-induced cell death in CGNs. This finding demonstrates that MCU-VDAC1 complex regulates mitochondrial Ca(2+) uptake and oxidative stress-induced apoptosis, which might represent therapeutic targets for oxidative stress related diseases.

  6. Inhaled Diesel Emissions Generated with Cerium Oxide Nanoparticle Fuel Additive Induce Adverse Pulmonary and Systemic Effects

    Science.gov (United States)

    Diesel exhaust (DE) exposure induces adverse cardiopulmonary effects. Cerium oxide nanoparticles added to diesel fuel (DECe) increases fuel burning efficiency but leads to altered emission characteristics and potentially altered health effects. Here, we evaluated whether DECe res...

  7. Charging effects during focused electron beam induced deposition of silicon oxide

    NARCIS (Netherlands)

    de Boer, Sanne K.; van Dorp, Willem F.; De Hosson, Jeff Th. M.

    2011-01-01

    This paper concentrates on focused electron beam induced deposition of silicon oxide. Silicon oxide pillars are written using 2, 4, 6, 8, 10-pentamethyl-cyclopenta-siloxane (PMCPS) as precursor. It is observed that branching of the pillar occurs above a minimum pillar height. The branching is attrib

  8. Metformin protects primary rat hepatocytes against oxidative stress-induced apoptosis

    NARCIS (Netherlands)

    Conde de la Rosa, Laura; Vrenken, Titia E; Buist-Homan, Manon; Faber, Klaas Nico; Moshage, Han

    2015-01-01

    The majority of chronic liver diseases are accompanied by oxidative stress, which induces apoptosis in hepatocytes and liver injury. Recent studies suggest that oxidative stress and insulin resistance are important in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and the pathophysiolo

  9. Electron beam induced oxidation of Ni3Al surfaces : electron flux effects

    NARCIS (Netherlands)

    Koch, S.A.; Palasantzas, G.; Agterveld, D.T.L. van; Hosson, J.Th.M. De

    2002-01-01

    Electron beam irradiation of polycrystalline boron doped Ni3Al (at 300 K and under ultrahigh vacuum conditions) induces fast oxidation. The rate and depth of oxidation initially increase with increasing electron flux as indicated by results from Auger electron spectroscopy. Curves of oxygen developm

  10. NRF2 Oxidative Stress Induced by Heavy Metals is Cell Type Dependent

    Science.gov (United States)

    Exposure to metallic environmental toxicants has been demonstrated to induce a variety of oxidative stress responses in mammalian cells. The transcription factor Nrf2 is activated in response to oxidative stress and coordinates the expression of antioxidant gene products. In this...

  11. Co-delivery of doxorubicin and arsenite with reduction and pH dual-sensitive vesicle for synergistic cancer therapy

    Science.gov (United States)

    Zhang, Lu; Xiao, Hong; Li, Jingguo; Cheng, Du; Shuai, Xintao

    2016-06-01

    Drug resistance is the underlying cause for therapeutic failure in clinical cancer chemotherapy. A prodrug copolymer mPEG-PAsp(DIP-co-BZA-co-DOX) (PDBD) was synthesized and assembled into a nanoscale vesicle comprising a PEG corona, a reduction and pH dual-sensitive hydrophobic membrane and an aqueous lumen encapsulating doxorubicin hydrochloride (DOX.HCl) and arsenite (As). The dual stimulation-sensitive design of the vesicle gave rise to rapid release of the physically entrapped DOX.HCl and arsenite inside acidic lysosomes, and chemically conjugated DOX inside the cytosol with high glutathione (GSH) concentration. In the optimized concentration range, arsenite previously recognized as a promising anticancer agent from traditional Chinese medicine can down-regulate the expressions of anti-apoptotic and multidrug resistance proteins to sensitize cancer cells to chemotherapy. Consequently, the DOX-As-co-loaded vesicle demonstrated potent anticancer activity. Compared to the only DOX-loaded vesicle, the DOX-As-co-loaded one induced more than twice the apoptotic ratio of MCF-7/ADR breast cancer cells at a low As concentration (0.5 μM), due to the synergistic effects of DOX and As. The drug loading strategy integrating chemical conjugation and physical encapsulation in stimulation-sensitive carriers enabled efficient drug loading in the formulation.Drug resistance is the underlying cause for therapeutic failure in clinical cancer chemotherapy. A prodrug copolymer mPEG-PAsp(DIP-co-BZA-co-DOX) (PDBD) was synthesized and assembled into a nanoscale vesicle comprising a PEG corona, a reduction and pH dual-sensitive hydrophobic membrane and an aqueous lumen encapsulating doxorubicin hydrochloride (DOX.HCl) and arsenite (As). The dual stimulation-sensitive design of the vesicle gave rise to rapid release of the physically entrapped DOX.HCl and arsenite inside acidic lysosomes, and chemically conjugated DOX inside the cytosol with high glutathione (GSH) concentration. In the

  12. Attenuating effect of daidzein on polychlorinated biphenyls-induced oxidative toxicity in mouse testicular cells*

    OpenAIRE

    Zhang, Da-lei; Mi, Yu-ling; Wang, Kai-Ming; Zeng, Wei-dong; Zhang, Cai-qiao

    2008-01-01

    The attenuating effect of daidzein (DAI) on oxidative toxicity induced by Aroclor 1254 (A1254) was investigated in mouse testicular cells. Cells were exposed to A1254 alone or with DAI. The oxidative damage was estimated by measuring malondialdehyde (MDA) formation, superoxide dismutase (SOD) activity and glutathione (GSH) content. Results show that A1254 induced a decrease of germ cell number, an elevation in thiobarbituric acid reactive substances (TBARS) but a decrease in SOD activity and ...

  13. Evaluating Oxidative Stress Factors Induced by Chlorpyrifos Poisoning in Plasma of Wistar Rat

    OpenAIRE

    Saberi, M.; A Zare’i Mahmoudabadi; M Fasihi Ramandi; A Kazemi; J Rasouli Vani

    2014-01-01

    Introduction: Chlorpyrifos (CPF) is a broad-spectrum organophosphorus insecticide that has been used abundantly over the globe during the past 40 years. Chemical pesticides may induce oxidative stress via generating free radicals and altering antioxidant levels of the free radical scavenging enzyme activity. Therefore, this study aimed to evaluate the toxicity of Chlorpyrifos-induced oxidative stress in the plasma samples of Wistar rat. Methods: Twenty-four male Wistar rats were selected r...

  14. Romo1 expression contributes to oxidative stress-induced death of lung epithelial cells

    Energy Technology Data Exchange (ETDEWEB)

    Shin, Jung Ar [Department of Internal Medicine, Yonsei University College of Medicine, Yonsei University Health System, Seoul 135-270 (Korea, Republic of); Chung, Jin Sil [Laboratory of Molecular Cell Biology, College of Life Sciences and Biotechnology, Korea University, Seoul 136-713 (Korea, Republic of); Cho, Sang-Ho [Department of Pathology, Pochon CHA University, College of Medicine, Gyeonggi-do (Korea, Republic of); Kim, Hyung Jung, E-mail: khj57@yuhs.ac.kr [Department of Internal Medicine, Yonsei University College of Medicine, Yonsei University Health System, Seoul 135-270 (Korea, Republic of); Yoo, Young Do, E-mail: ydy1130@korea.ac.kr [Laboratory of Molecular Cell Biology, College of Life Sciences and Biotechnology, Korea University, Seoul 136-713 (Korea, Republic of)

    2013-09-20

    Highlights: •Romo1 mediates oxidative stress-induced mitochondrial ROS production. •Romo1 induction by oxidative stress plays an important role in oxidative stress-induced apoptosis. •Romo1 overexpression correlates with epithelial cell death in patients with IPF. -- Abstract: Oxidant-mediated death of lung epithelial cells due to cigarette smoking plays an important role in pathogenesis in lung diseases such as idiopathic pulmonary fibrosis (IPF). However, the exact mechanism by which oxidants induce epithelial cell death is not fully understood. Reactive oxygen species (ROS) modulator 1 (Romo1) is localized in the mitochondria and mediates mitochondrial ROS production through complex III of the mitochondrial electron transport chain. Here, we show that Romo1 mediates mitochondrial ROS production and apoptosis induced by oxidative stress in lung epithelial cells. Hydrogen peroxide (H{sub 2}O{sub 2}) treatment increased Romo1 expression, and Romo1 knockdown suppressed the cellular ROS levels and cell death triggered by H{sub 2}O{sub 2} treatment. In immunohistochemical staining of lung tissues from patients with IPF, Romo1 was mainly localized in hyperplastic alveolar and bronchial epithelial cells. Romo1 overexpression was detected in 14 of 18 patients with IPF. TUNEL-positive alveolar epithelial cells were also detected in most patients with IPF but not in normal controls. These findings suggest that Romo1 mediates apoptosis induced by oxidative stress in lung epithelial cells.

  15. Dysregulated autophagy increased melanocyte sensitivity to H2O2-induced oxidative stress in vitiligo

    Science.gov (United States)

    He, Yuanmin; Li, Shuli; Zhang, Weigang; Dai, Wei; Cui, Tingting; Wang, Gang; Gao, Tianwen; Li, Chunying

    2017-01-01

    In vitiligo, melanocytes are particularly vulnerable to oxidative stress owing to the pro-oxidant state generated during melanin synthesis and to the genetic antioxidant defects. Autophagy is a controlled self-digestion process which can protect cells against oxidative damage. However, the exact role of autophagy in vitiligo melanocytes in response to oxidative stress and the mechanism involved are still not clear. To determine the implications of autophagy for melanocyte survival in response to oxidative stress, we first detected the autophagic flux in normal melanocytes exposure to H2O2, and found that autophagy was significantly enhanced in normal melanocytes, for protecting cells against H2O2-induced oxidative damage. Nevertheless, vitiligo melanocytes exhibited dysregulated autophagy and hypersensitivity to H2O2-induced oxidative injury. In addition, we confirmed that the impairment of Nrf2-p62 pathway is responsible for the defects of autophagy in vitiligo melanocytes. Noteworthily, upregulation of the Nrf2-p62 pathway or p62 reduced H2O2-induced oxidative damage of vitiligo melanocytes. Therefore, our data demonstrated that dysregulated autophagy owing to the impairment of Nrf2-p62 pathway increase the sensitivity of vitiligo melanocytes to oxidative stress, thus promote the development of vitiligo. Upregulation of p62-dependent autophagy may be applied to vitiligo treatment in the future. PMID:28186139

  16. Biliverdin Reductase-A correlates with inducible nitric oxide synthasein in atorvastatin treated aged canine brain

    Institute of Scientific and Technical Information of China (English)

    Fabio Di Domenico; Marzia Perluigi; Eugenio Barone

    2013-01-01

    Alzheimer’s disease is a neurodegenerative disorder characterized by progressive cognitive impairment and neuropathology. Recent preclinical and epidemiological studies proposed statins as a possible therapeutic drug for Alzheimer’s disease, but the exact mechanisms of action are stil unknown. Biliverdin reductase-A is a pleiotropic enzyme involved in cel ular stress responses. It not only transforms biliverdin-IX alpha into the antioxidant bilirubin-IX alpha but its serine/threonine/tyrosine kinase activity is able to modulate cel signaling networks. We previously reported the beneficial effects of atorvastatin treatment on biliverdin reductase-A and heme oxygenase-1 in the brains of a well characterized pre-clinical model of Alzheimer’s disease, aged beagles, together with observed improvement in cognition. Here we extend our knowledge of the effects of atorvastatin on inducible nitric oxide synthase in parietal cortex, cerebel um and liver of the same animals. We demonstrated that atorvastatin treatment (80 mg/day for 14.5 months) to aged beagles selectively increased inducible nitric oxide synthase in the parietal cortex but not in the cerebel um. In contrast, inducible nitric oxide synthase protein levels were significantly decreased in the liver. Significant positive correlations were found between biliverdin reductase-A and inducible nitric oxide synthase as wel as heme oxygenase-1 protein levels in the parietal cortex. The opposite was observed in the liver. Inducible nitric oxide synthase up-regulation in the parietal cortex was positively associated with improved biliverdin reductase-A functions, whereas the oxidative-induced impairment of biliverdin reductase-A in the liver negatively affected inducible nitric oxide synthase expression, thus suggesting a role for biliverdin reductase-A in atorvastatin-dependent inducible nitric oxide synthase changes. Interestingly, increased inducible nitric oxide synthase levels in the parietal cortex were not

  17. Determinants of exercise-induced fat oxidation in obese women and men.

    Science.gov (United States)

    Haufe, S; Engeli, S; Budziarek, P; Utz, W; Schulz-Menger, J; Hermsdorf, M; Wiesner, S; Otto, C; Fuhrmann, J C; Luft, F C; Boschmann, M; Jordan, J

    2010-03-01

    Endurance training at an intensity eliciting maximal fat oxidation may have a beneficial effect on body weight and glucose metabolism in obese patients. However, the exercise intensity at which maximal fat oxidation occurs and the factors limiting fat oxidation are not well studied in this population. Obese, otherwise healthy men (n=38) and women (n=91) performed an incremental exercise test up to exhaustion on a cycle ergometer. Substrate oxidation was estimated using indirect calorimetry. Magnetic resonance tomography and spectroscopy were conducted to assess body fat distribution and intramyocellular fat content. We determined the exercise intensity at which maximal body fat oxidation occurs and assessed whether body composition, body fat distribution, intramyocellular fat content, or oxidative capacity predict exercise-induced fat oxidation. Maximal exercise-induced fat oxidation was 0.30+/-0.02 g/min in men and 0.23+/-0.01 g/min in women (pobese subjects the capacity to oxidize fat during exercise appears to be limited by skeletal muscle mass and oxidative capacity rather than the availability of visceral or intramyocellular fat.

  18. Grape seed and skin extract protects kidney from doxorubicin-induced oxidative injury.

    Science.gov (United States)

    Mokni, Meherzia; Hamlaoui, Sonia; Kadri, Safwen; Limam, Ferid; Amri, Mohamed; Marzouki, Lamjed; Aouani, Ezzedine

    2016-05-01

    The study investigated the protective effect of grape seed and skin extract (GSSE) against doxorubicin-induced renal toxicity in healthy rats. Animals were treated with GSSE or not (control), for 8 days, administered with doxorubicin (20mg/kg) in the 4th day, and renal function as well as oxidative stress parameters were evaluated. Data showed that doxorubicin induced renal toxicity by affecting renal architecture and plasma creatinine. Doxorubicin also induced an oxidative stress characterized by an increase in malondialdehyde (MDA), calcium and H(2)O(2) and a decrease in catalase (CAT) and superoxide dismutase (SOD). Unexpectedly doxorubicin increased peroxidase (POD) and decreased carbonyl protein and plasma urea. Treatment with GSSE counteracted almost all adverse effects induced by doxorubicin. Data suggest that doxorubicin induced an oxidative stress into rat kidney and GSSE exerted antioxidant properties, which seem to be mediated by the modulation of intracellular calcium.

  19. Inducible nitric oxide synthase mediates bone loss in ovariectomized mice.

    NARCIS (Netherlands)

    Cuzzocrea, S.; Mazzon, E.; Dugo, L.; Genovese, T.; Paola, R. Di; Ruggeri, Z.; Vegeto, E.; Caputi, A.P.; Loo, F.A.J. van de; Puzzolo, D.; Maggi, A.

    2003-01-01

    Several clinical studies have shown that bone loss may be attributed to osteoclast recruitment induced by mediators of inflammation. In different experimental paradigms we have recently demonstrated that estrogen exhibits antiinflammatory activity by preventing the induction of inducible nitric

  20. Inflammation, gene mutation and photoimmunosuppression in response to UVR-induced oxidative damage contributes to photocarcinogenesis.

    Science.gov (United States)

    Halliday, Gary M

    2005-04-01

    Ultraviolet (UV) radiation causes inflammation, gene mutation and immunosuppression in the skin. These biological changes are responsible for photocarcinogenesis. UV radiation in sunlight is divided into two wavebands, UVB and UVA, both of which contribute to these biological changes, and therefore probably to skin cancer in humans and animal models. Oxidative damage caused by UV contributes to inflammation, gene mutation and immunosuppression. This article reviews evidence for the hypothesis that UV oxidative damage to these processes contributes to photocarcinogenesis. UVA makes a larger impact on oxidative stress in the skin than UVB by inducing reactive oxygen and nitrogen species which damage DNA, protein and lipids and which also lead to NAD+ depletion, and therefore energy loss from the cell. Lipid peroxidation induces prostaglandin production that in association with UV-induced nitric oxide production causes inflammation. Inflammation drives benign human solar keratosis (SK) to undergo malignant conversion into squamous cell carcinoma (SCC) probably because the inflammatory cells produce reactive oxygen species, thus increasing oxidative damage to DNA and the immune system. Reactive oxygen or nitrogen appears to cause the increase in mutational burden as SK progress into SCC in humans. UVA is particularly important in causing immunosuppression in both humans and mice, and UV lipid peroxidation induced prostaglandin production and UV activation of nitric oxide synthase is important mediators of this event. Other immunosuppressive events are likely to be initiated by UV oxidative stress. Antioxidants have also been shown to reduce photocarcinogenesis. While most of this evidence comes from studies in mice, there is supporting evidence in humans that UV-induced oxidative damage contributes to inflammation, gene mutation and immunosuppression. Available evidence implicates oxidative damage as an important contributor to sunlight-induced carcinogenesis in humans.

  1. Inflammation, gene mutation and photoimmunosuppression in response to UVR-induced oxidative damage contributes to photocarcinogenesis

    Energy Technology Data Exchange (ETDEWEB)

    Halliday, Gary M. [Dermatology Research Laboratories, Division of Medicine, Melanoma and Skin Cancer Research Institute, Royal Prince Alfred Hospital at the University of Sydney, Sydney, NSW (Australia)]. E-mail: garyh@med.usyd.edu.au

    2005-04-01

    Ultraviolet (UV) radiation causes inflammation, gene mutation and immunosuppression in the skin. These biological changes are responsible for photocarcinogenesis. UV radiation in sunlight is divided into two wavebands, UVB and UVA, both of which contribute to these biological changes, and therefore probably to skin cancer in humans and animal models. Oxidative damage caused by UV contributes to inflammation, gene mutation and immunosuppression. This article reviews evidence for the hypothesis that UV oxidative damage to these processes contributes to photocarcinogenesis. UVA makes a larger impact on oxidative stress in the skin than UVB by inducing reactive oxygen and nitrogen species which damage DNA, protein and lipids and which also lead to NAD+ depletion, and therefore energy loss from the cell. Lipid peroxidation induces prostaglandin production that in association with UV-induced nitric oxide production causes inflammation. Inflammation drives benign human solar keratosis (SK) to undergo malignant conversion into squamous cell carcinoma (SCC) probably because the inflammatory cells produce reactive oxygen species, thus increasing oxidative damage to DNA and the immune system. Reactive oxygen or nitrogen appears to cause the increase in mutational burden as SK progress into SCC in humans. UVA is particularly important in causing immunosuppression in both humans and mice, and UV lipid peroxidation induced prostaglandin production and UV activation of nitric oxide synthase is important mediators of this event. Other immunosuppressive events are likely to be initiated by UV oxidative stress. Antioxidants have also been shown to reduce photocarcinogenesis. While most of this evidence comes from studies in mice, there is supporting evidence in humans that UV-induced oxidative damage contributes to inflammation, gene mutation and immunosuppression. Available evidence implicates oxidative damage as an important contributor to sunlight-induced carcinogenesis in humans.

  2. An aquaporin PvTIP4;1 from Pteris vittata may mediate arsenite uptake.

    Science.gov (United States)

    He, Zhenyan; Yan, Huili; Chen, Yanshan; Shen, Hongling; Xu, Wenxiu; Zhang, Haiyan; Shi, Lei; Zhu, Yong-Guan; Ma, Mi

    2016-01-01

    The fern Pteris vittata is an arsenic hyperaccumulator. The genes involved in arsenite (As(III)) transport are not yet clear. Here, we describe the isolation and characterization of a new P. vittata aquaporin gene, PvTIP4;1, which may mediate As(III) uptake. PvTIP4;1 was identified from yeast functional complement cDNA library of P. vittata. Arsenic toxicity and accumulating activities of PvTIP4;1 were analyzed in Saccharomyces cerevisiae and Arabidopsis. Subcellular localization of PvTIP4;1-GFP fusion protein in P. vittata protoplast and callus was conducted. The tissue expression of PvTIP4;1 was investigated by quantitative real-time PCR. Site-directed mutagenesis of the PvTIP4;1 aromatic/arginine (Ar/R) domain was studied. Heterologous expression in yeast demonstrates that PvTIP4;1 was able to facilitate As(III) diffusion. Transgenic Arabidopsis showed that PvTIP4;1 increases arsenic accumulation and induces arsenic sensitivity. Images and FM4-64 staining suggest that PvTIP4;1 localizes to the plasma membrane in P. vittata cells. A tissue location study shows that PvTIP4;1 transcripts are mainly expressed in roots. Site-directed mutation in yeast further proved that the cysteine at the LE1 position of PvTIP4;1 Ar/R domain is a functional site. PvTIP4;1 is a new represented tonoplast intrinsic protein (TIP) aquaporin from P. vittata and the function and location results imply that PvTIP4;1 may be involved in As(III) uptake.

  3. Taurine chloramine-induced inactivation of cofilin protein through methionine oxidation.

    Science.gov (United States)

    Luo, Shen; Uehara, Hiroshi; Shacter, Emily

    2014-10-01

    Cofilin regulates reorganization of actin filaments (F-actin) in eukaryotes. A recent finding has demonstrated that oxidation of cofilin by taurine chloramine (TnCl), a physiological oxidant derived from neutrophils, causes cofilin to translocate to the mitochondria inducing apoptosis (F. Klamt et al. Nat. Cell Biol.11:1241-1246; 2009). Here we investigated the effect of TnCl on biological activities of cofilin in vitro. Our data show that TnCl-induced oxidation of recombinant human cofilin-1 inhibits its F-actin-binding and depolymerization activities. Native cofilin contains four free Cys and three Met residues. Incubation of oxidized cofilin with DTT does not lead to its reactivation. A double Cys to Ala mutation on the two C-terminal Cys shows similar biological activities as the wild type, but does not prevent the TnCl-induced inactivation. In contrast, incubation of oxidized cofilin with methionine sulfoxide reductases results in its reactivation. Phosphorylation is known to inhibit cofilin activities. We found that Met oxidation also prevents phosphorylation of cofilin, which is reversed by incubating oxidized cofilin with methionine sulfoxide reductases. Interestingly, intact protein mass spectrometry of the oxidized mutant indicated one major oxidation product with an additional mass of 16 Da, consistent with oxidation of one specific Met residue. This residue was identified as Met-115 by peptide mapping and tandem mass spectrometry. It is adjacent to Lys-114, a known residue on globular-actin-binding site, implying that oxidation of Met-115 disrupts the globular-actin-binding site of cofilin, which causes TnCl-induced inactivation. The findings identify Met-115 as a redox switch on cofilin that regulates its biological activity. Published by Elsevier Inc.

  4. Pressure-related activation of inducible nitric oxide synthase

    Institute of Scientific and Technical Information of China (English)

    2001-01-01

    A lot of reports suggested that inducible nitric oxide synthase (iNOS) has a very different nature from constitutive NOS including endothelial NOS (eNOS) and neural NOS (nNOS). When exposed to cytokines or bacterial products, iNOS could be greatly activated and produces hundreds or thousands fold more NO than it does usually. Whether iNOS activation is arterial pressure related is not clear. In the present experiment, we studied three groups(n=6) of Sprague Dawley (SD) rats with implanted aorta and venous catheters that were maintained on 1 mEq/d, 12.5 mEq/d and 25 mEq/d of sodium intake respectively. Pulsatile arterial pressure signals from the amplifier were sent to a digital computer and the urine samples were taken every other day for nitrate/nitrite excretion (UNOx) assay using Greiss Reaction. After 6 days infusion, the rats were euthanized with an overdose of sodium pentobarbital, and the renal medullas were rapidly removed and frozen on dry ice for iNOS activity assay. Morever separate groups of hypertensive rats including spontaneously hypertensive rat (SHR, n=6) and High NaCl-induced hypertensive rat (NaHR, n=6) were used to measure renal iNOS protein by Western Blotting. The results showed that the mean arterial pressure (MAP) were significantly increased with the increase intake of sodium, the MAP (mmHg) at day 6 were 99.6±3.5,116.65±4.2 and 125.43±4.5, and the iNOS activity (nmol*g-1 protein*min-1) were 122.3±23.4, 342.4±35.6 and 623.9±65.4 in 1 mEq/d, 12.5 mEq/d and 25 mEq/d of sodium intake-rats respectively. At the same time, UNOx at day 6 were also increased, in turn, to 5 865.6±343.0 (for 12.5 mEq/d intake-rats) and (9 642.8±1 045.3) (for 25 mEq/d sodium intake-rats) nmol/d from (3 834.9±234.8) nmol/d of 1 mEq/d sodium intake-rats respectively. Western blotting showed that the renal medullary iNOS protein in SHR and NaHR were increased by 178%±13% and 104%±9% of normal Wistar rats. The data indicates that elevated arterial pressure

  5. Protective Effect of Wheat Peptides against Indomethacin-Induced Oxidative Stress in IEC-6 Cells

    Directory of Open Access Journals (Sweden)

    Hong Yin

    2014-01-01

    Full Text Available Recent studies have demonstrated that wheat peptides protected rats against non-steroidal anti-inflammatory drugs-induced small intestinal epithelial cells damage, but the mechanism of action is unclear. In the present study, an indomethacin-induced oxidative stress model was used to investigate the effect of wheat peptides on the nuclear factor-κB(NF-κB-inducible nitric oxide synthase-nitric oxide signal pathway in intestinal epithelial cells-6 cells. IEC-6 cells were treated with wheat peptides (0, 125, 500 and 2000 mg/L for 24 h, followed by 90 mg/L indomethacin for 12 h. Wheat peptides significantly attenuated the indomethacin-induced decrease in superoxide dismutase and glutathione peroxidase activity. Wheat peptides at 2000 mg/L markedly decreased the expression of the NF-κB in response to indomethacin-induced oxidative stress. This study demonstrated that the addition of wheat peptides to a culture medium significantly inhibited the indomethacin-induced release of malondialdehyde and nitrogen monoxide, and increased antioxidant enzyme activity in IEC-6 cells, thereby providing a possible explanation for the protective effect proposed for wheat peptides in the prevention of indomethacin-induced oxidative stress in small intestinal epithelial cells.

  6. Cordyceps militaris Extract Protects Human Dermal Fibroblasts against Oxidative Stress-Induced Apoptosis and Premature Senescence

    Directory of Open Access Journals (Sweden)

    Jun Myoung Park

    2014-09-01

    Full Text Available Oxidative stress induced by reactive oxygen species (ROS is the major cause of degenerative disorders including aging and disease. In this study, we investigated whether Cordyceps militaris extract (CME has in vitro protective effects on hydrogen peroxide-induced oxidative stress in human dermal fibroblasts (HDFs. Our results showed that the 2,2-diphenyl-1-picrylhydrazyl (DPPH radical scavenging activity of CME was increased in a dose-dependent manner. We found that hydrogen peroxide treatment in HDFs increased ROS generation and cell death as compared with the control. However, CME improved the survival of HDFs against hydrogen peroxide-induced oxidative stress via inhibition of intracellular ROS production. CME treatment inhibited hydrogen peroxide-induced apoptotic cell death and apoptotic nuclear condensation in HDFs. In addition, CME prevented hydrogen peroxide-induced SA-β-gal-positive cells suggesting CME could inhibit oxidative stress-induced premature senescence. Therefore, these results suggest that CME might have protective effects against oxidative stress-induced premature senescence via scavenging ROS.

  7. Protective effect of wheat peptides against indomethacin-induced oxidative stress in IEC-6 cells.

    Science.gov (United States)

    Yin, Hong; Pan, Xingchang; Song, Zhixiu; Wang, Shaokang; Yang, Ligang; Sun, Guiju

    2014-01-29

    Recent studies have demonstrated that wheat peptides protected rats against non-steroidal anti-inflammatory drugs-induced small intestinal epithelial cells damage, but the mechanism of action is unclear. In the present study, an indomethacin-induced oxidative stress model was used to investigate the effect of wheat peptides on the nuclear factor-κB(NF-κB)-inducible nitric oxide synthase-nitric oxide signal pathway in intestinal epithelial cells-6 cells. IEC-6 cells were treated with wheat peptides (0, 125, 500 and 2000 mg/L) for 24 h, followed by 90 mg/L indomethacin for 12 h. Wheat peptides significantly attenuated the indomethacin-induced decrease in superoxide dismutase and glutathione peroxidase activity. Wheat peptides at 2000 mg/L markedly decreased the expression of the NF-κB in response to indomethacin-induced oxidative stress. This study demonstrated that the addition of wheat peptides to a culture medium significantly inhibited the indomethacin-induced release of malondialdehyde and nitrogen monoxide, and increased antioxidant enzyme activity in IEC-6 cells, thereby providing a possible explanation for the protective effect proposed for wheat peptides in the prevention of indomethacin-induced oxidative stress in small intestinal epithelial cells.

  8. Cordyceps militaris Extract Protects Human Dermal Fibroblasts against Oxidative Stress-Induced Apoptosis and Premature Senescence

    Science.gov (United States)

    Park, Jun Myoung; Lee, Jong Seok; Lee, Ki Rim; Ha, Suk-Jin; Hong, Eock Kee

    2014-01-01

    Oxidative stress induced by reactive oxygen species (ROS) is the major cause of degenerative disorders including aging and disease. In this study, we investigated whether Cordyceps militaris extract (CME) has in vitro protective effects on hydrogen peroxide-induced oxidative stress in human dermal fibroblasts (HDFs). Our results showed that the 2,2-diphenyl-1-picrylhydrazyl (DPPH) radical scavenging activity of CME was increased in a dose-dependent manner. We found that hydrogen peroxide treatment in HDFs increased ROS generation and cell death as compared with the control. However, CME improved the survival of HDFs against hydrogen peroxide-induced oxidative stress via inhibition of intracellular ROS production. CME treatment inhibited hydrogen peroxide-induced apoptotic cell death and apoptotic nuclear condensation in HDFs. In addition, CME prevented hydrogen peroxide-induced SA-β-gal-positive cells suggesting CME could inhibit oxidative stress-induced premature senescence. Therefore, these results suggest that CME might have protective effects against oxidative stress-induced premature senescence via scavenging ROS. PMID:25230212

  9. Vitamin D3 pretreatment alleviates renal oxidative stress in lipopolysaccharide-induced acute kidney injury.

    Science.gov (United States)

    Xu, Shen; Chen, Yuan-Hua; Tan, Zhu-Xia; Xie, Dong-Dong; Zhang, Cheng; Xia, Mi-Zhen; Wang, Hua; Zhao, Hui; Xu, De-Xiang; Yu, De-Xin

    2015-08-01

    Increasing evidence demonstrates that reactive oxygen species plays important roles in sepsis-induced acute kidney injury. This study investigated the effects of VitD3 pretreatment on renal oxidative stress in sepsis-induced acute kidney injury. Mice were intraperitoneally injected with lipopolysaccharide (LPS, 2.0mg/kg) to establish an animal model of sepsis-induced acute kidney injury. In VitD3+LPS group, mice were orally pretreated with three doses of VitD3 (25 μg/kg) at 1, 24 and 48 h before LPS injection. As expected, oral pretreatment with three daily recommended doses of VitD3 markedly elevated serum 25(OH)D concentration and efficiently activated renal VDR signaling. Interestingly, LPS-induced renal GSH depletion and lipid peroxidation were markedly alleviated in VitD3-pretreated mice. LPS-induced serum and renal nitric oxide (NO) production was obviously suppressed by VitD3 pretreatment. In addition, LPS-induced renal protein nitration, as determined by 3-nitrotyrosine residue, was obviously attenuated by VitD3 pretreatment. Further analysis showed that LPS-induced up-regulation of renal inducible nitric oxide synthase (inos) was repressed in VitD3-pretreated mice. LPS-induced up-regulation of renal p47phox and gp91phox, two NADPH oxidase subunits, were normalized by VitD3 pretreatment. In addition, LPS-induced down-regulation of renal superoxide dismutase (sod) 1 and sod2, two antioxidant enzyme genes, was reversed in VitD3-pretreated mice. Finally, LPS-induced tubular epithelial cell apoptosis, as determined by TUNEL, was alleviated by VitD3 pretreatment. Taken together, these results suggest that VitD3 pretreatment alleviates LPS-induced renal oxidative stress through regulating oxidant and antioxidant enzyme genes.

  10. Nitric oxide alleviates aluminum-induced oxidative damage through regulating the ascorbate-glutathione cycle in roots of wheat

    Institute of Scientific and Technical Information of China (English)

    Chengliang Sun; Lijuan Liu; Yan Yu; Wenjing Liu; Lingli Lu; Chongwei Jin; Xianyong Lin

    2015-01-01

    The possible association with nitric oxide (NO) and ascorbate-glutathione (AsA-GSH) cycle in regulating aluminum (Al) tolerance of wheat (Triticum aestivum L.) was investigated using two genotypes with different Al resistance. Exposure to Al inhibited root elongation, and triggered lipid peroxidation and oxidation of AsA to dehydroascorbate and GSH to glutathione disulfide in wheat roots. Exogenous NO significantly increased endogenous NO levels, and subsequently al eviated Al-induced inhibition of root elongation and oxidation of AsA and GSH to maintain the redox molecules in the reduced form in both wheat genotypes. Under Al stress, significantly increased activities and gene transcriptional levels of ascorbate peroxi-dase, glutathione reductase, and dehydroascorbate reductase, were observed in the root tips of the Al-tolerant genotype Jian-864. Nitric oxide application enhanced the activity and gene transcriptional level of these enzymes in both wheat geno-types. g-Glutamylcysteine synthetase was not significantly affected by Al or NO, but NO treatments increased the activity of glutathione peroxidase and glutathione S-transferase to a greater extent than the Al-treated wheat seedlings. Proline was significantly decreased by Al, while it was not affected by NO. These results clearly suggest that NO protects wheat root against Al-induced oxidative stress, possibly through its regulation of the AsA-GSH cycle.

  11. Visualization of Oxidative Stress Induced by Experimental Periodontitis in Keap1-Dependent Oxidative Stress Detector-Luciferase Mice.

    Science.gov (United States)

    Kataoka, Kota; Ekuni, Daisuke; Tomofuji, Takaaki; Irie, Koichiro; Kunitomo, Muneyoshi; Uchida, Yoko; Fukuhara, Daiki; Morita, Manabu

    2016-11-16

    The aim of this study was to investigate whether a Keap1-dependent oxidative stress detector-luciferase (OKD-LUC) mouse model would be useful for the visualization of oxidative stress induced by experimental periodontitis. A ligature was placed around the mandibular first molars for seven days to induce periodontitis. Luciferase activity was measured with an intraperitoneal injection of d-luciferin on days 0, 1, and 7. The luciferase activity in the periodontitis group was significantly greater than that in the control group at seven days. The expressions of heme oxygenase-1 (HO-1) and malondialdehyde in periodontal tissue were significantly higher in the periodontitis group than in the control group. Immunofluorescent analysis confirmed that the nuclear translocation of nuclear factor erythroid 2-related factor 2 (Nrf2) occurred more frequently in the periodontitis group than in the control group. This study found that under oxidative stress induced by experimental periodontitis, the Nrf2/antioxidant defense pathway was activated and could be visualized from the luciferase activity in the OKD-LUC model. Thus, the OKD-LUC mouse model may be useful for exploring the mechanism underlying the relationship between the Nrf2/antioxidant defense pathway and periodontitis by enabling the visualization of oxidative stress over time.

  12. Attenuating effect of daidzein on polychlorinated biphenyls-induced oxidative toxicity in mouse testicular cells

    Institute of Scientific and Technical Information of China (English)

    Da-lei ZHANG; Yu-ling MI; Kai-ming WANG; Wei-dong ZENG; Cai-qiao ZHANG

    2008-01-01

    The attenuating effect of daidzein (DAD on oxidative toxicity induced by Aroclor 1254 (A 1254) was investigated in mouse testicular cells. Cells were exposed to A1254 alone or with DAI. The oxidative damage was estimated by measuring malondialdehyde (MDA) formation, superoxide dismutase (SOD) activity and glutathione (GSH) content. Results show that A 1254 induced a decrease of germ cell number, an elevation in thiobarbituric acid reactive substances (TBARS) but a decrease in SOD activity and GSH content. However, simultaneous supplementation with DAI decreased TBARS level and increased SOD activity and GSH content. Consequently, dietary DAI may restore the intracellular antioxidant system to attenuate the oxidative toxicity of A1254 in testicular cells.

  13. Activation of the hypothalamic-pituitary-adrenal stress axis induces cellular oxidative stress

    Directory of Open Access Journals (Sweden)

    Jereme G. Spiers

    2015-01-01

    Full Text Available Glucocorticoids released from the adrenal gland in response to stress-induced activation of the hypothalamic-pituitary-adrenal (HPA axis induce activity in the cellular reduction-oxidation (redox system. The redox system is a ubiquitous chemical mechanism allowing the transfer of electrons between donor/acceptors and target molecules during oxidative phosphorylation while simultaneously maintaining the overall cellular environment in a reduced state. The objective of this review is to present an overview of the current literature discussing the link between HPA axis-derived glucocorticoids and increased oxidative stress, particularly focussing on the redox changes observed in the hippocampus following glucocorticoid exposure.

  14. [Biological consequences of oxidative stress induced by pesticides].

    Science.gov (United States)

    Grosicka-Maciąg, Emilia

    2011-06-17

    Pesticides are used to protect plants and numerous plant products. They are also utilized in several industrial branches. These compounds are highly toxic to living organisms. In spite of close supervision in the use of pesticides there is a serious risk that these agents are able to spread into the environment and contaminate water, soil, food, and feedstuffs. Recently, more and more studies have been focused on understanding the toxic mechanisms of pesticide actions. The data indicate that the toxic action of pesticides may include the induction of oxidative stress and accumulation of free radicals in the cell. Long-lasting or acute oxidative stress disturbs cell metabolism and is able to produce permanent changes in the structure of proteins, lipids, and DNA. The proteins that are oxidized may lose or enhance their activity. Moreover, the proteins oxidized are able to form aggregates that inhibit the systems responsible for protein degradation and lead to alterations of proteins in the cell. Once oxidized, lipids have the capacity to damage and depolarize cytoplasmic membranes. Free oxygen radicals are harmful to DNA including damage to single nitric bases, DNA strand breaks and adduct production. Many studies indicate that oxidative stress may accelerate development of numerous diseases including cancer and neurodegenerative ones such as Alzheimer’s and Parkinson’s disease and may also be responsible for infertility.

  15. Plasma levels of oxidative stress-responsive apoptosis inducing protein (ORAIP) in rats subjected to physicochemical oxidative stresses.

    Science.gov (United States)

    Yao, Takako; Fujimura, Tsutomu; Murayama, Kimie; Seko, Yoshinori

    2016-01-01

    Oxidative stress is known to play a pivotal role in the pathogenesis of various disorders including atherosclerosis, aging and especially ischaemia/reperfusion injury. It causes cell damage that leads to apoptosis. However, the precise mechanism has been uncertain. Recently, we identified an apoptosis-inducing humoral factor in a hypoxia/reoxygenated medium of cardiac myocytes. We named this novel post-translationally modified secreted form of eukaryotic translation initiation factor 5A (eIF5A) as oxidative stress-responsive apoptosis inducing protein (ORAIP). We developed a sandwich ELISA and confirmed that myocardial ischaemia/reperfusion markedly increased plasma levels of ORAIP. To investigate whether the role of ORAIP is common to various types of oxidative stress, we measured plasma ORAIP levels in rats subjected to three physicochemical models of oxidative stress including N2/O2 inhalation, cold/warm-stress (heat shock) and blood acidification. In all three models, plasma ORAIP levels significantly increased and reached a peak level at 10-30 min after stimulation, then decreased within 60 min. The (mean±S.E.M.) plasma ORAIP levels before and after (peak) stimulation were (16.4±9.6) and (55.2±34.2) ng/ml in N2/O2 inhalation, (14.1±12.4) and (34.3±14.6) ng/ml in cold/warm-stress, and (18.9±14.3) and (134.0±67.2) ng/ml in blood acidification study. These data strongly suggest that secretion of ORAIP in response to oxidative stress is universal mechanism and plays an essential role. ORAIP will be an important novel biomarker as well as a specific therapeutic target of these oxidative stress-induced cell injuries. © 2016 The Author(s).

  16. Aminoguanidine inhibits reactive oxygen species formation, lipid peroxidation, and oxidant-induced apoptosis.

    Science.gov (United States)

    Giardino, I; Fard, A K; Hatchell, D L; Brownlee, M

    1998-07-01

    Aminoguanidine (AG) treatment, like nerve growth factor (NGF) treatment, prevents diabetes-induced apoptosis of retinal Müller cells in the rat eye, but the mechanism involved is unknown. In this study, the effects of preincubation with AG on oxidant-induced apoptosis, oxidant-induced intracellular reactive oxygen species (ROS) production, and lipid peroxidation were determined in rat retinal Müller cells and compared with the effects of NGF, a protein that protects neuronal cells from oxidative stress. The effect of AG on rabbit vitreous lipid peroxide levels was also determined. After exposure to increasing concentrations of H2O2, there was a corresponding increase in the percentage of apoptotic Müller cells. Preincubation with AG for 48 h completely inhibited oxidant-induced apoptosis in response to 10 micromol/l H2O2 (+AG 0 vs. 10 micromol/l, NS), and reduced the percentage of apoptotic cells in response to 50 micromol/l H2O2 by 50% (+AG vs. -AG, P NGF. Both AG and NGF preincubation prevented the twofold increase in oxidant-induced lipid peroxides. The fivefold increase in oxidant-induced ROS production was decreased 100% by NGF, but only 61% by AG preincubation. The twofold increase in vitreous lipid peroxide level in diabetic rabbits was completely prevented by AG treatment. AG reduced H2O2-induced benzoate hydroxylation in a dose-dependent manner. Intracellular glutathione content was unchanged. These data demonstrate that AG can act as an antioxidant in vivo, quenching hydroxyl radicals and lipid peroxidation in cells and tissues and preventing oxidant-induced apoptosis.

  17. Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension

    Directory of Open Access Journals (Sweden)

    Magdalena Cristóbal-García

    2015-01-01

    Full Text Available We addressed if oxidative stress in the renal cortex plays a role in the induction of hypertension and mitochondrial alterations in hyperuricemia. A second objective was to evaluate whether the long-term treatment with the antioxidant Tempol prevents renal oxidative stress, mitochondrial alterations, and systemic hypertension in this model. Long-term (11-12 weeks and short-term (3 weeks effects of oxonic acid induced hyperuricemia were studied in rats (OA, 750 mg/kg BW, OA+Allopurinol (AP, 150 mg/L drinking water, OA+Tempol (T, 15 mg/kg BW, or vehicle. Systolic blood pressure, renal blood flow, and vascular resistance were measured. Tubular damage (urine N-acetyl-β-D-glucosaminidase and oxidative stress markers (lipid and protein oxidation along with ATP levels were determined in kidney tissue. Oxygen consumption, aconitase activity, and uric acid were evaluated in isolated mitochondria from renal cortex. Short-term hyperuricemia resulted in hypertension without demonstrable renal oxidative stress or mitochondrial dysfunction. Long-term hyperuricemia induced hypertension, renal vasoconstriction, tubular damage, renal cortex oxidative stress, and mitochondrial dysfunction and decreased ATP levels. Treatments with Tempol and allopurinol prevented these alterations. Renal oxidative stress induced by hyperuricemia promoted mitochondrial functional disturbances and decreased ATP content, which represent an additional pathogenic mechanism induced by chronic hyperuricemia. Hyperuricemia-related hypertension occurs before these changes are evident.

  18. Induction of heme oxygenase-1 inhibits the monocyte transmigration induced by mildly oxidized LDL.

    Science.gov (United States)

    Ishikawa, K; Navab, M; Leitinger, N; Fogelman, A M; Lusis, A J

    1997-09-01

    Heme catabolic processes produce the antioxidants biliverdin and bilirubin, as well as the potent prooxidant free iron. Since these products have opposing effects on oxidative stress, it is not clear whether heme catabolism promotes or inhibits inflammatory processes, including atherosclerotic lesion formation. Heme oxygenase (HO) catalyzes the rate-limiting step of heme catabolism. We used cocultures of human aortic endothelial cells and smooth muscle cells to examine the possible role of HO in early atherosclerosis. Heme oxygenase-1 (HO-1), the inducible isoform of HO, was highly induced by mildly oxidized LDL, and augmented induction was observed with hemin pretreatment. This augmented HO-1 induction resulted in the reduction of monocyte chemotaxis in response to LDL oxidation. Conversely, inhibition of HO by a specific inhibitor, Sn-protoporphyrin IX, enhanced chemotaxis. Furthermore, pretreatment with biliverdin or bilirubin, the products of HO, reduced chemotaxis. Oxidized phospholipids in the mildly oxidized LDL appear to be responsible for HO-1 induction, since oxidized but not native arachidonic acid-containing phospholipids also induced HO-1. These results suggest that HO-1 induced by mildly oxidized LDL may protect against the induction of inflammatory responses in artery wall cells through the production of the antioxidants biliverdin and bilirubin.

  19. Carvedilol inhibits pressure-induced increase in oxidative stress in coronary smooth muscle cells.

    Science.gov (United States)

    Yasunari, Kenichi; Maeda, Kensaku; Nakamura, Munehiro; Yoshikawa, Junichi

    2002-05-01

    The cellular mechanisms by which hypertension enhances atherosclerosis are still not known in detail. Recently, evidence has been obtained that oxidative stress plays a role in the pathogenesis of pressure-induced atherosclerosis. We examined the effects of pressure on oxidative stress in cultured human coronary smooth muscle cells (SMCs). Application of increased pressure (+100 mmHg) with He gas for 48 h increased oxidative stress of measured by flow cytometry by 71% and F2-isopretane by 77%. Increased pressure also increased the activities of phospholipase D (PLD), and particulate protein kinase C (PKC). The PLD inhibitor suramin 100 micromol/l, 1-butanol 40 mmol/l, and the PKC inhibitors chelerythrine 1 micromol/l and calphostin C 100 nmol/l and completely blocked the increase in oxidative stress induced by pressure. Carvedilol 1 micromol/l but not propranolol 1 micromol/l blocked pressure-induced increases in oxidative stress in cultured SMCs. These findings suggest that pressure increases oxidative stress and that carvedilol significantly inhibits pressure-induced increase in oxidative stress in cultured human coronary smooth muscle cells.

  20. Inducible nitric oxide synthase is responsible for nitric oxide release from murine pituicytes

    DEFF Research Database (Denmark)

    Kjeldsen, T H; Rivier, C; Lee, S;

    2003-01-01

    This study investigated whether pituicytes were able to produce and release nitric oxide (NO), and which type of nitric oxide synthase (NOS) would be responsible for this phenomenon. Lipopolysaccharide (LPS) 1 micro g/ml was used as inflammatory mediator. Because pituicytes are known to secrete...

  1. Cellular Automata Modelling of Photo-Induced Oxidation Processes in Molecularly Doped Polymers

    Directory of Open Access Journals (Sweden)

    David M. Goldie

    2016-11-01

    Full Text Available The possibility of employing cellular automata (CA to model photo-induced oxidation processes in molecularly doped polymers is explored. It is demonstrated that the oxidation dynamics generated using CA models exhibit stretched-exponential behavior. This dynamical characteristic is in general agreement with an alternative analysis conducted using standard rate equations provided the molecular doping levels are sufficiently low to prohibit the presence of safe-sites which are impenetrable to dissolved oxygen. The CA models therefore offer the advantage of exploring the effect of dopant agglomeration which is difficult to assess from standard rate equation solutions. The influence of UV-induced bleaching or darkening upon the resulting oxidation dynamics may also be easily incorporated into the CA models and these optical effects are investigated for various photo-oxidation product scenarios. Output from the CA models is evaluated for experimental photo-oxidation data obtained from a series of hydrazone-doped polymers.

  2. Arsenic toxicity induced endothelial dysfunction and dementia: Pharmacological interdiction by histone deacetylase and inducible nitric oxide synthase inhibitors

    Energy Technology Data Exchange (ETDEWEB)

    Sharma, Bhupesh, E-mail: drbhupeshresearch@gmail.com; Sharma, P.M.

    2013-11-15

    Arsenic toxicity has been reported to damage all the major organs including the brain and vasculature. Dementia including Alzheimer's disease (AD) and vascular dementia (VaD) are posing greater risk to the world population as it is now increasing at a faster rate. We have investigated the role of sodium butyrate, a selective histone deacetylase (HDAC) inhibitor and aminoguanidine, a selective inducible nitric oxide synthase (iNOS) inhibitor in pharmacological interdiction of arsenic toxicity induced vascular endothelial dysfunction and dementia in rats. Arsenic toxicity was done by administering arsenic drinking water to rats. Morris water-maze (MWM) test was used for assessment of learning and memory. Endothelial function was assessed using student physiograph. Oxidative stress (aortic superoxide anion, serum and brain thiobarbituric acid reactive species, brain glutathione) and nitric oxide levels (serum nitrite/nitrate) were also measured. Arsenic treated rats have shown impairment of endothelial function, learning and memory, reduction in serum nitrite/nitrate and brain GSH levels along with increase in serum and brain TBARS. Sodium butyrate as well as aminoguanidine significantly convalesce arsenic induced impairment of learning, memory, endothelial function, and alterations in various biochemical parameters. It may be concluded that arsenic induces endothelial dysfunction and dementia, whereas, sodium butyrate, a HDAC inhibitor as well as aminoguanidine, a selective iNOS inhibitor may be considered as potential agents for the management of arsenic induced endothelial dysfunction and dementia. - Highlights: • As has induced endothelial dysfunction (Edf) and vascular dementia (VaD). • As has increased oxidative stress, AChE activity and decreased serum NO. • Inhibitors of HDAC and iNOS have attenuated As induced Edf and VaD. • Both the inhibitors have attenuated As induced biochemical changes. • Inhibitor of HDAC and iNOS has shown good potential

  3. Role of Forkhead Transcription Factors in Diabetes-Induced Oxidative Stress

    Directory of Open Access Journals (Sweden)

    Bhaskar Ponugoti

    2012-01-01

    Full Text Available Diabetes is a chronic metabolic disorder, characterized by hyperglycemia resulting from insulin deficiency and/or insulin resistance. Recent evidence suggests that high levels of reactive oxygen species (ROS and subsequent oxidative stress are key contributors in the development of diabetic complications. The FOXO family of forkhead transcription factors including FOXO1, FOXO3, FOXO4, and FOXO6 play important roles in the regulation of many cellular and biological processes and are critical regulators of cellular oxidative stress response pathways. FOXO1 transcription factors can affect a number of different tissues including liver, retina, bone, and cell types ranging from hepatocytes to microvascular endothelial cells and pericytes to osteoblasts. They are induced by oxidative stress and contribute to ROS-induced cell damage and apoptosis. In this paper, we discuss the role of FOXO transcription factors in mediating oxidative stress-induced cellular response.

  4. Protective effects of propolis on inorganic mercury induced oxidative stress in mice.

    Science.gov (United States)

    Zhao, Jun-Quan; Wen, Yi-Fei; Bhadauria, Monika; Nirala, Satendra Kumar; Sharma, Abhilasha; Shrivastava, Sadhana; Shukla, Sangeeta; Agrawal, Om Prakash; Mathur, Ramesh

    2009-04-01

    Protective potential of propolis was evaluated against mercury induced oxidative stress and antioxidant enzymatic alterations in mice liver. Exposure to mercuric chloride (HgCl2; 5 mg/kg; ip) induced oxidative stress by increasing lipid peroxidation and oxidized glutathione level along with concomitant decrease in glutathione and various antioxidant enzymes. Mercury intoxication deviated the activity of liver marker enzymes in serum. Conjoint treatment of propolis (200 mg/kg; po) inhibited lipid peroxidation and oxidized glutathione level, whereas increased glutathione level. Activities of antioxidants enzymes, i.e., superoxide dismutase, catalase, glutathione-S-transferase and glucose-6-phosphate dehydrogenase were also restored concomitantly towards control after propolis administration. Release of serum transaminases, alkaline phosphatase, lactate dehydrogenase and y-glutamyl transpeptidase were significantly restored towards control after propolis treatment. Results suggest that propolis augments the antioxidants defense against mercury induced toxicity and provides evidence that it has therapeutic potential as hepatoprotective agent.

  5. Coordination of altered DNA repair and damage pathways in arsenite-exposed keratinocytes.

    Science.gov (United States)

    Hamadeh, Hisham K; Trouba, Kevin J; Amin, Rupesh P; Afshari, Cynthia A; Germolec, Dori

    2002-10-01

    Human exposure to arsenic, a ubiquitous and toxic environmental pollutant, is associated with an increased incidence of skin cancer. However, the mechanism(s) associated with AsIII-mediated toxicity and carcinogenesis at low levels of exposure remains elusive. Aberrations in cell proliferation, oxidative damage, and DNA-repair fidelity have been implicated in sodium arsenite (AsIII)-mediated carcinogenicity and toxicity, but these events have been examined in isolation in the majority of biological models of arsenic exposure. We hypothesized that the simultaneous interaction of these effects may be important in arsenic-mediated neoplasia in the skin. To evaluate this, normal human epidermal keratinocytes (NHEK) were exposed to nontoxic doses (0.005-5 micro M) of AsIII and monitored for several physiological endpoints at the times when cells were harvested for gene expression measurements (1-24 h). Two-fluor cDNA microarray analyses indicated that AsIII treatment decreased the expression of genes associated with DNA repair (e.g., p53 and Damage-specific DNA-binding protein 2) and increased the expression of genes indicative of the cellular response to oxidative stress (e.g., Superoxide dismutase 1, NAD(P)H quinone oxidoreductase, and Serine/threonine kinase 25). AsIII also modulated the expression of certain transcripts associated with increased cell proliferation (e.g., Cyclin G1, Protein kinase C delta), oncogenes, and genes associated with cellular transformation (e.g., Gro-1 and V-yes). These observations correlated with measurements of cell proliferation and mitotic measurements as AsIII treatment resulted in a dose-dependent increase in cellular mitoses at 24 h and an increase in cell proliferation at 48 h of exposure. Data in this manuscript demonstrates that AsIII exposure simultaneously modulates DNA repair, cell proliferation, and redox-related gene expression in nontransformed, normal NHEK. It is anticipated that data in this report will serve as a

  6. Significance of nitric oxide on the pathogenesis of steroid-induced femoral head necrosis

    Institute of Scientific and Technical Information of China (English)

    2000-01-01

    @@Steroid-induced femoral head necrosis is claimed to be an ischemic femoral head disease. But there is no discussion on the role of nitric oxide (NO) in the idiopathic disease. The concentration of NO indirectly in serum with steroid induced avascular necrosis of femoral head (ANFH) and in controls are studied in this article.

  7. High glucose-induced oxidative stress increases transient receptor potential channel expression in human monocytes

    DEFF Research Database (Denmark)

    Wuensch, Tilo; Thilo, Florian; Krueger, Katharina;

    2010-01-01

    Transient receptor potential (TRP) channel-induced cation influx activates human monocytes, which play an important role in the pathogenesis of atherosclerosis. In the present study, we investigated the effects of high glucose-induced oxidative stress on TRP channel expression in human monocytes....

  8. Modulatory effect of Tinospora cordifolia extract on Cd-induced oxidative stress in Wistar rats

    Directory of Open Access Journals (Sweden)

    Viswanadha Vijaya Padma

    2016-03-01

    Conclusion: Our results suggested that TCE with its antioxidant effect offered cytoprotection against Cd-induced toxicity in kidneys by restoring the altered cellular antioxidants and renal markers. TCE treatment for 28 days reversed ATPase activity and tissue glycoprotein levels. These results revealed the protective effect of TCE on Cd-induced toxicity in kidneys and oxidative stress.

  9. Electrochemical activity of heavy metal oxides in the process of chloride induced corrosion of steel reinforcement

    Indian Academy of Sciences (India)

    V Živica

    2002-10-01

    The influence of heavy metal oxides on the chloride induced corrosion of steel reinforcement in concrete was studied. Significant inhibition and stimulation of chloride induced corrosion have been observed. Basicity and acidity of the relevant metal ions, and their ability to form complexes are considered as the main factors of the observed effects.

  10. Changes in magmatic oxidation state induced by degassing

    Science.gov (United States)

    Brounce, M. N.; Stolper, E. M.; Eiler, J. M.

    2015-12-01

    Temporal variations in the oxygen fugacity (fO2) of the mantle may have been transmitted to Earth's atmosphere and oceans by volcanic degassing. However, it is unclear how redox states of volatiles relate to their source magmas because degassing and assimilation can impact fO2 before or during eruption. To explore this, we present µ-XANES measurements of the oxidation states of Fe and S and laser fluorination measurements of 18O/16O ratios in submarine glasses from two settings where degassing is recorded: 1) submarine glasses from the Reykjanes Ridge as it shoals to Iceland, including subglacial glasses from the Reykjanes Peninsula; and 2) submarine glasses from Mauna Kea recovered by the Hawaii Shield Drilling Program (HSDP). Glasses from both settings are basalts with 5.5-9.9 wt% MgO and 350-1790 ppm S. Submarine Reykjanes glasses are sulfide saturated. Subglacial Reykjanes and HSDP glasses are not sulfide saturated, and S and H2O contents are consistent with S+H2O degassing. Submarine Reykjanes glasses have 18O/16O indistinguishable from MORB and become progressively 18O-depleted as MgO decreases. Subglacial glasses have lower 18O/16O than submarine glasses at a given MgO, but both sample types project to a common 18O/16O near 10 wt% MgO, suggesting that 18O-depletion in these lavas is generated by fractional crystallization and assimilation of an 18O-depleted crustal component. The oxidation state of Fe increases only slightly as 18O/16O decrease, suggesting that the assimilant is not oxidized enough to change magmatic fO2. Fe and S do not oxidize or reduce with decreasing S or H2O, suggesting that relatively reduced magmas at depth degassed S+H2O without changing magmatic fO2, and that the fO2 of these lavas reflect the fO2of their mantle source. The oxidation states of Fe and S in HSDP glasses are broadly correlated and samples with the highest S concentrations are the most oxidized. Both Fe and S reduce with decreasing S and H2O contents. This suggests

  11. Brain oxidative stress induced by obstructive jaundice in rats.

    Science.gov (United States)

    Chroni, Elisabeth; Patsoukis, Nikolaos; Karageorgos, Nikolaos; Konstantinou, Dimitris; Georgiou, Christos

    2006-02-01

    The effect of experimental obstructive jaundice on the oxidative status of brain tissues in rats was examined. Twenty-four male Wistar rats were divided into 4 groups: Group I was the control, group II was the sham operated, and groups III and IV were bile duct ligated and killed on the 5th and the 10th day, respectively. Oxidative stress was assessed by measuring the thiol redox state (protein and nonprotein components) and lipid peroxidation level variations in samples from the cerebral cortex, midbrain, and cerebellar tissue in all animals. Results indicated the presence of oxidative stress in the jaundiced animals that was more pronounced on the 10th day as indicated by a decrease in reduced glutathione and protein thiol and an increase in protein disulphide and lipid peroxidation. A dramatic elevation of the level of total nonprotein mixed disulphide level was found specifically in the midbrain in the 10th day group. This suggests an accumulation of nonprotein disulfides other than oxidized glutathione, which remained unchanged, in this particular brain area. This study showed a correlation between experimental obstructive jaundice and the oxidative stress in the rats' brain, implying that a similar pathogenetic mechanism may play a key role in cholestatic liver disease, resulting in hepatic encephalopathy in humans.

  12. The role of oxidative/nitrosative stress in pathogenesis of paracetamol-induced toxic hepatitis

    Directory of Open Access Journals (Sweden)

    Ješić-Vukićević Rada

    2010-01-01

    Full Text Available Introduction. Paracetamol is an effective analgesic/antipyretic drug when used at therapeutic doses. However, the overdose of paracetamol can cause severe liver injury and liver necrosis. The mechanism of paracetamol-induced liver injury is still not completely understood. Reactive metabolite formation, depletion of glutathione and alkylation of proteins are the triggers of inhibition of mitochondrial respiration, adenosine triphosphate depletion and mitochondrial oxidant stress leading to hepatocellular necrosis. Role of oxidative stress in paracetamol-induced liver injury. The importance of oxidative stress in paracetamol hepatotoxicity is controversial. Paracetamol induced liver injury cause the formation of reactive oxygen species. The potent sources of reactive oxygen are mitochondria, neutrophils, Kupffer cells and the enzyme xatnine oxidase. Free radicals lead to lipid peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in paracetamol-induced oxidative stress. The production of mitochondrial reactive oxygen species is increased, and the glutathione content is decreased in paracetamol overdose. Oxidative stress in mitochondria leads to mito­chondrial dysfunction with adenosine triphosphate depletion, increase mitochondrial permeability transition, deoxyribonu­cleic acid fragmentation which contribute to the development of hepatocellular necrosis in the liver after paracetamol overdose. Role of Kupffer cells in paracetamol-induced liver injury. Paracetamol activates Kupffer cells, which then release numerous cytokines and signalling molecules, including nitric oxide and superoxide. Kupffer cells are important in peroxynitrite formation. On the other hand, the activated Kupffer cells release anti-inflammatory cytokines. Role of neutrophils in paracetamol-induced liver injury. Paracetamol-induced liver injury leads to the accumulation of neutrophils, which release lysosomal enzymes and generate superoxide anion

  13. Concentrations of Nitric Oxide in Rat Brain Tissues after Diffuse Brain Injury and Neuroprotection by the Selective Inducible Nitric Oxide Synthase Inhibitor Aminoguanidine

    Institute of Scientific and Technical Information of China (English)

    Yi-bao Wang; Shao-wu Ou; Guang-yu Li; Yun-hui Liu

    2005-01-01

    @@ To investigate the effects of nitric oxide (NO) and the selective inducible nitric oxide synthase (iNOS) inhibitor aminoguanidine (AG) on trauma, we explored the concentrations of nitric oxide in rat brain tissues at different time stamps after diffuse brain injury (DBI) with or without AG treatment.

  14. The antioxidant tempol decreases acute pulmonary thromboembolism-induced hemolysis and nitric oxide consumption.

    Science.gov (United States)

    Sousa-Santos, Ozelia; Neto-Neves, Evandro M; Ferraz, Karina C; Sertório, Jonas T; Portella, Rafael L; Tanus-Santos, Jose E

    2013-11-01

    Acute pulmonary thromboembolism (APT) is a critical condition associated with acute pulmonary hypertension. Recent studies suggest that oxidative stress and hemolysis contribute to APT-induced pulmonary hypertension, possibly as a result of increased nitric oxide (NO) consumption. We hypothesized that the antioxidant tempol could attenuate APT-induced hemolysis, and therefore attenuate APT-induced increases in plasma NO consumption. APT was induced in anesthetized sheep with autologous blood clots. The hemodynamic effects of tempol infused at 1.0mg/kg/min 30 min after APT were determined. Hemodynamic measurements were carried out every 15 min. To assess oxidative stress, serum 8-isoprostanes levels were measured by ELISA. Plasma cell-free hemoglobin concentrations and NO consumption by plasma samples were determined. An in vitro oxidative AAPH-induced hemolysis assay was used to further validate the in vivo effects of tempol. APT caused pulmonary hypertension, and increased pulmonary vascular resistance in proportion with the increases in 8-isoprostanes, plasma cell-free hemoglobin concentrations, and NO consumption by plasma (all Phemolysis (Phemolysis and nitric oxide consumption, thus attenuating APT-induced pulmonary hypertension. © 2013.

  15. Influence of Ring Oxidation-Induced Stack Faults on Efficiency in Silicon Solar Cells

    Institute of Scientific and Technical Information of China (English)

    ZHOU Chun-Lan; WANG Wen-Jing; LI Hai-Ling; ZHAO Lei; DIAO Hong-Wei; LI Xu-Dong

    2008-01-01

    @@ We observe a strong correlation between the ring oxidation-induced stack faults (OISF) formed in the course of phosphor diffusion and the efficiency of Czochralski-grown silicon solar cells. The main reason for ring-OISF formation and growth in substrate is the silicon oxidation and phosphorus diffusion process induced silicon self-interstitial point defect during POCl3 diffusion. The decreasing of minority carrier diffusion length in crystal silicon solar cell induced by ring-OISF defects is identified to be one of the major causes of efficiency loss.

  16. New nickel-uranium-arsenic mineral species from the oxidation zone of the Belorechenskoye deposit, Northern Caucasus, Russia. Pt. II. Dymkovite, Ni(UO{sub 2}){sub 2}(As{sup 3+}O{sub 3}){sub 2}.7H{sub 2}O, a seelite-related arsenite

    Energy Technology Data Exchange (ETDEWEB)

    Pekov, Igor V.; Bryzgalov, Igor A. [Moscow State Univ. (Russian Federation). Faculty of Geology; Levitskiy, Viktor V. [Russian Minerals Co., Moscow (Russian Federation); Krivovichev, Sergey V.; Zolotarev, Andrey A. [St Petersburg State Univ. (Russian Federation). Faculty of Geology; Chukanov, Nikita V. [Institute of Problems of Chemical Physics, Chernogolovka, Moscow (Russian Federation); Zadov, Aleksandr E. [NPP ' ' Teplokhim' ' , Moscow (Russian Federation)

    2012-07-01

    A new arsenite mineral species dymkovite, ideally Ni(UO{sub 2}){sub 2}(As{sup 3+}O{sub 3}){sub 2}.7H{sub 2}O (IMA no. 2010-087), was found at the Belorechenskoye deposit, Adygea Republic, Northern Caucasus, Russia. It is a supergene mineral associated with rauchite, annabergite, and goethite in cavities of a dolomite vein with primary uraninite (pitchblende), nickeline, and gersdorffite. Dymkovite forms longprismatic, lath-shaped to acicular crystals (≤0.5 mm long, ≤0.05 mm thick), which are elongated along [010]. They are combined in sprays or open-work, chaotic groups up to 1.5 mm across; crusts up to 2 x 2 mm{sup 2} and up to 0.05-mm-thick also occur. Dymkovite crystals are transparent and bright yellow, whereas crusts are translucent and light yellow to light greenish-yellow. The luster is vitreous. The mineral is brittle, the Mohs' hardness is ca. 3. Cleavage was not observed. D{sub calc} is 3.806 g cm{sup -3}. Dymkovite is optically biaxial (-), α = 1.625(2), β = 1.735(5), γ = 1.745(3), 2V{sub meas} = 20(10) , 2V{sub calc.} = 32 . Dispersion is strong, r > v. Pleochroism is strong: X = very pale yellowish-green, Y ∼ Z = light greenish yellow. In the IR spectrum, bands of As{sup 3+}O{sub 3} anions are strong, whereas bands of As{sup 5+}O{sub 4} anions are very weak. The average chemical composition (electron microprobe) is (in wt%): MgO = 1.11, FeO = 0.24, NiO = 5.40, ZnO = 0.23, As{sub 2}O{sub 3} = 19.57, P{sub 2}O{sub 5} = 0.58, UO{sub 3} = 59.43, H{sub 2}O{sub calc} = 13.44, total = 100.00. The empirical formula, calculated on the basis of 17 O apfu, is: (Ni{sub 0.69}Mg{sub 0.26}Fe{sub 0.03}Zn{sub 0.03}){sub Σ1.01} U{sub 1.97}(As{sup 3+}{sub 1.88}P{sub 0.08}){sub Σ1.96}O{sub 9.94}.7.06H{sub 2}O. Dymkovite is monoclinic, space group C2/m, a = 17.99(3), b = 7.033(7), c = 6.633(9) Aa, β = 99.62(11) , V = 827(3) Aa{sup 3}, Z = 2. The crystal structure was refined from single-crystal X-ray diffraction data (R{sub 1} = 0.063). The structure is

  17. Uncovering the polymerase-induced cytotoxicity of an oxidized nucleotide

    Science.gov (United States)

    Freudenthal, Bret D.; Beard, William A.; Perera, Lalith; Shock, David D.; Kim, Taejin; Schlick, Tamar; Wilson, Samuel H.

    2015-01-01

    Oxidative stress promotes genomic instability and human diseases. A common oxidized nucleoside is 8-oxo-7,8-dihydro-2'-deoxyguanosine, which is found both in DNA (8-oxo-G) and as a free nucleotide (8-oxo-dGTP). Nucleotide pools are especially vulnerable to oxidative damage. Therefore cells encode an enzyme (MutT/MTH1) that removes free oxidized nucleotides. This cleansing function is required for cancer cell survival and to modulate Escherichia coli antibiotic sensitivity in a DNA polymerase (pol)-dependent manner. How polymerases discriminate between damaged and non-damaged nucleotides is not well understood. This analysis is essential given the role of oxidized nucleotides in mutagenesis, cancer therapeutics, and bacterial antibiotics. Even with cellular sanitizing activities, nucleotide pools contain enough 8-oxo-dGTP to promote mutagenesis. This arises from the dual coding potential where 8-oxo-dGTP(anti) base pairs with cytosine and 8-oxo-dGTP(syn) uses its Hoogsteen edge to base pair with adenine. Here we use time-lapse crystallography to follow 8-oxo-dGTP insertion opposite adenine or cytosine with human pol β, to reveal that insertion is accommodated in either the syn- or anti-conformation, respectively. For 8-oxo-dGTP(anti) insertion, a novel divalent metal relieves repulsive interactions between the adducted guanine base and the triphosphate of the oxidized nucleotide. With either templating base, hydrogen-bonding interactions between the bases are lost as the enzyme reopens after catalysis, leading to a cytotoxic nicked DNA repair intermediate. Combining structural snapshots with kinetic and computational analysis reveals how 8-oxo-dGTP uses charge modulation during insertion that can lead to a blocked DNA repair intermediate.

  18. Progesterone modulates the LPS-induced nitric oxide production by a progesterone-receptor independent mechanism.

    Science.gov (United States)

    Wolfson, Manuel Luis; Schander, Julieta Aylen; Bariani, María Victoria; Correa, Fernando; Franchi, Ana María

    2015-12-15

    Genital tract infections caused by Gram-negative bacteria induce miscarriage and are one of the most common complications of human pregnancy. LPS administration to 7-day pregnant mice induces embryo resorption after 24h, with nitric oxide playing a fundamental role in this process. We have previously shown that progesterone exerts protective effects on the embryo by modulating the inflammatory reaction triggered by LPS. Here we sought to investigate whether the in vivo administration of progesterone modulated the LPS-induced nitric oxide production from peripheral blood mononuclear cells from pregnant and non-pregnant mice. We found that progesterone downregulated LPS-induced nitric oxide production by a progesterone receptor-independent mechanism. Moreover, our results suggest a possible participation of glucocorticoid receptors in at least some of the anti-inflammatory effects of progesterone.

  19. Inflammatory cytokines protect retinal pigment epithelial cells from oxidative stress-induced death

    DEFF Research Database (Denmark)

    Juel, Helene B; Faber, Carsten; Svendsen, Signe Goul

    2013-01-01

    expression of anti-oxidative enzymes, and protein expression was validated by immunoblotting. RESULTS: Viability of RPE cells was reduced by exposure to inflammatory agents (PCM, IFNγ+/-TNFα) or to oxidative agents (H2O2 or NaIO3). Unexpectedly, cells treated with either H2O2 or NaIO3 were partially......-cultured with activated T cells, or treated with cytokines showed increased expression of anti-oxidative genes, with upregulation of superoxide dismutase 2 protein following PCM treatment. CONCLUSION: Oxidative stress-induced cell death was reduced by concomitant inflammatory stress. This is likely due to the cytokine......-mediated induction of the anti-oxidative stress response, upregulating protective anti-oxidant pathway(s). These findings suggest caution for the clinical use of anti-inflammatory agents in the management of immune-associated eye diseases such as age-related macular degeneration....

  20. Periodontal Disease-Induced Atherosclerosis and Oxidative Stress

    Directory of Open Access Journals (Sweden)

    Tomoko Kurita-Ochiai

    2015-09-01

    Full Text Available Periodontal disease is a highly prevalent disorder affecting up to 80% of the global population. Recent epidemiological studies have shown an association between periodontal disease and cardiovascular disease, as oxidative stress plays an important role in chronic inflammatory diseases such as periodontal disease and cardiovascular disease. In this review, we focus on the mechanisms by which periodontopathic bacteria cause chronic inflammation through the enhancement of oxidative stress and accelerate cardiovascular disease. Furthermore, we comment on the antioxidative activity of catechin in atherosclerosis accelerated by periodontitis.

  1. C-phycocyanin ameliorates doxorubicin-induced oxidative stress and apoptosis in adult rat cardiomyocytes.

    Science.gov (United States)

    Khan, Mahmood; Varadharaj, Saradhadevi; Shobha, Jagdish C; Naidu, Madireddi U; Parinandi, Narasimham L; Kutala, Vijay Kumar; Kuppusamy, Periannan

    2006-01-01

    Doxorubicin (DOX), a potent antineoplastic agent, poses limitations for its therapeutic use due to the associated risk of developing cardiomyopathy and congestive heart failure. The cardiotoxicity of doxorubicin is associated with oxidative stress and apoptosis. We have recently shown that Spirulina, a blue-green alga with potent antioxidant properties, offered significant protection against doxorubicin-induced cardiotoxicity in mice. The aim of the present study was to establish the possible protective role of C-phycocyanin, one of the active ingredients of Spirulina, against doxorubicin-induced oxidative stress and apoptosis. The study was carried out using cardiomyocytes isolated from adult rat hearts. Doxorubicin significantly enhanced the formation of reactive oxygen species (ROS) in cells as measured by the 2',7'-dichlorodihydrofluorescein diacetate and dihydroethidium fluorescence. The doxorubicin-induced reactive oxygen species formation was significantly attenuated in cells pretreated with C-phycocyanin. It was further observed that the doxorubicin-induced DNA fragmentation and apoptosis, as assayed by TUNEL assay and flow cytometry coupled with BrdU-FITC/propidium iodide staining, were markedly attenuated by C-phycocyanin. C-phycocyanin also significantly attenuated the doxorubicin-induced increase in the expression of Bax protein, release of cytochrome c, and increase in the activity of caspase-3 in cells. In summary, C-phycocyanin ameliorated doxorubicin-induced oxidative stress and apoptosis in cardiomyocytes. This study further supports the crucial role of the antioxidant nature of C-phycocyanin in its cardioprotection against doxorubicin-induced oxidative stress and apoptosis.

  2. Expression of Endothelial Nitric Oxide Synthase Traffic Inducer in the Placenta of Pregnancy Induced Hypertension

    Institute of Scientific and Technical Information of China (English)

    XIANG Wenpei; CHEN Hanping; GUO Yuzhen; SHEN Hongling

    2006-01-01

    The expression of endothelial nitric oxide synthase traffic inducer (NOSTRIN) in the placenta of the patients with pregnancy induced hypertension (PIH) was detected and its role in the pathogenesis of PIH was studied. The pathological changes in placental vessels were observed by HE staining. NO2-/NO3- , the stable metabolic end products of NO, was measured with nitrate reductase. The eNOS activity in placental tissues was assayed by spectrophotometry. Western blot analysis was applied to detect NOSTRIN expression. The incidence of thickening and fibronoid necrosis of placental vessels was significantly higher in women with PIH than in the normal group (P<0.01). The levels of placental NO2-/NO3- in PIH patients (27.53±7.48 μmol/mg) were significantly lower than in normal group (54.27±9.53 μmol/mg, P<0.01). The activity of eNOS was significantly decreased in PIH group (12. 826±3.61 U/mg) as compared with that in normal group (21. 72±3.83 U/mg, P<0.01). Western blot analysis revealed that both groups expressed 58 kD NOSTRIN, but the protein level was significantly higher in women with PIH than in the normal group (P<0.01). A significant negative correlation existed between the expression of NOSTRIN protein and the activity of eNOS in placental tissue of women with PIH (r=-0. 57, P<0. 01). It was concluded that the level of NOSTRIN expression in placenta of women with PIH was increased, which may play an important role in the pathogenesis of PIH.

  3. ATM protects against oxidative stress induced by oxidized low-density lipoprotein

    OpenAIRE

    2011-01-01

    Chronic oxidative stress is involved in the pathogenesis of multiple inflammatory diseases, including cardiovascular disease and atherosclerosis. The rare autosomal recessive disorder Ataxia-telangiectasia (A-T) is characterized by progressive cerebellar ataxia secondary to Purkinje cell death, immunodeficiency, and increased cancer incidence. ATM, the protein mutated in A-T, plays a key role in cellular DNA-damage responses. A-T cells show poor cellular anti-oxidant defences and increased ox...

  4. Hypochlorite-induced oxidation of amino acids, peptides and proteins

    DEFF Research Database (Denmark)

    Hawkins, C L; Pattison, D I; Davies, Michael Jonathan

    2003-01-01

    Activated phagocytes generate the potent oxidant hypochlorite (HOCl) via the release of the enzyme myeloperoxidase and hydrogen peroxide. HOCl is known to react with a number of biological targets including proteins, DNA, lipids and cholesterol. Proteins are likely to be major targets for reaction...

  5. Cigarette smoke-induced mitochondrial dysfunction and oxidative stress in

    NARCIS (Netherlands)

    Toorn, Marco van der

    2009-01-01

    In this thesis we studied the effects of cigarette smoke (CS) on mitochondrial function and oxidative stress in epithelial cells and discussed the potential of these phenomena in the pathogenesis of chronic obstructive pulmonary diseases (COPD). In the first three chapters we demonstrated that CS di

  6. Carbon monoxide-induced reduction and healing of graphene oxide

    NARCIS (Netherlands)

    Narayanan, B.; Weeks, S. L.; Jariwala, B. N.; Macco, B.; Weber, J.; Rathi, S. J.; M. C. M. van de Sanden,; Sutter, P.; Agarwal, S.; Ciobanu, C. V.

    2013-01-01

    Graphene oxide holds promise as a carbon-based nanomaterial that can be produced inexpensively in large quantities. However, its structural and electrical properties remain far from those of the graphene sheets obtained by mechanical exfoliation or by chemical vapor deposition unless efficient reduc

  7. Oxidative stress induces idiopathic infertility in Egyptian males

    African Journals Online (AJOL)

    Yomi

    2012-01-19

    Jan 19, 2012 ... Oxidative stress (OS) would play a vital role in etiology of ... To examine OS effect on Egyptian men fertility, sperm samples were obtained from infertile .... 1 ml semen. According to seminal quality profile, the infertile patients were .... donors and idiopathic men in terms of semen volume (ml) and leukocytes ...

  8. Carbon monoxide-induced reduction and healing of graphene oxide

    NARCIS (Netherlands)

    Narayanan, B.; Weeks, S. L.; Jariwala, B. N.; Macco, B.; Weber, J.; Rathi, S. J.; M. C. M. van de Sanden,; Sutter, P.; Agarwal, S.; Ciobanu, C. V.

    2013-01-01

    Graphene oxide holds promise as a carbon-based nanomaterial that can be produced inexpensively in large quantities. However, its structural and electrical properties remain far from those of the graphene sheets obtained by mechanical exfoliation or by chemical vapor deposition unless efficient reduc

  9. Textile industrial effluent induces mutagenicity and oxidative DNA damage and exploits oxidative stress biomarkers in rats.

    Science.gov (United States)

    Akhtar, Muhammad Furqan; Ashraf, Muhammad; Anjum, Aftab Ahmad; Javeed, Aqeel; Sharif, Ali; Saleem, Ammara; Akhtar, Bushra

    2016-01-01

    Exposure to complex mixtures like textile effluent poses risks to animal and human health such as mutations, genotoxicity and oxidative damage. Aim of the present study was to quantify metals in industrial effluent and to determine its mutagenic, genotoxic and cytotoxic potential and effects on oxidative stress biomarkers in effluent exposed rats. Metal analysis revealed presence of high amounts of zinc, copper, chromium, iron, arsenic and mercury in industrial effluent. Ames test with/without enzyme activation and MTT assay showed strong association of industrial effluent with mutagenicity and cytotoxicity respectively. In-vitro comet assay revealed evidence of high oxidative DNA damage. When Wistar rats were exposed to industrial effluent in different dilutions for 60 days, then activities of total superoxide dismutase and catalase and hydrogen peroxide concentration were found to be significantly lower in kidney, liver and blood/plasma of effluent exposed rats than control. Vitamin C in a dose of 50 mg/kg/day significantly reduced oxidative effects of effluent in rats. On the basis of this study it is concluded that industrial effluent may cause mutagenicity, in-vitro oxidative stress-related DNA damage and cytotoxicity and may be associated with oxidative stress in rats. Vitamin C may have ameliorating effect when exposed to effluent.

  10. Blockade of Drp1 rescues oxidative stress-induced osteoblast dysfunction

    Energy Technology Data Exchange (ETDEWEB)

    Gan, Xueqi; Huang, Shengbin; Yu, Qing [Department of Pharmacology and Toxicology and Higuchi Bioscience Center, University of Kansas, Lawrence, KS, 66047 (United States); State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041 (China); Yu, Haiyang [State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University, Chengdu, 610041 (China); Yan, Shirley ShiDu, E-mail: shidu@ku.edu [Department of Pharmacology and Toxicology and Higuchi Bioscience Center, University of Kansas, Lawrence, KS, 66047 (United States)

    2015-12-25

    Osteoblast dysfunction, induced by oxidative stress, plays a critical role in the pathophysiology of osteoporosis. However, the underlying mechanisms remain unclarified. Imbalance of mitochondrial dynamics has been closely linked to oxidative stress. Here, we reveal an unexplored role of dynamic related protein 1(Drp1), the major regulator in mitochondrial fission, in the oxidative stress-induced osteoblast injury model. We demonstrate that levels of phosphorylation and expression of Drp1 significantly increased under oxidative stress. Blockade of Drp1, through pharmaceutical inhibitor or gene knockdown, significantly protected against H{sub 2}O{sub 2}-induced osteoblast dysfunction, as shown by increased cell viability, improved cellular alkaline phosphatase (ALP) activity and mineralization and restored mitochondrial function. The protective effects of blocking Drp1 in H{sub 2}O{sub 2}-induced osteoblast dysfunction were evidenced by increased mitochondrial function and suppressed production of reactive oxygen species (ROS). These findings provide new insights into the role of the Drp1-dependent mitochondrial pathway in the pathology of osteoporosis, indicating that the Drp1 pathway may be targetable for the development of new therapeutic approaches in the prevention and the treatment of osteoporosis. - Highlights: • Oxidative stress is an early pathological event in osteoporosis. • Imbalance of mitochondrial dynamics are linked to oxidative stress in osteoporosis. • The role of the Drp1-dependent mitochondrial pathway in osteoporosis.

  11. Differential inhibition of oxidized LDL-induced apoptosis in human endothelial cells treated with different flavonoids.

    Science.gov (United States)

    Jeong, Yu-Jin; Choi, Yean-Jung; Kwon, Hyang-Mi; Kang, Sang-Wook; Park, Hyoung-Sook; Lee, Myungsook; Kang, Young-Hee

    2005-05-01

    High plasma level of cholesterol is a well-known risk factor for atherosclerotic diseases. Oxidized LDL induces cellular and nuclear damage that leads to apoptotic cell death. We tested the hypothesis that flavonoids may function as antioxidants with regard to LDL incubated with 5 microm-Cu(2+) alone or in combination with human umbilical vein endothelial cells (HUVEC). Cytotoxicity and formation of thiobarbituric acid-reactive substances induced by Cu(2+)-oxidized LDL were examined in the presence of various subtypes of flavonoid. Flavanols, flavonols and flavanones at a non-toxic dose of 50 microm markedly inhibited LDL oxidation by inhibiting the formation of peroxidative products. In contrast, the flavones luteolin and apigenin had no such effect, with >30 % of cells killed after exposure to 0.1 mg LDL/ml. Protective flavonoids, especially (-)-epigallocatechin gallate, quercetin, rutin and hesperetin, inhibited HUVEC nuclear condensation and fragmentation induced by Cu(2+)-oxidized LDL. In addition, immunochemical staining and Western blot analysis revealed that anti-apoptotic Bcl-2 expression was enhanced following treatment with these protective flavonoids. However, Bax expression and caspase-3 cleavage stimulated by 18 h incubation with oxidized LDL were reduced following treatment with these protective flavonoids. The down-regulation of Bcl-2 and up-regulation of caspase-3 activation were reversed by the cytoprotective flavonoids, (-)-epigallocatechin gallate, quercetin and hesperetin, at >/=10 microm. These results suggest that flavonoids may differentially prevent Cu(2+)-oxidized LDL-induced apoptosis and promote cell survival as potent antioxidants. Survival potentials of certain flavonoids against cytotoxic oxidized LDL appeared to stem from their disparate chemical structure. Furthermore, dietary flavonoids may have therapeutic potential for protecting the endothelium from oxidative stress and oxidized LDL-triggered atherogenesis.

  12. Permethrin-induced oxidative stress and toxicity and metabolism. A review.

    Science.gov (United States)

    Wang, Xu; Martínez, María-Aránzazu; Dai, Menghong; Chen, Dongmei; Ares, Irma; Romero, Alejandro; Castellano, Victor; Martínez, Marta; Rodríguez, José Luis; Martínez-Larrañaga, María-Rosa; Anadón, Arturo; Yuan, Zonghui

    2016-08-01

    Permethrin (PER), the most frequently used synthetic Type I pyrethroid insecticide, is widely used in the world because of its high activity as an insecticide and its low mammalian toxicity. It was originally believed that PER exhibited low toxicity on untargeted animals. However, as its use became more extensive worldwide, increasing evidence suggested that PER might have a variety of toxic effects on animals and humans alike, such as neurotoxicity, immunotoxicity, cardiotoxicity, hepatotoxicity, reproductive, genotoxic, and haematotoxic effects, digestive system toxicity, and cytotoxicity. A growing number of studies indicate that oxidative stress played critical roles in the various toxicities associated with PER. To date, almost no review has addressed the toxicity of PER correlated with oxidative stress. The focus of this article is primarily to summarise advances in the research associated with oxidative stress as a potential mechanism for PER-induced toxicity as well as its metabolism. This review summarises the research conducted over the past decade into the reactive oxygen species (ROS) generation and oxidative stress as a consequence of PER treatments, and ultimately their correlation with the toxicity and the metabolism of PER. The metabolism of PER involves various CYP450 enzymes, alcohol or aldehyde dehydrogenases for oxidation and the carboxylesterases for hydrolysis, through which oxidative stress might occur, and such metabolic factors are also reviewed. The protection of a variety of antioxidants against PER-induced toxicity is also discussed, in order to further understand the role of oxidative stress in PER-induced toxicity. This review will throw new light on the critical roles of oxidative stress in PER-induced toxicity, as well as on the blind spots that still exist in the understanding of PER metabolism, the cellular effects in terms of apoptosis and cell signaling pathways, and finally strategies to help to protect against its oxidative

  13. Oxidative stress-induced epigenetic changes associated with malignant transformation of human kidney epithelial cells.

    Science.gov (United States)

    Mahalingaiah, Prathap Kumar S; Ponnusamy, Logeswari; Singh, Kamaleshwar P

    2016-09-17

    Renal Cell Carcinoma (RCC) in humans is positively influenced by oxidative stress status in kidneys. We recently reported that adaptive response to low level of chronic oxidative stress induces malignant transformation of immortalized human renal tubular epithelial cells. Epigenetic alterations in human RCC are well documented, but its role in oxidative stress-induced malignant transformation of kidney cells is not known. Therefore, the objective of this study was to evaluate the potential role of epigenetic changes in chronic oxidative stress-induced malignant transformation of HK-2, human renal tubular epithelial cells. The results revealed aberrant expression of epigenetic regulatory genes involved in DNA methylation (DNMT1, DNMT3a and MBD4) and histone modifications (HDAC1, HMT1 and HAT1) in HK-2 cells malignantly transformed by chronic oxidative stress. Additionally, both in vitro soft agar assay and in vivo nude mice study showing decreased tumorigenic potential of malignantly transformed HK-2 cells following treatment with DNA de-methylating agent 5-aza 2' dC further confirmed the crucial role of DNA hypermethyaltion in oxidative stress-induced malignant transformation. Changes observed in global histone H3 acetylation (H3K9, H3K18, H3K27 and H3K14) and decrease in phospho-H2AX (Ser139) also suggest potential role of histone modifications in increased survival and malignant transformation of HK-2 cells by oxidative stress. In summary, the results of this study suggest that epigenetic reprogramming induced by low levels of oxidative stress act as driver for malignant transformation of kidney epithelial cells. Findings of this study are highly relevant in potential clinical application of epigenetic-based therapeutics for treatments of kidney cancers.

  14. Overweight and Obesity-Induced Oxidative Stress in Children

    Institute of Scientific and Technical Information of China (English)

    YOU-GEN ZHU; SHU-MEI ZHANG; JI-YUE WANG; WEI-QIANG XIAO; XIN-YU WANG; JUN-FU ZHOU

    2006-01-01

    Objective To investigate whether overweight and obesity might cause oxidative stress and potential oxidative damage in overweight and obese children, and to explore its possible mechanism. Methods Eighty-five overweight and obese children(OOC), and eighty-five age-matched healthy children (HC) were recruited in this case-control study. The present study analyzed spectrophotometrically vitamin C (VC), vitamin E (VE), and β-carotene (β-CAR) in plasma, as well as the activities of superoxide dismutase (SOD), catalase (CAT), and the level of malondialdehyde (MDA) in erythrocytes. Results Compared with those of VC, VE, β-CAR, SOD, CAT and MDA in the HC group, the average values of VC, VE, β-CAR, SOD, and CAT in the OOC group were significantly decreased (P<0.001), while the average value of MDA in the OOC group was significantly increased (P<0.001). The regression analysis demonstrated that VC, VE, β-CAR, SOD, and CAT were negatively correlated (P<0.05-0.01), and MDA was positively correlated with BMI (P<0.05). Fitting to the model of multiple stepwise regression of BMI on VC, VE, β-CAR, SOD, CAT, and MDA in 85 OOC was Y = 27.0041 + 0.2541MDA - 2.1448β-CAR - 0.0090CAT, where F =43.8088, P<0.001, r= 0.7866, r2= 0.6187, adjusted r2= 0.6046. The findings from the reliability analysis for VC, VE, β-CAR, SOD, CAT, and MDA used to reflect increased oxidative stress and potential oxidative damage in the OOC showed that the reliability coefficients (alpha, 6 items) = 0.7231, P<0.0001, and that the standardized item alpha = 0.9207, P<0.0001. Conclusion The present study suggests that there exists an increased oxidative stress in overweight and obese children.

  15. Organ damage in zymosan-induced multiple organ dysfunction syndrome in mice is not mediated by inducible nitric oxide synthase.

    NARCIS (Netherlands)

    Volman, T.J.H.; Goris, R.J.A.; Jagt, M. van der; Loo, F.A.J. van de; Hendriks, T.

    2002-01-01

    OBJECTIVE: To examine the role of inducible nitric oxide synthase (iNOS) in the development of the multiple organ dysfunction syndrome (MODS) in a murine model by using either a selective iNOS inhibitor or iNOS knockout mice. DESIGN: Prospective randomized laboratory study. SETTING: Central animal

  16. In vitro investigation of ultrasound-induced oxidative stress on human lens epithelial cells.

    Science.gov (United States)

    Rwei, Patrick; Alex Gong, Cihun-Siyong; Luo, Li-Jyuan; Lin, Meng-Bo; Lai, Jui-Yang; Liu, Hao-Li

    2017-01-22

    The effect of ultrasound exposure on human lens epithelial cells (HLE-B3) was investigated in vitro, specifically on the generation of oxidative stress upon ultrasound application using various clinically-relevant settings. In addition to ultrasound-induced heat effects, oxidative stress has been recently proposed as one of the main mechanisms for ultrasound-induced effects on human cells. In this work, the levels of biocompatibility and generation of oxidative stress by exposure of ultrasound to HLE-B3 were evaluated quantitatively and qualitatively by the MTT assay, Live/Dead assay, reactive oxygen species (ROS) and intracellular calcium level. Oxidative stress induction is traditionally achieved through administrations of H2O2 and thus the administration of H2O2 was used as the positive control group for comparison herein. Concerning the administrations of H2O2 are considered invasive and may potentially have side effects, ultrasound as physical stimulation could be a safer and non-invasive method to induce similar oxidative stress environments. The effect of ultrasound on cell viability and induction of oxidative stress increases with ultrasound intensity. The result reveals that the continuous ultrasound has a positive impact on the oxidative stress levels but does negatively on the cell viability, as compared to the pulsed ultrasound. Furthermore, our work demonstrates that the exposure of 58 kPa continuous ultrasound without microbubbles can maintain acceptable cell viability and produce oxidative stress effects similar to the traditional administrations of H2O2. In summary, exposure of ultrasound can generate oxidative stress comparable to traditional administrations of H2O2. The effect of generating oxidative stress is adjustable through ultrasound parameters, including the pulsed or continuous wave, the intensity of ultrasound and addition of microbubbles.

  17. The effect of HDL-bound and free PON1 on copper-induced LDL oxidation.

    Science.gov (United States)

    Bayrak, Ahmet; Bayrak, Tülin; Bodur, Ebru; Kılınç, Kamer; Demirpençe, Ediz

    2016-09-25

    Oxidative modification of LDL plays an important role in the development of atherosclerosis. High-density lipoprotein (HDL) confers protection against atherosclerosis and the antioxidative properties of paraoxonase 1 (PON1) has been suggested to contribute to this effect of HDL. The PON1 exist in two major polymorphic forms (Q and R), which regulate the concentration and activity of the enzyme and alter its ability to prevent lipid oxidation. However, the association of Q192R polymorphism with PON1's capacity to protect against LDL lipoperoxidation is controversial. The aim of this study was to evaluate the effects of the purified PON1 Q192R and the partially purified HDL-bound PON1 Q192R isoenzymes (HDL-PON1 Q192R) on LDL oxidation, with respect to their arylesterase/homocysteine thiolactonase (HTLase) activities. Cupric ion-induced LDL oxidation was reduced up to 48% by purified PON1 Q192, but only 33% by an equivalent activity of PON1 R192. HDL-PON1 Q192 isoenzyme caused a 65% reduction, whereas HDL-PON1 R192 isoenzyme caused only 46% reduction in copper ion-induced LDL oxidation. These findings reflect the fact that PON1 Q and PON1 R allozymes may have different protective characteristics against LDL oxidation. The protection against LDL oxidation provided by HDL-PON1 Q192R isoenzymes is more prominent than the purified soluble enzymes. Inhibition of the Ca(+2)-dependent PON1 Q192R arylesterase/HTLase by the metal chelator EDTA, did not alter PON1's ability to inhibit LDL oxidation. These studies indicate that the active site involvement of the purified enzyme is not similar to the HDL-bound one, in terms of both PON1 arylesterase/HTLase activity and the protection of LDL from copper ion-induced oxidation. Moreover, PON1's ability to protect LDL from oxidation does not seem to require calcium.

  18. Effect of curcumin on kidney histopathological changes, lipid peroxidation and total antioxidant capacity of serum in sodium arsenite-treated mice.

    Science.gov (United States)

    Momeni, Hamid Reza; Eskandari, Najmeh

    2017-02-01

    Sodium arsenite is an environmental pollutant with the ability to generate free radicals and curcumin acts as a potent antioxidant. This study investigates the effect of curcumin on kidney histopathology, lipid peroxidation and antioxidant capacity of serum in the mice treated with sodium arsenite. Adult male mice were divided into four groups: control, sodium arsenite, curcumin and curcumin+sodium arsenite. The treatments were delivered for 5 weeks. After the treatment period, blood samples were collected and the concentrations of malondialdehyde (MDA) and total antioxidant capacity of serum were determined. Left kidney was dissected, weighed and used for histopathological and histomorphometrical studies. Sodium arsenite-treated mice showed a significant decrease in the diameter of glomerulus and proximal tubule, glomerular area, total antioxidant capacity of serum as well as a significant increase in serum concentration of MDA compared to the control group. However, no significant difference was found in kidney weight, area and diameter of Bowman's capsule as well as the diameter of distal tubule in mice treated with sodium arsenite compared to the control. In curcumin+sodium arsenite group, curcumin significantly reversed the adverse effects of sodium arsenite on the diameter of glomerulus and proximal tubule, glomerular area, total antioxidant capacity of serum and serum concentration of MDA compared to the sodium arsenite group. The application of curcumin alone significantly increased the total antioxidant capacity of serum compared to the control. Curcumin compensated the adverse effects of sodium arsenite on kidney tissue, lipid peroxidation and total antioxidant capacity of serum.

  19. Lewis acid catalysis and Green oxidations: sequential tandem oxidation processes induced by Mn-hyperaccumulating plants.

    Science.gov (United States)

    Escande, Vincent; Renard, Brice-Loïc; Grison, Claude

    2015-04-01

    Among the phytotechnologies used for the reclamation of degraded mining sites, phytoextraction aims to diminish the concentration of polluting elements in contaminated soils. However, the biomass resulting from the phytoextraction processes (highly enriched in polluting elements) is too often considered as a problematic waste. The manganese-enriched biomass derived from native Mn-hyperaccumulating plants of New Caledonia was presented here as a valuable source of metallic elements of high interest in chemical catalysis. The preparation of the catalyst Eco-Mn1 and reagent Eco-Mn2 derived from Grevillea exul exul and Grevillea exul rubiginosa was investigated. Their unusual polymetallic compositions allowed to explore new reactivity of low oxidative state of manganese-Mn(II) for Eco-Mn1 and Mn(IV) for Eco-Mn2. Eco-Mn1 was used as a Lewis acid to catalyze the acetalization/elimination of aldehydes into enol ethers with high yields; a new green and stereoselective synthesis of (-)-isopulegol via the carbonyl-ene cyclization of (+)-citronellal was also performed with Eco-Mn1. Eco-Mn2 was used as a mild oxidative reagent and controlled the oxidation of aliphatic alcohols into aldehydes with quantitative yields. Oxidative cleavage was interestingly noticed when Eco-Mn2 was used in the presence of a polyol. Eco-Mn2 allowed direct oxidative iodination of ketones without using iodine, which is strongly discouraged by new environmental legislations. Finally, the combination of the properties in the Eco-Mn catalysts and reagents gave them an unprecedented potential to perform sequential tandem oxidation processes through new green syntheses of p-cymene from (-)-isopulegol and (+)-citronellal; and a new green synthesis of functionalized pyridines by in situ oxidation of 1,4-dihydropyridines.

  20. Therapeutic role of Cuminum cyminum on ethanol and thermally oxidized sunflower oil induced toxicity.

    Science.gov (United States)

    Aruna, K; Rukkumani, R; Varma, P Suresh; Menon, Venugopal P

    2005-05-01

    Ethanol is one of the most widely used and abused drugs, increasing lipid levels in humans and experimental animals. Heating of oil rich in polyunsaturated fatty acids (PUFA) produces various lipid peroxidative end products that can aggravate the pathological changes produced by ethanol. In the present communication, the effect of Cuminum cyminum was investigated on alcohol and thermally oxidized oil induced hyperlipidaemia. The results showed increased activity of aspartate transaminase (AST), alkaline phosphatase (ALP) and gamma glutamyl transferase (GGT) and increased levels of cholesterol, triglycerides and phospholipids in the plasma of rats given alcohol, thermally oxidized oil and alcohol+thermally oxidized oil when compared with the normal control group. The levels of tissue (liver and kidney) cholesterol and triglycerides were increased significantly in rats groups given alcohol, thermally oxidized oil and alcohol+thermally oxidized oil when compared with the normal control rats. The levels were decreased when cumin was given along with alcohol and thermally oxidized oil. The level of phospholipids decreased significantly in the liver and kidney of groups given alcohol, thermally oxidized oil and alcohol+thermally oridized oil when compared with the normal control rats. The level increased when cumin was administered along with alcohol and thermally oxidized oil. The activity of phospholipase A and C increased significantly in the liver of groups given alcohol, thermally oxidized oil and alcohol+thermally oxidized oil when compared with the normal control rats, whereas the activity was decreased with the cumin treatment. The results obtained indicate that cumin can decrease the lipid levels in alcohol and thermally oxidized oil induced hepatotoxicity.

  1. Arsenic augments the uptake of oxidized LDL by upregulating the expression of lectin-like oxidized LDL receptor in mouse aortic endothelial cells

    Energy Technology Data Exchange (ETDEWEB)

    Hossain, Ekhtear [Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi (Japan); Ota, Akinobu, E-mail: aota@aichi-med-u.ac.jp [Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi (Japan); Karnan, Sivasundaram; Damdindorj, Lkhagvasuren [Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi (Japan); Takahashi, Miyuki [Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi (Japan); Division of Hematology, Department of Internal Medicine, Aichi Medical University School of Medicine, Nagakute, Aichi (Japan); Konishi, Yuko; Konishi, Hiroyuki; Hosokawa, Yoshitaka [Department of Biochemistry, Aichi Medical University School of Medicine, Nagakute, Aichi (Japan)

    2013-12-15

    Although chronic arsenic exposure is a well-known risk factor for cardiovascular diseases, including atherosclerosis, the molecular mechanism underlying arsenic-induced atherosclerosis remains obscure. Therefore, this study aimed to elucidate this molecular mechanism. We examined changes in the mRNA level of the lectin-like oxidized LDL (oxLDL) receptor (LOX-1) in a mouse aortic endothelial cell line, END-D, after sodium arsenite (SA) treatment. SA treatment significantly upregulated LOX-1 mRNA expression; this finding was also verified at the protein expression level. Flow cytometry and fluorescence microscopy analyses showed that the cellular uptake of fluorescence (Dil)-labeled oxLDL was significantly augmented with SA treatment. In addition, an anti-LOX-1 antibody completely abrogated the augmented uptake of Dil-oxLDL. We observed that SA increased the levels of the phosphorylated forms of nuclear factor of kappa light polypeptide gene enhancer in B cells (NF-κB)/p65. SA-induced upregulation of LOX-1 protein expression was clearly prevented by treatment with an antioxidant, N-acetylcysteine (NAC), or an NF-κB inhibitor, caffeic acid phenethylester (CAPE). Furthermore, SA-augmented uptake of Dil-oxLDL was also prevented by treatment with NAC or CAPE. Taken together, our results indicate that arsenic upregulates LOX-1 expression through the reactive oxygen species-mediated NF-κB signaling pathway, followed by augmented cellular oxLDL uptake, thus highlighting a critical role of the aberrant LOX-1 signaling pathway in the pathogenesis of arsenic-induced atherosclerosis. - Highlights: • Sodium arsenite (SA) increases LOX-1 expression in mouse aortic endothelial cells. • SA enhances cellular uptake of oxidized LDL in dose-dependent manner. • SA-induced ROS generation enhances phosphorylation of NF-κB. • SA upregulates LOX-1 expression through ROS-activated NF-κB signaling pathway.

  2. Nivalenol induces oxidative stress and increases deoxynivalenol pro-oxidant effect in intestinal epithelial cells.

    Science.gov (United States)

    Del Regno, Marisanta; Adesso, Simona; Popolo, Ada; Quaroni, Andrea; Autore, Giuseppina; Severino, Lorella; Marzocco, Stefania

    2015-06-01

    Mycotoxins are secondary fungal metabolites often found as contaminants in almost all agricultural commodities worldwide, and the consumption of food or feed contaminated by mycotoxins represents a major risk for human and animal health. Reactive oxygen species are normal products of cellular metabolism. However, disproportionate generation of reactive oxygen species poses a serious problem to bodily homeostasis and causes oxidative tissue damage. In this study we analyzed the effect of two trichothecenes mycotoxins: nivalenol and deoxynivalenol, alone and in combination, on oxidative stress in the non-tumorigenic intestinal epithelial cell line IEC-6. Our results indicate the pro-oxidant nivalenol effect in IEC-6, the stronger pro-oxidant effect of nivalenol when compared to deoxynivalenol and, interestingly, that nivalenol increases deoxynivalenol pro-oxidative effects. Mechanistic studies indicate that the observed effects were mediated by NADPH oxidase, calcium homeostasis alteration, NF-kB and Nrf2 pathways activation and by iNOS and nitrotyrosine formation. The toxicological interaction by nivalenol and deoxynivalenol reported in this study in IEC-6, points out the importance of the toxic effect of these mycotoxins, mostly in combination, further highlighting the risk assessment process of these toxins that are of growing concern. Copyright © 2015 Elsevier Inc. All rights reserved.

  3. Oxidation Degradation of Aqueous Carbofuran Induced by Low Temperature Plasma

    Science.gov (United States)

    Pu, Lumei; Gao, Jinzhang; Hu, Yusen; Liang, Huiguang; Xiao, Wen; Wang, Xingmin

    2008-06-01

    The oxidative degradation of aqueous carbofuran, a heavily used toxic carbamate insecticide by low temperature plasma, was investigated. The results show that the treatment efficiency increases with the increase in initial concentration. Raising the treatment temperature and changing the pH value can result in enhanced degradation of carbofuran in solution. The results also show that low temperature plasma treatment can effectively remove chemical oxygen demand (COD) of carbofuran in the solution.

  4. Oxidation Degradation of Aqueous Carbofuran Induced by Low Temperature Plasma

    Institute of Scientific and Technical Information of China (English)

    PU Lumei; GAO Jinzhang; HU Yusen; LIANG Huiguang; XIAO Wen; WANG Xingmin

    2008-01-01

    The oxidative degradation of aqueous carbofuran, a heavily used toxic carbamate insecticide by low temperature plasma, was investigated. The results show that the treatment efficiency increases with the increase in initial concentration. Raising the treatment temperature and changing the pH value can result in enhanced degradation of carbofuran in solution. The results also show that low temperature plasma treatment can effectively remove chemical oxygen demand (COD) of carbofuran in the solution.

  5. Role of malaria induced oxidative stress on anaemia in pregnancy

    Institute of Scientific and Technical Information of China (English)

    Akanbi OM; Odaibo AB; Olatoregun R; Ademowo AB

    2010-01-01

    Objective:To assess the role of oxidative stress on anaemia in pregnancy.Methods:Blood samples were collected from pregnant and non-pregnant women who came for antenatal clinic and medical check at Comprehensive Health Center, Akungba-Akoko and Iwaro General Hospital in Akoko Area of Ondo State, Nigeria. Thick and thin blood films were prepared and used for malaria parasite counts. Haemoglobin level was determined by colorimetric method using Drabkin's solution. Oxidative status was determined using malondiadelhyde level as an indicator of lipid peroxidation, while ascorbic acid and reduced glutathione levels were measured by standard spectrophotometric methods.Results: Mean parasite density was significantly higher in pregnant women than non-pregnant women (P<0.05). Haemoglobin level was significantly reduced in malaria positive pregnant and non-pregnant women than malaria negative (8.3-10.0 g/dL) (P<0.05). The oxidative status indicated that malondialdehyde(MDA) was significantly increased in pregnant [(2.5±0.7) nmol/mL] than non-pregnant women [(1.8±0.1) nmol/mL] (P<0.05), while Vit C and superoxide dismutase(SOD) levels were significantly reduced in pregnant than non-pregnant women(P<0.05). There was an inverse correlation between Hb and MDA levels in pregnant women studied. Positive correlation was observed between the mean MDA level and parasite density (r = 0.53). The Hb level decreased as the parasite density and MDA level increased in pregnant women.Conclusions:This study shows that oxidative stress, caused by malaria infection could be part of the contributing factors responsible for anaemia in pregnancy.

  6. A STUDY ON HOT-CARRIER-INDUCED GATE OXIDE BREAKDOWN IN PARTIALLY DEPLETED SIMOX MOSFET'S

    Institute of Scientific and Technical Information of China (English)

    Liu Hongxia; Hao Yue; Zhu Jiangang

    2002-01-01

    The hot-carrier-induced oxide regions in the front and back interfaces are systematically studied for partially depleted SOI MOSFET's. The gate oxide properties are investigated for channel hot-carrier effects. The hot-carrier-induced device degradations are analyzed using stress experiments with three typical hot-carrier injection, i.e., the maximum gate current, maximum substrate current and parasitic bipolar transistor action. Experiments show that PMOSFET's degradation is caused by hot carriers injected into the drain side of the gate oxide and the types of trapped hot carrier depend on the bias conditions, and NMOSFET's degradation is caused by hot holes. This paper reports for the first time that the electric characteristics of NMOSFET's and PMOSFET's are significantly different after the gate oxide breakdown, and an extensive discussion of the experimental findings is provided.

  7. A STUDY ON HOT-CARRIER-INDUCED GATE OXIDE BREAKDOWN IN PARTIALLY DEPLETED SIMOX MOSFET'S

    Institute of Scientific and Technical Information of China (English)

    2002-01-01

    The hot-carrier-induced oxide regions in the front and back interfaces are systematic-cally studied for partially depleted SOI MOSFET's .The gate oxide properties are investigated for channel hot-carrier effects.The hot-carrier-induced device degradations are analyzed using stress experiments with three typical hot-carrier injection,i.e.the maximum gate current, maximum substrate current and parasitic bipolaf transistor action.Experiments show that PMOSFET's degradation is caused by hot carriers injected into the drain side of the gate oxide and the types of trapped hot carrier depend on the bias conditions, and NMOSFET's degradation is caused by hot holes.This paper reports for the first time that the electric characteristics of NMOSFET's and PMOSFET's are significantly different after the gate oxide breakdown, and an extensive discussion of the experimental findings is provided.

  8. Lipids and Oxidative Stress Associated with Ethanol-Induced Neurological Damage

    Directory of Open Access Journals (Sweden)

    José A. Hernández

    2016-01-01

    Full Text Available The excessive intake of alcohol is a serious public health problem, especially given the severe damage provoked by chronic or prenatal exposure to alcohol that affects many physiological processes, such as memory, motor function, and cognitive abilities. This damage is related to the ethanol oxidation in the brain. The metabolism of ethanol to acetaldehyde and then to acetate is associated with the production of reactive oxygen species that accentuate the oxidative state of cells. This metabolism of ethanol can induce the oxidation of the fatty acids in phospholipids, and the bioactive aldehydes produced are known to be associated with neurotoxicity and neurodegeneration. As such, here we will review the role of lipids in the neuronal damage induced by ethanol-related oxidative stress and the role that lipids play in the related compensatory or defense mechanisms.

  9. Wet air oxidation induced enhanced biodegradability of distillery effluent.

    Science.gov (United States)

    Malik, S N; Saratchandra, T; Tembhekar, P D; Padoley, K V; Mudliar, S L; Mudliar, S N

    2014-04-01

    The present study reports the feasibility of Wet Air Oxidation (WAO) as a pretreatment option for enhanced biodegradation of complex distillery effluent. Initially, the distillery effluent was pretreated by WAO at different process conditions (pressure, temperature and time) to facilitate enhancement in the biodegradability index (BI = BOD5: COD ratio). The biodegradability of WAO pretreated effluent was evaluated by subjecting it to aerobic biodegradation and anaerobic followed by aerobic biodegradation. Aerobic biodegradation of pretreated effluent with enhanced biodegradability index (BI = 0.4-0.8) showed enhanced COD reduction of up to 67.7%, whereas the untreated effluent (BI = 0.17) indicated poor COD reduction of only 22.5%. Anaerobic followed by aerobic biodegradation of pretreated effluent has shown up to 87.9% COD reduction, while the untreated effluent has shown only 43.1% COD reduction. Bio-kinetic parameters also confirmed the increased rate of bio-oxidation at enhanced BIs. The results indicate that the WAO pretreatment facilitates enhanced bio-oxidation/bio-degradation of complex effluents like the distillery spent wash.

  10. REGULATION OF INDUCIBLE NITRIC OXIDE SYNTHASE IN COLLAGENOUS COLITIS

    DEFF Research Database (Denmark)

    Andresen, Lars

    2004-01-01

    Produktionen af nitrogen oxid og ekspressionen af enzymet, inducerbar nitrogen oxid syntase (iNOS), er markant øget i den inflammerede kolonslimhinde. Kollagen kolit er en inflammatorisk tarmsygdom af ukendt ætiologi, som er karakteriseret klinisk ved kronisk vandig diaré, trods en endoskopisk...... normal slimhinde, og histologisk ved et øget antal lymfocytter og plasmaceller i lamina propria, et fortykket subepitelialt kollagen bånd og et abnormt højt antal intraepiteliale lymfocytter. Ved denne sygdomstilstand er observeret en lige så høj – eller højere – produktion af nitrogen oxid som ved...... patienter med henholdsvis kollagen kolit, ulcerøs kolit (positive kontroller) og funktionel tarmsygdom (negative kontroller) undersøgt. Der fandtes en øget ekspression af iNOS og aktivering af NF-B ved både kollagen kolit og ulcerøs kolit. Da destruktiv, sårdannende betændelse aldrig forekommer ved...

  11. The endogenous nitric oxide mediates selenium-induced phytotoxicity by promoting ROS generation in Brassica rapa.

    Directory of Open Access Journals (Sweden)

    Yi Chen

    Full Text Available Selenium (Se is suggested as an emerging pollutant in agricultural environment because of the increasing anthropogenic release of Se, which in turn results in phytotoxicity. The most common consequence of Se-induced toxicity in plants is oxidative injury, but how Se induces reactive oxygen species (ROS burst remains unclear. In this work, histofluorescent staining was applied to monitor the dynamics of ROS and nitric oxide (NO in the root of Brassica rapa under Se(IV stress. Se(IV-induced faster accumulation of NO than ROS. Both NO and ROS accumulation were positively correlated with Se(IV-induced inhibition of root growth. The NO accumulation was nitrate reductase (NR- and nitric oxide synthase (NOS-dependent while ROS accumulation was NADPH oxidase-dependent. The removal of NO by NR inhibitor, NOS inhibitor, and NO scavenger could alleviate Se(IV-induced expression of Br_Rbohs coding for NADPH oxidase and the following ROS accumulation in roots, which further resulted in the amelioration of Se(IV-induced oxidative injury and growth inhibition. Thus, we proposed that the endogenous NO played a toxic role in B. rapa under Se(IV stress by triggering ROS burst. Such findings can be used to evaluate the toxic effects of Se contamination on crop plants.

  12. Lanthanum Chloride Inhibiting Expression of Inducible Nitric Oxide Synthase in RAW264.7 Macrophages Induced by Lipopolysaccharide

    Institute of Scientific and Technical Information of China (English)

    Guo Fei; Lou Yuanlei; Wang Yang; Xie An; Li Guohui

    2007-01-01

    Nitric oxide (NO) and its reaction products were key players in the pathophysiology of sepsis and shock. The present study was designed to explore the effects of lanthanum chloride (LaCl3) on inducible nitric oxide synthase (iNOS) expression, at both gene and protein levels, in RAW264.7 macrophages induced by Lipopolysaccharide (LPS). Reverse transcription polymerase chain reaction (RT-PCR), immunofluorescence, and western blot were employed to measure iNOS gene expression, localization, and protein expression respectively. NO production in culture supernatants was detected by the nitrate reductase method. The results showed that LaCl3 significantly attenuated the iNOS gene and protein expression, as well as NO production in RAW264.7cells induced by LPS.

  13. Hydrogen Sulfide Induces Oxidative Damage to RNA and DNA in a Sulfide-Tolerant Marine Invertebrate

    OpenAIRE

    Joyner-Matos, Joanna; Predmore, Benjamin L.; Stein, Jenny R.; Leeuwenburgh, Christiaan; Julian, David

    2010-01-01

    Hydrogen sulfide acts as an environmental toxin across a range of concentrations and as a cellular signaling molecule at very low concentrations. Despite its toxicity, many animals, including the mudflat polychaete Glycera dibranchiata, are periodically or continuously exposed to sulfide in their environment. We tested the hypothesis that a broad range of ecologically relevant sulfide concentrations induces oxidative stress and oxidative damage to RNA and DNA in G. dibranchiata. Coelomocytes ...

  14. Isorhamnetin attenuates collagen-induced arthritis via modulating cytokines and oxidative stress in mice

    OpenAIRE

    Wang, Xuewen; Zhong, Wei

    2015-01-01

    Inflammation and oxidative stress were involved in the development and progression of rheumatoid arthritis (RA). Isorhamnetin has anti-inflammatory and anti-oxidative activities, but its effects on RA have not been investigated. In order to observe the possible therapeutic effects of isorhamnetin on RA, we established a collagen-induced arthritis mouse model and treated the animal with isorhamnetin for 3 weeks. Besides, fibroblast-like synoviocytes (FLS) were treated with lipopolysaccharide (...

  15. Spirulina maxima and its effect on antioxidant activity in fructose induced oxidative stress with histopathological observations

    OpenAIRE

    Jarouliya Urmila; Zacharia Anish; Keservani Raj K.; Prasad Godavarthi B.K.S

    2015-01-01

    Diabetes mellitus is a metabolic disorder characterised by hyperglycemia and oxidative stress. The aim of the present study is to explore the antioxidant effect of Spirulina maxima in rat model along with the histopathological observations. Diabetes was induced by feeding 10% fructose solution orally to Wistar rats (n = 6) for 30 days, analysed for plasma blood glucose and the markers of the oxidative stress [catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH) and thiobarbit...

  16. Anti-oxidative effects of Rooibos tea (Aspalathus linearis on immobilization-induced oxidative stress in rat brain.

    Directory of Open Access Journals (Sweden)

    In-Sun Hong

    Full Text Available Exposure to chronic psychological stress may be related to increased reactive oxygen species (ROS or free radicals, and thus, long-term exposure to high levels of oxidative stress may cause the accumulation of oxidative damage and eventually lead to many neurodegenerative diseases. Compared with other organs, the brain appears especially susceptible to excessive oxidative stress due to its high demand for oxygen. In the case of excessive ROS production, endogenous defense mechanisms against ROS may not be sufficient to suppress ROS-associated oxidative damage. Dietary antioxidants have been shown to protect neurons against a variety of experimental neurodegenerative conditions. In particular, Rooibos tea might be a good source of antioxidants due to its larger proportion of polyphenolic compounds. An optimal animal model for stress should show the features of a stress response and should be able to mimic natural stress progression. However, most animal models of stress, such as cold-restraint, electric foot shock, and burn shock, usually involve physical abuse in addition to the psychological aspects of stress. Animals subjected to chronic restraint or immobilization are widely believed to be a convenient and reliable model to mimic psychological stress. Therefore, in the present study, we propose that immobilization-induced oxidative stress was significantly attenuated by treatment with Rooibos tea. This conclusion is demonstrated by Rooibos tea's ability to (i reverse the increase in stress-related metabolites (5-HIAA and FFA, (ii prevent lipid peroxidation (LPO, (iii restore stress-induced protein degradation (PD, (iv regulate glutathione metabolism (GSH and GSH/GSSG ratio, and (v modulate changes in the activities of antioxidant enzymes (SOD and CAT.

  17. Protective role of quercetin on PCBs-induced oxidative stress and apoptosis in hippocampus of adult rats.

    Science.gov (United States)

    Selvakumar, Kandaswamy; Bavithra, Senthamilselvan; Suganthi, Muralidharan; Benson, Chellakan Selvanesan; Elumalai, Perumal; Arunkumar, Ramachandran; Krishnamoorthy, Gunasekaran; Venkataraman, Prabhu; Arunakaran, Jagadeesan

    2012-04-01

    Polychlorinated biphenyls (PCBs) exposure produces neurodegeneration and induces oxidative stress. Neuroprotective role of quercetin, on PCBs induced apoptosis in hippocampus has not yet been studied. The present study is focused to see whether quercetin supplementation precludes against PCBs induced oxidative stress and hippocampal apoptosis. The results have shown that quercetin at 50 mg/kg bwt/30 days has protected oxidative stress in hippocampus of adult male rats. Quercetin, a free radical scavenger decreased the levels of oxidative stress markers in the hippocampus of simultaneous PCB+quercetin treated rats. The pro-apoptotic and anti-apoptotic molecules such as Bad, Bid, Bax and Bcl2 were altered in the hippocampus of experimental animals. PCBs increased the DNA damage and induced neurodegeneration were assessed by histological studies. PCB induced ROS may be linked to increased hippocampal neuronal apoptosis. Quercetin supplementation decreased the neuronal damage and scavenged the free radicals induced by PCBs and protects PCBs induced apoptosis and oxidative stress.

  18. H2 O2-induced higher order chromatin degradation: A novel mechanism of oxidative genotoxicity

    Indian Academy of Sciences (India)

    Gregory W Konat

    2003-02-01

    The genotoxicity of reactive oxygen species (ROS) is well established. The underlying mechanism involves oxidation of DNA by ROS. However, we have recently shown that hydrogen peroxide (H2O2), the major mediator of oxidative stress, can also cause genomic damage indirectly. Thus, H2O2 at pathologically relevant concentrations rapidly induces higher order chromatin degradation (HOCD), i.e. enzymatic excision of chromatin loops and their oligomers at matrix-attachment regions. The activation of endonuclease that catalyzes HOCD is a signalling event triggered specifically by H2O2. The activation is not mediated by an influx of calcium ions, but resting concentrations of intracellular calcium ions are required for the maintenance of the endonuclease in an active form. Although H2O2-induced HOCD can efficiently dismantle the genome leading to cell death, under sublethal oxidative stress conditions H2O2-induced HOCD may be the major source of somatic mutations.

  19. Alpha-tocopherol ameliorates cypermethrin-induced toxicity and oxidative stress in the nematode Caenorhabdtis elegans.

    Science.gov (United States)

    Shashikumar, Shivaiah; Rajini, P S

    2011-06-01

    Oxidative stress and other effects induced by cypermethrin (CYP, 15 mM) and their amelioration by alpha-tocopherol (400 microM) was studied in the nematode Caenorhabditis elegans. The worms exposed for 4 h to CYP showed increased levels of reactive oxygen species (46%), H2O2 (37%) and protein carbonyls (29%), accompanied by decreased lifespan and brood size. However, exposure to both CYP and alpha-tocopherol resulted in diminution of above alterations with the worms exhibiting relatively lower levels of ROS (30%), H2O2 (15%), protein carbonyls (14%), altered antioxidant enzyme activities and normal lifespan and brood size. The results suggest that CYP induces oxidative stress in C. elegans and the strategy of intervention with alpha-tocopherol could be exploited to offset this induced oxidative stress.

  20. Protective effect of bacoside-A against morphine-induced oxidative stress in rats

    Directory of Open Access Journals (Sweden)

    T Sumathi

    2011-01-01

    Full Text Available In the present study, we investigated the protective effect of bacoside-A the active principle isolated from the plant Bacopa monniera against oxidative damage induced by morphine in rat brain. Morphine intoxicated rats received 10-160 mg/kg b.w. of morphine hydrochloride intraperitoneally for 21 days. Bacoside-A pretreated rats were administered with bacoside-A (10 mg/kg b.w/day orally, 2 h before the injection of morphine for 21 days. Pretreatment with bacoside-A has shown to possess a significant protective role against morphine induced brain oxidative damage in the antioxidant status (total reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase and lipid peroxidation and membrane bound ATP-ases(Na + /K + ATPase. Ca 2+ and Mg 2+ ATPases activities in rat. The results of the present study indicate that bacoside-A protects the brain from oxidative stress induced by morphine.

  1. Protective Effect of Bacoside-A against Morphine-Induced Oxidative Stress in Rats.

    Science.gov (United States)

    Sumathi, T; Nathiya, V C; Sakthikumar, M

    2011-07-01

    In the present study, we investigated the protective effect of bacoside-A the active principle isolated from the plant Bacopa monniera against oxidative damage induced by morphine in rat brain. Morphine intoxicated rats received 10-160 mg/kg b.w. of morphine hydrochloride intraperitoneally for 21 days. Bacoside-A pretreated rats were administered with bacoside-A (10 mg/kg b.w/day) orally, 2 h before the injection of morphine for 21 days. Pretreatment with bacoside-A has shown to possess a significant protective role against morphine induced brain oxidative damage in the antioxidant status (total reduced glutathione, superoxide dismutase, catalase, glutathione peroxidase and lipid peroxidation) and membrane bound ATP-ases(Na(+)/K(+)ATPase. Ca(2+) and Mg(2+) ATPases) activities in rat. The results of the present study indicate that bacoside-A protects the brain from oxidative stress induced by morphine.

  2. Sesamin ameliorates oxidative liver injury induced by carbon tetrachloride in rat.

    Science.gov (United States)

    Lv, Dan; Zhu, Chang-Qing; Liu, Li

    2015-01-01

    Sesamin is naturally occurring lignan from sesame oil with putative antioxidant property. The present study was designed to investigate the protective role of sesamin against carbon tetrachloride induced oxidative liver injury. Male Wistar albino rats (180-200 g) were divided in to 5 groups (n=6). Hepatotoxicity was induced by the administration of CCl4 (0.1 ml/100 g bw., 50% v/v with olive oil) intraperitoneally. Sesamin was administered in two different dose (5 and 10 ml/kg bw) to evaluate the hepatoprotective activity. Sesamin significantly reduced the elevated serum liver marker enzymes (Psesamin treated groups shows the amelioration of oxidative stress induced by CCl4. Histopathological report also supported the hepatoprotection offered by sesamin. Sesamin effects in both the dose were in comparable to reference standard drug silymarin. From these above findings it has been concluded that sesamin ameliorate the oxidative liver injury in terms of reduction of lipid peroxidation and enhancement of liver antioxidant enzymes.

  3. Nordihydroguaiaretic Acid Attenuates the Oxidative Stress-Induced Decrease of CD33 Expression in Human Monocytes

    Directory of Open Access Journals (Sweden)

    Silvia Guzmán-Beltrán

    2013-01-01

    Full Text Available Nordihydroguaiaretic acid (NDGA is a natural lignan with recognized antioxidant and beneficial properties that is isolated from Larrea tridentata. In this study, we evaluated the effect of NDGA on the downregulation of oxidant stress-induced CD33 in human monocytes (MNs. Oxidative stress was induced by iodoacetate (IAA or hydrogen peroxide (H2O2 and was evaluated using reactive oxygen species (ROS production, and cell viability. NDGA attenuates toxicity, ROS production and the oxidative stress-induced decrease of CD33 expression secondary to IAA or H2O2 in human MNs. It was also shown that NDGA (20 μM attenuates cell death in the THP-1 cell line that is caused by treatment with either IAA or H2O2. These results suggest that NDGA has a protective effect on CD33 expression, which is associated with its antioxidant activity in human MNs.

  4. Modulation of Hypercholesterolemia-Induced Oxidative/Nitrative Stress in the Heart

    Science.gov (United States)

    Sárközy, Márta; Pipicz, Márton; Dux, László; Csont, Tamás

    2016-01-01

    Hypercholesterolemia is a frequent metabolic disorder associated with increased risk for cardiovascular morbidity and mortality. In addition to its well-known proatherogenic effect, hypercholesterolemia may exert direct effects on the myocardium resulting in contractile dysfunction, aggravated ischemia/reperfusion injury, and diminished stress adaptation. Both preclinical and clinical studies suggested that elevated oxidative and/or nitrative stress plays a key role in cardiac complications induced by hypercholesterolemia. Therefore, modulation of hypercholesterolemia-induced myocardial oxidative/nitrative stress is a feasible approach to prevent or treat deleterious cardiac consequences. In this review, we discuss the effects of various pharmaceuticals, nutraceuticals, some novel potential pharmacological approaches, and physical exercise on hypercholesterolemia-induced oxidative/nitrative stress and subsequent cardiac dysfunction as well as impaired ischemic stress adaptation of the heart in hypercholesterolemia. PMID:26788247

  5. Protective role of erdosteine on vancomycin-induced oxidative stress in rat liver.

    Science.gov (United States)

    Sahin, Mehmet; Cam, Hakan; Olgar, Seref; Tunc, Sevket Ercan; Arslan, Cagatay; Uz, Efkan; Yilmaz, H Ramazan

    2006-10-01

    Drug-induced liver toxicity is a common cause of liver injury. This study was designed to elucidate whether high dose vancomycin (VCM) induces oxidative stress in liver and to investigate the protective effects of erdosteine, an expectorant agent. Twenty-two young Wistar rats were divided into three groups as follows: control group, VCM, and VCM plus erdosteine. VCM was administered intraperitoneally in the dosage of 200 mg/kg twice daily for 7 days. Erdosteine was administered orally administered once a day at a dose of 10 mg/kg body weight. The activities of antioxidant enzymes such as superoxide dismutase and catalase as well as the concentration of malondialdehyde, as an indicator of lipid peroxidation, were measured to evaluate oxidative stress in homogenates of the liver. VCM administration increased malondialdehyde levels (p Erdosteine co-administration with VCM injections caused significantly decreased malondialdehyde levels (p erdosteine may prevent VCM-induced oxidative changes in liver by reducing reactive oxygen species.

  6. Nordihydroguaiaretic acid attenuates the oxidative stress-induced decrease of CD33 expression in human monocytes.

    Science.gov (United States)

    Guzmán-Beltrán, Silvia; Pedraza-Chaverri, José; Gonzalez-Reyes, Susana; Hernández-Sánchez, Fernando; Juarez-Figueroa, Ulises E; Gonzalez, Yolanda; Bobadilla, Karen; Torres, Martha

    2013-01-01

    Nordihydroguaiaretic acid (NDGA) is a natural lignan with recognized antioxidant and beneficial properties that is isolated from Larrea tridentata. In this study, we evaluated the effect of NDGA on the downregulation of oxidant stress-induced CD33 in human monocytes (MNs). Oxidative stress was induced by iodoacetate (IAA) or hydrogen peroxide (H(2)O(2)) and was evaluated using reactive oxygen species (ROS) production, and cell viability. NDGA attenuates toxicity, ROS production and the oxidative stress-induced decrease of CD33 expression secondary to IAA or H(2)O(2) in human MNs. It was also shown that NDGA (20  μ M) attenuates cell death in the THP-1 cell line that is caused by treatment with either IAA or H(2)O(2). These results suggest that NDGA has a protective effect on CD33 expression, which is associated with its antioxidant activity in human MNs.

  7. Application of a novel plasma-induced CD/MWCNT/iron oxide composite in zinc decontamination.

    Science.gov (United States)

    Yang, Shitong; Guo, Zhiqiang; Sheng, Guodong; Wang, Xiangke

    2012-10-01

    Herein, β-cyclodextrin (β-CD) was grafted onto magnetic MWCNT/iron oxide particles by using low temperature plasma-induced technique to synthesize a novel nanocomposite. The prepared composite (denoted as CD/MWCNT/iron oxide) exhibited high magnetic property (saturation magnetization M(s)=37.8 emu/g) and good dispersion property in aqueous solution. Batch experiments were conducted to evaluate the application potential of CD/MWCNT/iron oxide in the decontamination of Zn(II) from aqueous solutions. The sorption amount of Zn(II) on CD/MWCNT/iron oxide was higher than that of Zn(II) on MWCNT/iron oxides and oxidized MWCNTs, indicating that the grafted β-CD could enhance the sorption capacity of CD/MWCNT/iron oxide composite toward Zn(II) by providing multiple hydroxyl functional groups. Due to its high magnetic, CD/MWCNT/iron oxide could be easily separated from aqueous solution with an external magnetic field. Regeneration studies suggested that CD/MWCNT/iron oxide can support long term use as a cost-effective material in sewage treatment with minimum replacement costs.

  8. Protective effects of Asian green vegetables against oxidant induced cytotoxicity

    Institute of Scientific and Technical Information of China (English)

    Peter Rose; Choon Nam Ong; Matt Whiteman

    2005-01-01

    AIM: To evaluate the antioxidant and phase Ⅱ detoxification enzyme inducing ability of green leaf vegetables consumed in Asia.METHODS: The antioxidant properties of six commonly consumed Asian vegetables were determined using the ABTS, DPPH, deoxyribose, PR bleaching and ironascorbate induced lipid peroxidation assay. Induce of phase Ⅱ detoxification enzymes was also determined for each respective vegetable extract. Protection against authentic ONOO- and HOCI mediated cytotoxicity in human colon HCT116 cells was determined using the MTT 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrasodium bromide) viability assay.RESULTS: All of the extracts derived from green leaf vegetables exhibited antioxidant properties, while also having cytoprotective effects against ONOO- and HOCI mediated cytotoxicity. In addition, evaluation of the phase Ⅱ enzyme inducing ability of each extract,as assessed by quinone reductase and glutathioneS-transferase activities, showed significant variation between the vegetables analyzed.CONCLUSION: Green leaf vegetables are potential sources of antioxidants and phase Ⅱ detoxification enzyme inducers in the Asian diet. It is likely that consumption of such vegetables is a major source of beneficial phytochemical constituents that may protect against colonic damage.

  9. Prenatal Exposure to Sodium Arsenite Alters Placental Glucose 1, 3, and 4 Transporters in Balb/c Mice

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    Daniela Sarahí Gutiérrez-Torres

    2015-01-01

    Full Text Available Inorganic arsenic (iAs exposure induces a decrease in glucose type 4 transporter (GLUT4 expression on the adipocyte membrane, which may be related to premature births and low birth weight infants in women exposed to iAs at reproductive age. The aim of this study was to analyze the effect of sodium arsenite (NaAsO2 exposure on GLUT1, GLUT3, and GLUT4 protein expression and on placental morphology. Female Balb/c mice (n=15 were exposed to 0, 12, and 20 ppm of NaAsO2 in drinking water from 8th to 18th day of gestation. Morphological changes and GLUT1, GLUT3, and GLUT4 expression were evaluated in placentas by immunohistochemical and image analysis and correlated with iAs and arsenical species concentration, which were quantified by atomic absorption spectroscopy. NaAsO2 exposure induced a significant decrease in fetal and placental weight (P<0.01 and increases in infarctions and vascular congestion. Whereas GLUT1 expression was unchanged in placentas from exposed group, GLUT3 expression was found increased. In contrast, GLUT4 expression was significantly lower (P<0.05 in placentas from females exposed to 12 ppm. The decrease in placental GLUT4 expression might affect the provision of adequate fetal nutrition and explain the low fetal weight observed in the exposed groups.

  10. Neuroprotective effect of ginger on anti-oxidant enzymes in streptozotocin-induced diabetic rats.

    Science.gov (United States)

    Shanmugam, Kondeti Ramudu; Mallikarjuna, Korivi; Kesireddy, Nishanth; Sathyavelu Reddy, Kesireddy

    2011-04-01

    The aim of the present study was to investigate the effect of ginger on oxidative stress markers in the mitochondrial fractions of cerebral cortex (CC), cerebellum (CB), hippocampus (HC) and hypothalamus (HT) of diabetic rats. Diabetes exacerbates neuronal injury induced by hyperglycemia mediated oxidative damage. A marked decrease in anti-oxidant marker enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), reduced glutathione (GSH) and increase in malondialdehyde (MDA) was observed in the diabetic rats. Decreased activities of anti-oxidant enzymes in diabetic rats were augmented on oral administration of ginger. Moreover, ginger administration depleted the MDA level, which was earlier increased in the diabetic rats. These results suggest that ginger exhibit a neuroprotective effect by accelerating brain anti-oxidant defense mechanisms and down regulating the MDA levels to the normal levels in the diabetic rats. Thus, ginger may be used as therapeutic agent in preventing complications in diabetic patients.

  11. Genetically Engineering Bacillus subtilis with a Heat-Resistant Arsenite Methyltransferase for Bioremediation of Arsenic-Contaminated Organic Waste.

    Science.gov (United States)

    Huang, Ke; Chen, Chuan; Shen, Qirong; Rosen, Barry P; Zhao, Fang-Jie

    2015-10-01

    Organic manures may contain high levels of arsenic (As) due to the use of As-containing growth-promoting substances in animal feed. To develop a bioremediation strategy to remove As from organic waste, Bacillus subtilis 168, a bacterial strain which can grow at high temperature but is unable to methylate and volatilize As, was genetically engineered to express the arsenite S-adenosylmethionine methyltransferase gene (CmarsM) from the thermophilic alga Cyanidioschyzon merolae. The genetically engineered B. subtilis 168 converted most of the inorganic As in the medium into dimethylarsenate and trimethylarsine oxide within 48 h and volatized substantial amounts of dimethylarsine and trimethylarsine. The rate of As methylation and volatilization increased with temperature from 37 to 50°C. When inoculated into an As-contaminated organic manure composted at 50°C, the modified strain significantly enhanced As volatilization. This study provides a proof of concept of using genetically engineered microorganisms for bioremediation of As-contaminated organic waste during composting.

  12. Green tea polyphenols protect spinal cord neurons against hydrogen peroxide-induced oxidative stress

    Institute of Scientific and Technical Information of China (English)

    Jianbo Zhao; Shiqiang Fang; Yajiang Yuan; Zhanpeng Guo; Jinhao Zeng; Yue Guo; Peifu Tang; Xifan Mei

    2014-01-01

    Green tea polyphenols are strong antioxidants and can reduce free radical damage. To investigate their neuroprotective potential, we induced oxidative damage in spinal cord neurons using hy-drogen peroxide, and applied different concentrations (50-200 µg/mL) of green tea polyphenol to the cell medium for 24 hours. Measurements of superoxide dismutase activity, malondial-dehyde content, and expression of apoptosis-related genes and proteins revealed that green tea polyphenol effectively alleviated oxidative stress. Our results indicate that green tea polyphenols play a protective role in spinal cord neurons under oxidative stress.

  13. Modification of radiation-induced oxidative damage in liposomal and microsomal membrane by eugenol

    Energy Technology Data Exchange (ETDEWEB)

    Pandey, B.N. [Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Mumbai 400 085 (India); Lathika, K.M. [Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Mumbai 400 085 (India); Mishra, K.P. [Radiation Biology and Health Sciences Division, Bhabha Atomic Research Centre, Mumbai 400 085 (India)]. E-mail: kpm@magnum.barc.ernet.in

    2006-03-15

    Radiation-induced membrane oxidative damage, and their modification by eugenol, a natural antioxidant, was investigated in liposomes and microsomes. Liposomes prepared with DPH showed decrease in fluorescence after {gamma}-irradiation, which was prevented significantly by eugenol and correlated with magnitude of oxidation of phospholipids. Presence of eugenol resulted in substantial inhibition in MDA formation in irradiated liposomes/microsomes, which was less effective when added after irradiation. Similarly, the increase in phospholipase C activity observed after irradiation i