Atorvastatin protected from paraquat-induced cytotoxicity in alveolar macrophages via down-regulation of TLR-4

NARCIS (Netherlands)

Alizadeh-Tabrizi, Nazli; Malekinejad, Hassan; Varasteh, Soheil; Cheraghi, Hadi

2017-01-01

The current study designed to clarify the mechanism of paraquat-induced cytotoxicity and protective effects of Atorvastatin on freshly isolated alveolar macrophages (AMs). AMs were collected via bronchoalveolar lavage and exposed to various concentrations of paraquat in the presence and absence of

Protective effects of exogenous β-hydroxybutyrate on paraquat toxicity in rat kidney

Energy Technology Data Exchange (ETDEWEB)

Wei, Teng; Tian, Wulin; Liu, Fangning; Xie, Guanghong, E-mail: xiegh@jlu.edu.cn

2014-05-16

Highlights: • β-Hydroxybutyrate inhibits paraquat-induced toxicity in rat kidney. • β-Hydroxybutyrate inhibits lipid peroxidation and caspase-mediated apoptosis. • β-Hydroxybutyrate increases the activities of SOD and CAT. • The study describes a novel finding for the renoprotective ability of β-hydroxybutyrate. - Abstract: In this study, we demonstrated the protective effects of β-hydroxybutyrate (β-HB) against paraquat (PQ)-induced kidney injury and elucidated the underlying molecular mechanisms. By histological examination and renal dysfunction specific markers (serum BUN and creatinine) assay, β-HB could protect the PQ-induced kidney injury in rat. PQ-induced kidney injury is associated with oxidative stress, which was measured by increased lipid peroxidation (MDA) and decreased intracellular anti-oxidative abilities (SOD, CAT and GSH). β-HB pretreatment significantly attenuated that. Caspase-mediated apoptosis pathway contributed importantly to PQ toxicity, as revealed by the activation of caspase-9/-3, cleavage of PARP, and regulation of Bcl-2 and Bax, which were also effectively blocked by β-HB. Moreover, treatment of PQ strongly decreased the nuclear Nrf2 levels. However, pre-treatment with β-HB effectively suppressed this action of PQ. This may imply the important role of β-HB on Nrf2 pathway. Taken together, this study provides a novel finding that β-HB has a renoprotective ability against paraquat-induced kidney injury.

Thirty-five cases of S-carboxymethylcysteine use in paraquat poisoning.

Science.gov (United States)

Lugo-Vallín, Nelly; Maradei-Irastorza, Idania; Pascuzzo-Lima, Carmine; Ramírez-Sánchez, Manuel; Montesinos, Claudia

2003-02-01

The herbicide paraquat is associated with a high mortality rate. It produces multiorgan damage through the induction of acute oxidative stress, by generation of reactive oxygen species that cause oxidative damage to biomolecules. In addition to general supportive measures, the management of paraquat poisoning includes gastric washing, forced diuresis, haemodialysis and the use of antioxidants, such as N-acetylcysteine. However, this drug is rather unavailable in Venezuela and S-carboxymethylcysteine has been used. We report 35 patients with mild to severe paraquat poisoning, which beside standard supportive treatment received 1500 mg S-carboxymethylcysteine, up to 2-3 w. The mortality rate was 22.86% (8 deaths/35 cases) and was related to the severity of paraquat poisoning (as assessed by urine dithionite tests). We conclude that S-carboxymethylcysteine is a reliable alternative in managing patients with paraquat poisoning.

DNA damage in grasshopper Chorthippus brunneus (Orthoptera) hatchlings following paraquat exposure.

Science.gov (United States)

Augustyniak, M; Nocoń, Ł; Kędziorski, A; Łaszczyca, P; Sawczyn, T; Tarnawska, M; Zawisza-Raszka, A

2015-04-01

Comet assay was applied to study genotoxic damage induced by paraquat (PQ) in brain cells of Chorthippus brunneus (Insecta: Orthoptera) hatchlings. Percentage of the comet fluorescence in the tail (TDNA), length of the comet tail (TL) and Olive tail moment (OTM) were used for quantitative assessment of the DNA damage. Multiple regression analysis supplemented standard statistical elaboration of the results. Increasing PQ concentrations applied either directly to the brain cells suspension (10, 50, and 250 μM PQ final concentration--in vitro protocol) or indirectly (50, 250, and 1250 μM PQ final concentration--in vivo protocol) provoked significant increase of oxidative damage to DNA (higher median TDNA and OTM values). The damage increased with time of exposure (0, 5, 15, and 30 min) following in vitro application, but decreased in longer interval (3 vs 24 h) after in vivo administration of paraquat. On contrary, median TL values did not correlate with paraquat concentration irrespectively of the exposure protocol. Possible reason of this discrepancy in light of paraquat toxicity is discussed. Copyright © 2015 Elsevier Ltd. All rights reserved.

Compensatory role of the Nrf2–ARE pathway against paraquat toxicity: Relevance of 26S proteasome activity

Directory of Open Access Journals (Sweden)

Yasuhiko Izumi

2015-11-01

Full Text Available Oxidative stress and the ubiquitin–proteasome system play a key role in the pathogenesis of Parkinson disease. Although the herbicide paraquat is an environmental factor that is involved in the etiology of Parkinson disease, the role of 26S proteasome in paraquat toxicity remains to be determined. Using PC12 cells overexpressing a fluorescent protein fused to the proteasome degradation signal, we report here that paraquat yielded an inhibitory effect on 26S proteasome activity without an obvious decline in 20S proteasome activity. Relative low concentrations of proteasome inhibitors caused the accumulation of nuclear factor erythroid 2-related factor 2 (Nrf2, which is targeted to the ubiquitin–proteasome system, and activated the antioxidant response element (ARE-dependent transcription. Paraquat also upregulated the protein level of Nrf2 without increased expression of Nrf2 mRNA, and activated the Nrf2–ARE pathway. Consequently, paraquat induced expression of Nrf2-dependent ARE-driven genes, such as γ-glutamylcysteine synthetase, catalase, and hemeoxygenase-1. Knockdown of Nrf2 or inhibition of γ-glutamylcysteine synthetase and catalase exacerbated paraquat-induced toxicity, whereas suppression of hemeoxygenase-1 did not. These data indicate that the compensatory activation of the Nrf2–ARE pathway via inhibition of 26S proteasome serves as part of a cellular defense mechanism to protect against paraquat toxicity.

Edaravone Decreases Paraquat Toxicity in A549 Cells and Lung Isolated Mitochondria

OpenAIRE

Shokrzadeh, Mohammad; Shaki, Fatemeh; Mohammadi, Ebrahim; Rezagholizadeh, Neda; Ebrahimi, Fatemeh

2014-01-01

Edaravone, an antioxidant and radical scavenger, showed protective effects against oxidative stress-like condition. Paraquat (PQ) is toxic herbicide considerable evidence suggests that oxidative stress and mitochondrial dysfunction contribute to PQ toxicity. In this study, protective effect of edaravone against PQ induced toxicity and reactive oxygen species (ROS) generation in A549 cells and lung isolated mitochondria were evaluated. A549 cells and lung isolated mitochondria were divided int...

Effect of paraquat-induced oxidative stress on gene expression and aging of the filamentous ascomycete Podospora anserina

Directory of Open Access Journals (Sweden)

Matthias Wiemer

2014-06-01

Full Text Available Aging of biological systems is influenced by various factors, conditions and processes. Among others, processes allowing organisms to deal with various types of stress are of key importance. In particular, oxidative stress as the result of the generation of reactive oxygen species (ROS at the mitochondrial respiratory chain and the accumulation of ROS-induced molecular damage has been strongly linked to aging. Here we view the impact of ROS from a different angle: their role in the control of gene expression. We report a genome-wide transcriptome analysis of the fungal aging model Podospora anserina grown on medium containing paraquat (PQ. This treatment leads to an increased cellular generation and release of H2O2, a reduced growth rate, and a decrease in lifespan. The combined challenge by PQ and copper has a synergistic negative effect on growth and lifespan. The data from the transcriptome analysis of the wild type cultivated under PQ-stress and their comparison to those of a longitudinal aging study as well as of a copper-uptake longevity mutant of P. anserina revealed that PQ-stress leads to the up-regulation of transcripts coding for components involved in mitochondrial remodeling. PQ also affects the expression of copper-regulated genes suggesting an increase of cytoplasmic copper levels as it has been demonstrated earlier to occur during aging of P. anserina and during senescence of human fibroblasts. This effect may result from the induction of the mitochondrial permeability transition pore via PQ-induced ROS, leading to programmed cell death as part of an evolutionary conserved mechanism involved in biological aging and lifespan control.

Paraquat, but not maneb, induces synucleinopathy and tauopathy in striata of mice through inhibition of proteasomal and autophagic pathways.

Directory of Open Access Journals (Sweden)

Jonathan Wills

Full Text Available SNCA and MAPT genes and environmental factors are important risk factors of Parkinson's disease [PD], the second-most common neurodegenerative disease. The agrichemicals maneb and paraquat selectively target dopaminergic neurons, leading to parkinsonism, through ill-defined mechanisms. In the current studies we have analyzed the ability of maneb and paraquat, separately and together, to induce synucleinopathy and tauopathy in wild type mice. Maneb was ineffective in increasing α-synuclein [α-Syn] or p-Tau levels. By contrast, paraquat treatment of mice resulted in robust accumulation of α-Syn and hyperphosphorylation of Tau in striata, through activation of p-GSK-3β, a major Tau kinase. Co-treatment with maneb did not enhance the effects of paraquat. Increased hyperacetylation of α-tubulin was observed in paraquat-treated mice, suggesting cytoskeleton remodeling. Paraquat, but not maneb, inhibited soluble proteasomal activity on a peptide substrate but this was not associated with a decreased expression of 26S proteasome subunits. Both paraquat and maneb treatments increased levels of the autophagy inhibitor, mammalian target of rapamycin, mTOR, suggesting impaired axonal autophagy, despite increases in certain autophagic proteins, such as beclin 1 and Agt12. Autophagic flux was also impaired, as ratios of LC3 II to LC3 I were reduced in treated animals. Increased mTOR was also observed in postmortem human PD striata, where there was a reduction in the LC3 II to LC3 I ratio. Heat shock proteins were either increased or unchanged upon paraquat-treatment suggesting that chaperone-mediated autophagy is not hampered by the agrichemicals. These studies provide novel insight into the mechanisms of action of these agrichemicals, which indicate that paraquat is much more toxic than maneb, via its inhibitory effects on proteasomes and autophagy, which lead to accumulation of α-Syn and p-Tau.

Metabolomic Analysis Provides Insights on Paraquat-Induced Parkinson-Like Symptoms in Drosophila melanogaster.

Science.gov (United States)

Shukla, Arvind Kumar; Ratnasekhar, Ch; Pragya, Prakash; Chaouhan, Hitesh Singh; Patel, Devendra Kumar; Chowdhuri, Debapratim Kar; Mudiam, Mohana Krishna Reddy

2016-01-01

Paraquat (PQ) exposure causes degeneration of the dopaminergic neurons in an exposed organism while altered metabolism has a role in various neurodegenerative disorders. Therefore, the study presented here was conceived to depict the role of altered metabolism in PQ-induced Parkinson-like symptoms and to explore Drosophila as a potential model organism for such studies. Metabolic profile was generated in control and in flies that were fed PQ (5, 10, and 20 mM) in the diet for 12 and 24 h concurrent with assessment of indices of oxidative stress, dopaminergic neurodegeneration, and behavioral alteration. PQ was found to significantly alter 24 metabolites belonging to different biological pathways along with significant alterations in the above indices. In addition, PQ attenuated brain dopamine content in the exposed organism. The study demonstrates that PQ-induced alteration in the metabolites leads to oxidative stress and neurodegeneration in the exposed organism along with movement disorder, a phenotype typical of Parkinson-like symptoms. The study is relevant in the context of Drosophila and humans because similar alteration in the metabolic pathways has been observed in both PQ-exposed Drosophila and in postmortem samples of patients with Parkinsonism. Furthermore, this study provides advocacy towards the applicability of Drosophila as an alternate model organism for pre-screening of environmental chemicals for their neurodegenerative potential with altered metabolism.

Salvianolic acid B protects against paraquat-induced pulmonary injury by mediating Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling

Energy Technology Data Exchange (ETDEWEB)

Liu, Bin, E-mail: iamicehe@163.com [Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Logistic University of Chinese People' s Armed Police Force, Tianjin 300162 (China); Cao, Bo, E-mail: caobo19814@126.com [Logistics University of Chinese People' s Armed Police Force, Tianjin 300162 (China); Tianjin Key Laboratory of Cardiovascular Remodeling and Target Organ Injury, Tianjin, 300162 (China); Zhang, Di, E-mail: zhangdibad@163.com [Department of Otorhinolaryngology Head and Neck Surgery, Institute of Otorhinolaryngology, Tianjin First Center Hospital, Tianjin 300192 (China); Xiao, Na [Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Logistic University of Chinese People' s Armed Police Force, Tianjin 300162 (China); Chen, Hong [Logistics University of Chinese People' s Armed Police Force, Tianjin 300162 (China); Li, Guo-qiang; Peng, Shou-chun [Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Logistic University of Chinese People' s Armed Police Force, Tianjin 300162 (China); Wei, Lu-qing, E-mail: luqing-wei@163.com [Department of Respiratory and Critical Care Medicine, Affiliated Hospital of Logistic University of Chinese People' s Armed Police Force, Tianjin 300162 (China)

2016-10-15

The present study was aimed at exploring the protective effects of Salvianolic acid B (SalB) against paraquat (PQ)-induced lung injury in mice. Lung fibrotic injuries were induced in mice by a single intragastrical administration of 300 mg/kg PQ, then the mice were administrated with 200 mg/kg, 400 mg/kg SalB, 100 mg/kg vitamin C (Vit C) and dexamethasone (DXM) for 14 days. PQ-triggered structure distortion, collagen overproduction, excessive inflammatory infiltration, pro-inflammatory cytokine release, and oxidative stress damages in lung tissues and mortality of mice were attenuated by SalB in a dose-dependent manner. Furthermore, SalB was noted to enhance the expression and nuclear translocation of nuclear factor erythroid 2–related factor 2 (Nrf2) and reduce expression of the reactive oxygen species-generating enzyme Nox4 [NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase-4]. SalB also inhibited the increasing expression of transforming growth factor (TGF)-β1 and the phosphorylation of its downstream target Smad3 which were enhanced by PQ. These results suggest that SalB may exert protective effects against PQ-induced lung injury and pulmonary fibrosis. Its mechanisms involve the mediation of Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling. - Highlights: • Salvianolic acid B (SalB) reduced Paraquat-induced mortality and pulmonary injury in mice. • SalB has anti-oxidation, anti-inflammatory and anti-fibrogenic effects simultaneously. • Its mechanisms were targeting Nrf2-Nox4 redox balance and TGF-β1/Smad3 signaling.

Salvianolic acid B protects against paraquat-induced pulmonary injury by mediating Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling

International Nuclear Information System (INIS)

Liu, Bin; Cao, Bo; Zhang, Di; Xiao, Na; Chen, Hong; Li, Guo-qiang; Peng, Shou-chun; Wei, Lu-qing

2016-01-01

The present study was aimed at exploring the protective effects of Salvianolic acid B (SalB) against paraquat (PQ)-induced lung injury in mice. Lung fibrotic injuries were induced in mice by a single intragastrical administration of 300 mg/kg PQ, then the mice were administrated with 200 mg/kg, 400 mg/kg SalB, 100 mg/kg vitamin C (Vit C) and dexamethasone (DXM) for 14 days. PQ-triggered structure distortion, collagen overproduction, excessive inflammatory infiltration, pro-inflammatory cytokine release, and oxidative stress damages in lung tissues and mortality of mice were attenuated by SalB in a dose-dependent manner. Furthermore, SalB was noted to enhance the expression and nuclear translocation of nuclear factor erythroid 2–related factor 2 (Nrf2) and reduce expression of the reactive oxygen species-generating enzyme Nox4 [NADPH (reduced form of nicotinamide adenine dinucleotide phosphate) oxidase-4]. SalB also inhibited the increasing expression of transforming growth factor (TGF)-β1 and the phosphorylation of its downstream target Smad3 which were enhanced by PQ. These results suggest that SalB may exert protective effects against PQ-induced lung injury and pulmonary fibrosis. Its mechanisms involve the mediation of Nrf2/Nox4 redox balance and TGF-β1/Smad3 signaling. - Highlights: • Salvianolic acid B (SalB) reduced Paraquat-induced mortality and pulmonary injury in mice. • SalB has anti-oxidation, anti-inflammatory and anti-fibrogenic effects simultaneously. • Its mechanisms were targeting Nrf2-Nox4 redox balance and TGF-β1/Smad3 signaling.

Binding of paraquat to cell walls of paraquat resistant and susceptible biotypes of Hordeum glaucum

International Nuclear Information System (INIS)

Alizadeh, H.M.; Preston, C.; Powles, S.B.

1997-01-01

Full text: Paraquat is a widely used, non-selective, light activated contact herbicide acting as a photosystem electron acceptor. Resistance to paraquat in weed species has occurred in Australia and world-wide following extensive use of this herbicide. The mechanism of resistance to paraquat in 'Hordeum glaucum' is correlated with reduced herbicide translocation and may be due to sequestration of herbicide away from its site of action by either binding to cell walls or other means. We measured paraquat binding to a cell wall fraction in resistant and susceptible biotypes of H. glaucum to determine whether differences in binding of paraquat to cell walls could explain herbicide resistance. The cell wall fraction was isolated from leaves of resistant and susceptible biotypes and incubated with 14 C-labelled paraquat. Of the total paraquat - absorbed by a cell wall preparation, about 80% remains strongly bind to the cell wall and doesn't readily exchange with solution in the absence of divalent cations. Divalent cations (Ca 2+ ,putrescine and paraquat) can competitively exchange for paraquat tightly bound to the cell wall. From kinetic experiments it seems that there are two types of binding sites in the cell wall with different affinities for paraquat. No significant differences between cell wall, characteristics of resistant and susceptible biotypes of H. glaucum have been found in any of our experiments. Therefore, increased binding of paraquat to the cell wall appears not to be a mechanism for exclusion of paraquat in resistant biotype

Paraquat and maneb co-exposure induces noradrenergic locus coeruleus neurodegeneration through NADPH oxidase-mediated microglial activation

International Nuclear Information System (INIS)

Hou, Liyan; Zhang, Cong; Wang, Ke; Liu, Xiaofang; Wang, Hongwei; Che, Yuning; Sun, Fuqiang; Zhou, Xueying; Zhao, Xiulan; Wang, Qingshan

2017-01-01

Highlights: • Microglial activation induced by paraquat and maneb precedes noradrenergic neurodegeneration in locus coeruleus. • NADPH oxidase activation contributes to microglia-mediated neuroinflammation and related noradrenergic neurodegeneration. • Inhibition of NADPH oxidase by apocynin protects noradrenergic neurons against paraquat and maneb-induced toxicity. - Abstract: Co-exposure to paraquat (PQ) and maneb (Mb) has been shown to increase the risk of Parkinson’s disease (PD) and dopaminergic (DA) neurodegeneration in the substantia nigra pars compacta (SNpc) is observed in PQ and Mb-treated experimental animals. The loss of noradrenergic locus coeruleus (LC/NE) neurons in brainstem is a common feature shared by multiple neurodegenerative diseases, including PD. However, whether PQ and Mb is able to damage LC/NE neurons remains undefined. In this study, mice treated with combined PQ and Mb displayed progressive LC/NE neurodegeneration. Time course studies revealed that the activation of microglia preceded LC/NE neurodegeneration. Mechanistically, the activation of NADPH oxidase contributed to microglial activation and subsequent LC/NE neurodegeneration. We found that PQ and Mb co-exposure induced activation of NADPH oxidase as shown by increased superoxide production and membrane translocation of p47 phox , a cytosolic subunit of NADPH oxidase. Inhibition of NADPH oxidase by apocynin, a widely used NADPH oxidase inhibitor, suppressed microglial activation and gene expressions of proinflammatory factors. Furthermore, reduced activation of nuclear factor-κB (NF-κB) pathway was observed in apocynin-treated mice. More importantly, inhibition of NADPH oxidase by apocynin afforded LC/NE neuroprotection against PQ and Mb-induced neurotoxicity. Thus, our findings revealed the critical role NADPH oxidase-mediated microglial activation in driving LC/NE neurodegeneration induced by PQ and Mb, providing new insights into the pathogenesis of environmental

PARAQUAT TOLERANCE3 Is an E3 Ligase That Switches off Activated Oxidative Response by Targeting Histone-Modifying PROTEIN METHYLTRANSFERASE4b.

Directory of Open Access Journals (Sweden)

Chao Luo

2016-09-01

Full Text Available Oxidative stress is unavoidable for aerobic organisms. When abiotic and biotic stresses are encountered, oxidative damage could occur in cells. To avoid this damage, defense mechanisms must be timely and efficiently modulated. While the response to oxidative stress has been extensively studied in plants, little is known about how the activated response is switched off when oxidative stress is diminished. By studying Arabidopsis mutant paraquat tolerance3, we identified the genetic locus PARAQUAT TOLERANCE3 (PQT3 as a major negative regulator of oxidative stress tolerance. PQT3, encoding an E3 ubiquitin ligase, is rapidly down-regulated by oxidative stress. PQT3 has E3 ubiquitin ligase activity in ubiquitination assay. Subsequently, we identified PRMT4b as a PQT3-interacting protein. By histone methylation, PRMT4b upregulates the expression of APX1 and GPX1, encoding two key enzymes against oxidative stress. On the other hand, PRMT4b is recognized by PQT3 for targeted degradation via 26S proteasome. Therefore, we have identified PQT3 as an E3 ligase that acts as a negative regulator of activated response to oxidative stress and found that histone modification by PRMT4b at APX1 and GPX1 loci plays an important role in oxidative stress tolerance.

Mitigating effects of pollen during paraquat exposure on gene expression and pathogen prevalence in Apis mellifera L.

Science.gov (United States)

de Mattos, Igor Medici; Soares, Ademilson E E; Tarpy, David R

2018-01-01

Honey bee (Apis mellifera L.) populations have been experiencing notable mortality in Europe and North America. No single cause has been identified for these dramatic losses, but rather multiple interacting factors are likely responsible (such as pesticides, malnutrition, habitat loss, and pathogens). Paraquat is one of the most widely used non-selective herbicides, especially in developing countries. This herbicide is considered slightly toxic to honey bees, despite being reported as a highly effective inducer of oxidative stress in a wide range of living systems. Here, we test the effects of paraquat on the expression of detoxification and antioxidant-related genes, as well as on the dynamics of pathogen titers. Moreover, we tested the effects of pollen as mitigating factor to paraquat exposure. Our results show significant changes in the expression of several antioxidant-related and detoxification-related genes in the presence of paraquat, as well as an increase of pathogens titers. Finally, we demonstrate a mitigating effect of pollen through the up-regulation of specific genes and improvement of survival of bees exposed to paraquat. The presence of pollen in the diet was also correlated with a reduced prevalence of Nosema and viral pathogens. We discuss the importance of honey bees' nutrition, especially the availability of pollen, on colony losses chronically reported in the USA and Europe.

Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure

OpenAIRE

Tang, Suk Peng; Kuttulebbai Nainamohamed Salam, Sirajudeen; Jaafar, Hasnan; Gan, Siew Hua; Muzaimi, Mustapha; Sulaiman, Siti Amrah

2017-01-01

Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2?mL/kg/day), Tualang honey (1.0?g/kg/day), or ubiquinol (0.2?g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were i...

Paraquat and psychological stressor interactions as pertains to Parkinsonian co-morbidity

Directory of Open Access Journals (Sweden)

Chris Rudyk

2015-01-01

Full Text Available A number of epidemiological and experimental studies have implicated the non-selective herbicide, paraquat, in the development of sporadic Parkinson's disease (PD. While preclinical research has focused mainly on elucidating the nigrostriatal effects of paraquat, relatively little data are available concerning non-motor brain systems and inflammatory immune processes (which have been implicated in PD. Hence, in the present study, we sought to take a multi-system approach to characterize the influence of paraquat upon extra-nigrostriatal brain regions, as well ascertain whether the impact of the pesticide might be enhanced in the context of chronic intermittent stressor exposure. Our findings support the contention that paraquat itself acted as a systemic stressor, with the pesticide increasing plasma corticosterone, as well as altering neurochemical activity in the locus coeruleus, paraventricular nucleus of the hypothalamus, nucleus accumbens, dorsal striatum, and central amygdala. However, with the important exception striatal dopamine turnover, the stressor treatment did not further augment these effects. Additionally, paraquat altered inter-cytokine correlations and, to a lesser extent, circulating cytokine levels, and concomitant stress exposure modulated some of these effects. Finally, paraquat provoked significant (albeit modest reductions of sucrose preference and weight gain, hinting at possible anhendonic-like or sickness responses. These data suggest that, in addition to being a well known oxidative stress generator, paraquat can act as a systemic stressor affecting hormonal and neurochemical activity, but largely not interacting with a concomitant stressor regimen.

77 FR 47539 - Paraquat Dichloride; Pesticide Tolerances

Science.gov (United States)

2012-08-09

... effects of paraquat. The effects of paraquat in lungs are considered systemic effects. There are no dermal toxicity studies suitable for evaluation of systemic lung effects in the toxicity database for paraquat... (PAM) Vol. II, is available for enforcing tolerances for residues of paraquat in/on plant commodities...

An assessment of the role of redox cycling in mediating the toxicity of paraquat and nitrofurantoin

Energy Technology Data Exchange (ETDEWEB)

Adam, A.; Cohen, G.M. (Univ. of London (England)); Smith, L.L. (Imperial Chemical Industries plc, Cheshire (England))

1990-04-01

The abilities of paraquat, diquat, and nitrofurantoin to undergo cyclic oxidation and reduction with rat microsomal systems have been assessed and compared to that of the potent redox cycler, menadione. Diquat and menadione were found to be potent redox cyclers with comparable abilities to elicit a nonstoichiometric increase in both the consumption of O{sub 2} and the oxidation of NADPH, compared to the amounts of substrate added. In contrast, paraquat and nitrofurantoin redox cycled poorly, being an order of magnitude less potent than either diquat or menadione. This was reflected in kinetic studies using lung and liver microsomes. In order to assess redox cycling of the substrates in an intact lung system, the O{sub 2} consumption of rat lung slices was measured in the presence of all four compounds. A small increase in lung slice O{sub 2} uptake was observed with paraquat in the first 2.5 hr of incubation, possibly because of redox cycling of a high intracellular concentration of paraquat resulting from active accumulation into target cells. This stimulation in O{sub 2} uptake was no longer observed when slices were incubated for a longer period or with higher paraquat concentrations (10{sup {minus}4}M), possibly because of toxic effects in target cells. These results together with the poor ability to redox cycle with microsomes and the absence of a specific uptake system highlight the problem of associating redox cycling and oxidative stress in the mechanism of nitrofurantoin toxicity.

Mucuna pruriens seed extract reduces oxidative stress in nigrostriatal tissue and improves neurobehavioral activity in paraquat-induced Parkinsonian mouse model.

Science.gov (United States)

Yadav, Satyndra Kumar; Prakash, Jay; Chouhan, Shikha; Singh, Surya Pratap

2013-06-01

Parkinson's disease (PD) is a neurodegenerative disease which causes rigidity, resting tremor and postural instability. Treatment for this disease is still under investigation. Mucuna pruriens (L.), is a traditional herbal medicine, used in India since 1500 B.C., as a neuroprotective agent. In this present study, we evaluated the therapeutic effects of aqueous extract of M. pruriens (Mp) seed in Parkinsonian mouse model developed by chronic exposure to paraquat (PQ). Results of our study revealed that the nigrostriatal portion of Parkinsonian mouse brain showed significantly increased levels of nitrite, malondialdehyde (MDA) and reduced levels of catalase compared to the control. In the Parkinsonian mice hanging time was decreased, whereas narrow beam walk time and foot printing errors were increased. Treatment with aqueous seed extract of Mp significantly increased the catalase activity and decreased the MDA and nitrite level, compared to untreated Parkinsonian mouse brain. Mp treatment also improved the behavioral abnormalities. It increased hanging time, whereas it decreased narrow beam walk time and foot printing error compared to untreated Parkinsonian mouse brain. Furthermore, we observed a significant reduction in tyrosine hydroxylase (TH) immunoreactivity in the substantia nigra (SN) and striatum region of the brain, after treatment with PQ which was considerably restored by the use of Mp seed extract. Our result suggested that Mp seed extract treatment significantly reduced the PQ induced neurotoxicity as evident by decrease in oxidative damage, physiological abnormalities and immunohistochemical changes in the Parkinsonian mouse. Copyright © 2013 Elsevier Ltd. All rights reserved.

Paraquat intoxication and associated pathological findings in three dogs in South Africa

Directory of Open Access Journals (Sweden)

June H. Williams

2016-11-01

Full Text Available Paraquat is a bipyridylium non-selective contact herbicide commonly used worldwide. When ingestion occurs by humans and animals either accidentally, intentionally or maliciously, paraquat selectively accumulates in the lungs resulting in the production of oxygen-free radicals, causing membrane damage and cell death. Intoxicated subjects typically show progressive and fatal pulmonary haemorrhage, collapse and oedema. In individuals surviving the acute phase, pulmonary fibrosis develops. Gastrointestinal-, renal- and central nervous system clinical signs may also occur. Owing to the lack of effective treatment and absence of an antidote, the prognosis is poor. The clinical presentation, clinicopathological findings and treatment are briefly described of three dogs from one South African household, intoxicated with paraquat. Macroscopic and microscopic lesions in one dog that was necropsied, as well as pulmonary ultrastructure are detailed and illustrated for academic reference. All dogs presented with tachypnoea and dyspnoea 2–3 days after accidental paraquat ingestion. Treatment was aimed at reducing gastrointestinal absorption, enhancing elimination by diuresis and avoiding further oxidative damage by administration of antioxidants. All dogs, however, became progressively hypoxic despite treatment and were euthanised. Paraquat toxicity should be a differential diagnosis in dogs with unexplained progressive respiratory and gastrointestinal signs and renal failure. The local veterinary profession should be aware of accidental or intentional paraquat toxicity of animals. Existing literature, variations possible in canine clinical signs, measured parameters, lesions, as well as possible treatments, promising experimental antidotes and management options are discussed.

Paraquat use among farmers in Korea after the ban.

Science.gov (United States)

Bang, Ye Jin; Kim, Jaeyoung; Lee, Won Jin

2017-07-04

The purpose of this study was to examine the proportion of paraquat use among farmers and to describe their epidemiologic characteristics after the paraquat ban in 2012. We interviewed 249 farmers in Korea in 2014. Approximately 20% of the farmers reported using paraquat in 2014. Farmers with longer farming experience, longer pesticide application years, and upland farming reported an increased risk of paraquat use although the trend was not statistically significant. The majority of the farmers used preexisting paraquat (85.7%), but some farmers purchased it illegally (14.3%). Farmers who used paraquat perceived paraquat as a dangerous chemical; however, they disagreed with the necessity of the paraquat ban.

Paraquat poisoning in the dog

International Nuclear Information System (INIS)

O'Sullivan, S.P.

1989-01-01

Recovery from paraquat poisoning in the dog is rare. This is a report of a case of recovery from confirmed paraquat poisoning in a clinical setting. The dog exhibited the usual signs of paraquat poisoning. The diagnosis was confirmed on toxicological analysis of urine using an ion exchange technique. The dog was treated with frusemide, nicotinamide, corticosteroids, α-tocopherol, vitamin A, etamiphylline camsylate and ampicillin. He recovered after seven weeks of intensive therapy. Alternative treatments are discussed

Mechanisms Underlying Early Rapid Increases in Creatinine in Paraquat Poisoning

Science.gov (United States)

Mohamed, Fahim; Endre, Zoltan; Jayamanne, Shaluka; Pianta, Timothy; Peake, Philip; Palangasinghe, Chathura; Chathuranga, Umesh; Jayasekera, Kithsiri; Wunnapuk, Klintean; Shihana, Fathima; Shahmy, Seyed; Buckley, Nicholas

2015-01-01

Background Acute kidney injury (AKI) is common after severe paraquat poisoning and usually heralds a fatal outcome. The rapid large increases in serum creatinine (Cr) exceed that which can be explained by creatinine kinetics based on loss of glomerular filtration rate (GFR). Methods and Findings This prospective multi-centre study compared the kinetics of two surrogate markers of GFR, serum creatinine and serum cystatin C (CysC), following paraquat poisoning to understand and assess renal functional loss after paraquat poisoning. Sixty-six acute paraquat poisoning patients admitted to medical units of five hospitals were included. Relative changes in creatinine and CysC were monitored in serial blood and urine samples, and influences of non-renal factors were also studied. Results Forty-eight of 66 patients developed AKI (AKIN criteria), with 37 (56%) developing moderate to severe AKI (AKIN stage 2 or 3). The 37 patients showed rapid increases in creatinine of >100% within 24 hours, >200% within 48 hours and >300% by 72 hours and 17 of the 37 died. CysC concentration increased by 50% at 24 hours in the same 37 patients and then remained constant. The creatinine/CysC ratio increased 8 fold over 72 hours. There was a modest fall in urinary creatinine and serum/urine creatinine ratios and a moderate increase in urinary paraquat during first three days. Conclusion Loss of renal function contributes modestly to the large increases in creatinine following paraquat poisoning. The rapid rise in serum creatinine most probably represents increased production of creatine and creatinine to meet the energy demand following severe oxidative stress. Minor contributions include increased cyclisation of creatine to creatinine because of acidosis and competitive or non-competitive inhibition of creatinine secretion. Creatinine is not a good marker of renal functional loss after paraquat poisoning and renal injury should be evaluated using more specific biomarkers of renal injury

Effect of Antioxidants on the Outcome of Therapy in Paraquat ...

African Journals Online (AJOL)

Erah

1Department of Anesthesiology and Intensive Care, School of Medicine, 2Isfahan Clinical Toxicology Research. Center, 3Noor ... patients received conventional treatment protocol consisting of fluid replacement, oral absorbents, ... toxic effects via oxidative stress-mediated ... administration of paraquat to rats, the vitamin.

Ulinastatin suppresses endoplasmic reticulum stress and apoptosis in the hippocampus of rats with acute paraquat poisoning

Directory of Open Access Journals (Sweden)

Hai-feng Li

2015-01-01

Full Text Available Lung injury is the main manifestation of paraquat poisoning. Few studies have addressed brain damage after paraquat poisoning. Ulinastatin is a protease inhibitor that can effectively stabilize lysosomal membranes, prevent cell damage, and reduce the production of free radicals. This study assumed that ulinastatin would exert these effects on brain tissues that had been poisoned with paraquat. Rat models of paraquat poisoning were intraperitoneally injected with ulinastatin. Simultaneously, rats in the control group were administered normal saline. Hematoxylin-eosin staining showed that most hippocampal cells were contracted and nucleoli had disappeared in the paraquat group. Fewer cells in the hippocampus were concentrated and nucleoli had disappeared in the ulinastatin group. Western blot assay showed that expressions of GRP78 and cleaved-caspase-3 were significantly lower in the ulinastatin group than in the paraquat group. Immunohistochemical findings showed that CHOP immunoreactivity was significantly lower in the ulinastatin group than in the paraquat group. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining showed that the number of apoptotic cells was reduced in the paraquat and ulinastatin groups. These data confirmed that endoplasmic reticular stress can be induced by acute paraquat poisoning. Ulinastatin can effectively inhibit this stress as well as cell apoptosis, thereby exerting a neuroprotective effect.

Age and Chronicity of Administration Dramatically Influenced the Impact of Low Dose Paraquat Exposure on Behavior and Hypothalamic-Pituitary-Adrenal Activity

Directory of Open Access Journals (Sweden)

Chris A. Rudyk

2017-07-01

Full Text Available Little is known of the age-dependent and long-term consequences of low exposure levels of the herbicide and dopaminergic toxicant, paraquat. Thus, we assessed the dose-dependent effects of paraquat using a typical short-term (3 week exposure procedure, followed by an assessment of the effects of chronic (16 weeks exposure to a very low dose (1/10th of what previously induced dopaminergic neuronal damage. Short term paraquat treatment dose-dependently induced deficits in locomotion, sucrose preference and Y-maze performance. Chronic low dose paraquat treatment had a very different pattern of effects that were also dependent upon the age of the animal: in direct contrast to the short-term effects, chronic low dose paraquat increased sucrose consumption and reduced forced swim test (FST immobility. Yet these effects were age-dependent, only emerging in mice older than 13 months. Likewise, Y-maze spontaneous alternations and home cage activity were dramatically altered as a function of age and paraquat chronicity. In both the short and long-term exposure studies, increased corticosterone and altered hippocampal glucocorticoid receptor (GR levels were induced by paraquat, but surprisingly these effects were blunted in the older mice. Thus, paraquat clearly acts as a systemic stressor in terms of corticoid signaling and behavioral outcomes, but that paradoxical effects may occur with: (a repeated exposure at; (b very low doses; and (c older age. Collectively, these data raise the possibility that repeated “hits” with low doses of paraquat in combination with aging processes might have promoted compensatory outcomes.

Antioxidant effects of selenium on lung injury in paraquat intoxicated rats

Science.gov (United States)

Kim, K.S.; Suh, G.J.; Kwon, W.Y.; Kwak, Y.H.; Lee, Kenneth; Lee, H.J.; Jeong, K.Y.; Lee, M.W.

2012-01-01

CONTEXT: Paraquat (PQ) causes lethal intoxication by inducing oxidant injury to the lung. Selenium is a cofactor for glutathione peroxidase (GPx), which is one of the major endogenous antioxidant enzymes. OBJECTIVE: To determine whether selenium post-treatment activates GPx, decreases lung injury, and improves survival in PQ intoxicated rats. MATERIALS AND METHODS: Male Spraque-Dawley rats were categorized into three groups: sham (n = 6), PQ (n = 12), and PQ + Se (n = 12). In the PQ and PQ + Se groups, 50 mg/kg of PQ was administered intraperitoneally. After 10 minutes, 60 μg/kg of Se (PQ + Se) or saline (PQ) was administered via the tail vein. Six rats per group were euthanized 6 hours or 24 hours later. Lung tissues were harvested for the measurement of GPx activity, reduced glutathione (GSH), glutathione disulfide (GSSG) and malondialdehyde (MDA) and for histological analysis. Using separated set of rats, survival of PQ (n = 10) and PQ + Se (n = 10) were observed for 72 hours. RESULTS: GPx activity in the PQ group at the 6-hour and 24-hour time points was lower than in the sham group (p CONCLUSION: Single dose of selenium post-treatment activates GPx and attenuates lipid peroxidation and lung injury early after paraquat intoxication, but does not improve 72 hours of survival.

Intoxicación por paraquat: descripción de un caso clínico Paraquat poisoning: a case report

Directory of Open Access Journals (Sweden)

Julieth Hernández

2008-07-01

Full Text Available El paraquat es el herbicida más vendido en todo el mundo. Se absorbe por las vías digestiva e inhalatoria. Si llega a los pulmones, produce congestión, edema alveolar con aumento de macrófagos que progresa a fibrosis y edema pulmonar, los cuales se presentan hasta 14 días después de la exposición si el afectado no recibió tratamiento oportuno y correcto. El paraquat se dirige fundamentalmente a los pulmones y genera allí radicales libres oxidantes; por eso, en los casos de intoxicación aguda está totalmente contraindicado usar oxígeno excepto cuando la presión parcial de oxigeno en sangre arterial sea inferior a 50 mmHg. Se presenta un caso clínico de un paciente quien desarrolló un síndrome de distress respiratorio del adulto (SDRA secundario a ingesta intencional de paraquat. El manejo inicial se realizó con lavado gástrico y tierra de Fuller en solución acuosa al 30%. Posteriormente, el paciente desarrolló compromiso pulmonar y renal, los cuales fueron manejados con pulso de ciclofosfamida a 15 mg/kg/día por 2 días, metilprednisolona 1g/día por 3 días y posteriormente dexametasona 5 mg IV cada 6 horas por 5 días con una evolución clínica satisfactoria.Paraquat is the best-selling herbicide throughout the world, It is absorbed by the digestive and inhalatory routes. If it reaches the lungs, congestion with swelling is developed, increased alveolar macrophages that progresses to fibrosis and pulmonary edema, which occur until 14 days after exposure if not treated timely and correct. Paraquat is directed primarily to the lungs and therefore generates free radicals oxidants, which is why, in cases of acute poisoning is absolutely forbidden to use oxygen except where arterial blood partial pressure of oxygen in is less than 50 mm Hg. A patient who developed an adult respiratory distress syndrome (ARDS secondary to deliberate ingestion of paraquat is presented. Initial patient management was performed with gastric lavage

Early Pulomonary Irradiation in Paraquat (Gramoxone) Poisoning

International Nuclear Information System (INIS)

Lee, Chang Geol; Kim, Gwi Eon; Suh, Chang Ok

1995-01-01

Purpose : To evaluate whether the early pulmonary irradiation can prevent or decrease the pulmonary damage and contribute to improve ultimate survival in paraquat lung. Materials and Methods : From Jun. 1987 to Aug. 1993, thirty patients with paraquat poisoning were evaluated. Fourteen of these patients were received pulmonary irradiation(RT). All of the patients ere managed with aggressive supportive treatment such as gastric lavage, forced diuresis, antioxidant agents and antifibrosis agents. Ingested amounts of paraquat were estimated into three groups(A: minimal 50cc). Pulmonary irradiation was started within 24 hours after admission(from day 1 to day 11 after ingestion of paraquat). Both whole lungs were irradiated with AP/PA parallel opposing fields using C0-60 teletherapy machine. A total of 10Gy(2Gy/fr. X 5 days)was delivered without correction of lung density. Results : In group A, all patients were alive regardless of pulmonary irradiation and in group C, all of the patients were died due o multi-organ failure, especially pulmonary fibrosis regardless of pulmonary irradiation. However, in group B, six of 7 patients(86%) with no RT were died due to respiratory failure, but 4 of 8 patients with RT were alive and 4 of 5 patients who received pulmonary irradiation within 4 days after ingestion of paraquat were all alive though radiological pulmonary fibrosis. All 3 patients who were received pulmonary irradiation after 4 days after ingestion were died due to pulmonary fibrosis in spite of recovery from renal and hepatic toxicity. Conclusion : It is difficult to find out the effect of pulmonary irradiation on the course of the paraquat lung because the precise plasma and urine paraquat concentration were not available between control and irradiation groups. But early pulmonary irradiation within 4 days after paraquat poisoning with aggressive supportive treatment appears to decrease pulmonary toxicity and contribute survival in patients with mouthful ingestion

Removal of paraquat solution onto zeolite material

Science.gov (United States)

Sirival, Rujikarn; Patdhanagul, Nopbhasinthu; Preecharram, Sutthidech; Photharin, Somkuan

2018-04-01

The purpose of this research was to study the adsorption of paraquat herbicides onto zeolite Y materials by the batch method. Three adsorbents material: Zeolite-3, Zeolite-10, and Zeolite-100 were Si/Al ratio at 3.58, 8.57 and 154.37, respectively. The factors for adsorption of paraquat as follows, adsorption time, initial concentrations of paraquat, pH and adsorption isotherm were investigated. The results showed that zeolite-10 had higher adsorption capacity than zeolite-3 and zeolite-100. The appropriate conditions for adsorption were 24 h., Zeolite 0.1 g., Initial paraquat concentration 100 ppm at pH 6. The adsorption isotherm was found to correspond with Langmuir Isotherm and the maximum paraquat adsorption is 26.38 mg/g for zeolite-10, 21.41 mg/g and 9.60 mg/g for zeolite-3 and zeolite-100, respectively. The characterization of zeolite material with XRD, XRF and BET. Furthermore, the zeolite materials applied to remove other organic and inorganic wastewater.

The autoradiographic localization of paraquat in the lung

International Nuclear Information System (INIS)

Webb, D.B.

1980-01-01

Paraquat poisoning in mammals results in a characteristic lung lesion manifested principally as progressive pulmonary fibrosis. Paraquat is actively concentrated into the lung but the site of uptake remains undefined. A method is described for the autoradiographic localization of paraquat in rats. Preliminary evidence for the site of uptake implicates the bronchiol. (author)

Curcumin-induced Activation of the Nrf2 Antioxidant System Attenuates Paraquat-induced InsuIin Resistance%姜黄素激活Nrf2抗氧化系统缓解百草枯诱导的胰岛素抵抗

Institute of Scientific and Technical Information of China (English)

杨含艳; 展平; 任丽伟; 于志文

2015-01-01

目的：观察姜黄素是否具有改善百草枯（ Paraquat，PQ）所致氧化应激诱导的胰岛素抵抗作用并探讨其改善胰岛素抵抗的效应机理。方法将实验小鼠随机分成对照组（ Control组），百草枯组（ PQ组）以及PQ加姜黄素组（ Cur组）。 PQ和Cur组连续腹腔注射百草枯7天造模成功后。 Cur组继续Cur灌胃干预。7天后，取胰岛素敏感组织肌肉，用蛋白免疫印迹方法（ Western blot，WB）检测蛋白水平和磷酸化变化，并检测脂质过氧化指标MDA。结果在PQ诱导的小鼠胰岛素抵抗模型中，姜黄素可改善小鼠葡萄糖耐量并对抗 PQ 所致的胰岛素信号蛋白 PKB－Ser473磷酸化损害；姜黄素还可明显降低肌肉MDA水平，激活小鼠Nrf2系统，促进Nrf2核转位和NQO－1的表达，同时能增强IкBα的水平，缓解氧化应激及炎症反应。结论姜黄素通过增强内源性Nrf2系统功能和胰岛素信号水平，对抗PQ诱导的氧化应激，是其缓解胰岛素抵抗的重要机理。%OBJECTIVE To observe the effect and explore the mechanism of curcumin on the paraquat-media-ted oxidative stress and insulin resistance.METHODS Thirty mice were randomly divided into 3 groups:control group,paraquat group and curcumin intervention group.Paraquat group and curcumin intervention group were contin-uously intraperitoneal injection of paraquat for 7 days to induce the models of insulin resistance.The curcumin inter-vention group was continuously gavaged with curcumin for another 7 days.Then,all mice were euthanized for muscle collection.The protein and phosphorylation levels in muscle tissue were examed by Western blot and the content of malonaldchyde ( MDA) indicated for lipid peroxidation was determined.RESULTS Curcumin improved the glucose tolerance in paraquat-induced insulin resistance in mice together with attenuation of PQ-caused impairment in PKB-Ser473 phosphorylation.Curcumin also significantly reduced

Paraquat-poisoning in the rabbit lungs: high resolution computed tomographic findings and pathologic correlation

International Nuclear Information System (INIS)

Lee, Kyung Soo; Kim, Eui Han; Lee, Byoung Ho; Kim, Kun Sang

1992-01-01

The authors evaluated high resolution computed tomographic (HRCT) findings of the isolated rabbit lungs with paraquat poisoning, and the findings were correlated with pathologic specimens. The purposes of this study are 1) to obtain the HRCT findings of the normal rabbit lung. 2) to find out if pulmonary pathology can be induced in rabbits by paraquat, and 3) to correlate the HRCT findings to those of pathology. Thirty rabbits were divided into three groups: group I included four control rabbits; group II included 16 rabbits given paraquat intraperitoneally (IP group); and group III included 10 rabbits given paraquat intravenously (IV group). The rabbits were sacrificed seven, 10, and 14 days after injection of various amount of paraquat, and then the lungs were isolated for HRCT and pathologic studies. Gross and microscopic findings of the three groups of control and paraquat-injected rabbit lungs were correlated with HRCT findings. Pulmonary congestion, mild thickening of alveolar walls and septae, and multifocal micro-atelectasis were the man pathologic findings of the lungs in both groups of the rabbits. Pulmonary hemorrhage was noted in five (31%) of 16 rabbits of IP group and three (30%) of 10 IV group. Pulmonary edema was seen in one rabbits (6%) of IP and four (40%) of IV group. Typical pulmonary fibrosis was seen in one rabbit of IP (6%) and IV (10%) group, respectively. There was no correlation between the amount of paraquat and frequency of the pulmonary pathology. Pulmonary fibrosis was seen at least one week after the paraquat injection. On HRCT, pulmonary hemorrhage and edema appeared as diffuse air-space consolidation and pulmonary fibrosis as linear or band-like opacities. However, minimal changes such as mild congestion

Efectos del herbicida Paraquat sobre el zooplancton Effects of Paraquat herbicide on zooplankton

Directory of Open Access Journals (Sweden)

Ana María Gagneten

2002-09-01

Full Text Available The effects of 0.1; 0.2; 0.4 and 0.8 mlPQ/L were analized on a zooplankton community, to determine the most sensitive species and to analize the occurence of physical abnormalities. A total of 40 taxa were determined. Paraquat affected significantly the zooplankton density but not the species richness. A progressive state of deformation of these organisms was also observed. Paraquat showed to be highly toxic for the zooplankton, so this herbicide should be strictly regulated in aquatic and terrestrial ecosystems.

Influence of age on the passage of paraquat through the blood-brain barrier in rats: a distribution and pathological examination

International Nuclear Information System (INIS)

Widdowson, P.S.; Farnworth, M.J.; Simpson, M.G.; Lock, E.A.

1996-01-01

Experiments were performed to determine the extent of paraquat entry into the brain of neonatal and elderly rats, as compared with adult rats, which may be dependent on the efficacy of the blood-brain barrier. A single, median lethal dose (20 mg/kg s.c.) of paraquat containing [14C]paraquat was administered to neonatal (10 day old), adult (3 month old) and elderly (18 month old) rats. In contrast to the adult and elderly rats where paraquat levels fell over the 24 h post-dosing period to negligible levels, paraquat concentrations in neonatal brains did not decrease with time between 0.5 and 24 h following dosing. The distribution of [14C]paraquat was measured in selective brain regions using quantitative autoradiography in all three age groups of rats, 30 min and 24 h following dosing. Autoradiography demonstrated that brain paraquat distributions were similar in the rat age groups. Most of the paraquat was confined to regions outside the blood-brain barrier and to brain regions that lack a complete blood-brain barrier e.g. dorsal hypothalamus, area postrema and the anterior olfactory bulb. Between 0.5 h and 24 h following dosing, paraquat concentrations in deeper brain structures, some distance away from the sites of entry, began to slowly increase in all the rat age groups. By 24 h following dosing, a majority of brain regions examined using quantitative autoradiography revealed significantly higher paraquat concentrations in neonatal brains as compared to brain regions of adult and elderly rats. Despite increased paraquat entry into neonatal brain, we could find no evidence for paraquat-induced neuronal cell damage following a detailed histopathological examination of perfused-fixed brains. In conclusion, impaired blood-brain barrier integrity in neonatal brain thus permitting more paraquat to enter than in adult brain, did not result in neuronal damage

Curcumin-induced Activation of the Nrf2 Antioxidant System Attenuates Paraquat-induced InsuIin Resistance%姜黄素激活Nrf2抗氧化系统缓解百草枯诱导的胰岛素抵抗

Institute of Scientific and Technical Information of China (English)

杨含艳; 展平; 任丽伟; 于志文

2015-01-01

目的：观察姜黄素是否具有改善百草枯（ paraquat，PQ）所致氧化应激诱导的胰岛素抵抗作用并探讨其改善胰岛素抵抗的效应机理。方法将实验小鼠随机分成对照组（ Control组），百草枯组（ PQ组）以及PQ加姜黄素组（ Cur组）。 PQ和Cur组连续腹腔注射百草枯7天造模成功后。 Cur组继续Cur灌胃干预。7天后，取胰岛素敏感组织肌肉，用蛋白免疫印迹方法（ Western blot，WB）检测蛋白水平和磷酸化变化，并检测脂质过氧化指标MDA。结果在PQ诱导的小鼠胰岛素抵抗模型中，姜黄素可改善小鼠葡萄糖耐量并对抗 PQ 所致的胰岛素信号蛋白 PKB－Ser473磷酸化损害；姜黄素还可明显降低肌肉MDA水平，激活小鼠Nrf2系统，促进Nrf2核转位和NQO－1的表达，同时能增强IкBα的水平，缓解氧化应激及炎症反应。结论姜黄素通过增强内源性Nrf2系统功能和胰岛素信号水平，对抗PQ诱导的氧化应激，是其缓解胰岛素抵抗的重要机理。%OBJECTIVE To examine the effect of curcumin on the paraquat-mediated oxidative stress and insu-lin resistance ,and to further explore the working mechanism underlying its effect .METHODS Thirty mice were randomly divided into 3 groups:control group , paraquat group and curcumin intervention group .Paraquat group and curcumin intervention group were continuously intraperitoneal injection of paraquat for 7 days to induce the models of insulin resistance.The curcumin intervention group was continuously gavaged with curcumin for another 7 days.Then,all mice were euthanized for muscle collection .The protein and phosphorylation levels in muscle tissue were examed by Western blot and the content of malonaldchyde ( MDA) indicated for lipid peroxidation was deter-mined.Results Curcumin improved the glucose tolerance in paraquat-induced insulin resistance in mice together with attenuation of PQ-caused impairment in PKBSer473

Paraquat and Maneb Exposure Alters Rat Neural Stem Cell Proliferation by Inducing Oxidative Stress: New Insights on Pesticide-Induced Neurodevelopmental Toxicity.

Science.gov (United States)

Colle, Dirleise; Farina, Marcelo; Ceccatelli, Sandra; Raciti, Marilena

2018-06-01

Pesticide exposure has been linked to the pathogenesis of neurodevelopmental and neurodegenerative disorders including autism spectrum disorders, attention deficit/hyperactivity, and Parkinson's disease (PD). Developmental exposure to pesticides, even at low concentrations not harmful for the adult brain, can lead to neuronal loss and functional deficits. It has been shown that prenatal or early postnatal exposure to the herbicide paraquat (PQ) and the fungicide maneb (MB), alone or in combination, causes permanent toxicity in the nigrostriatal dopamine system, supporting the idea that early exposure to these pesticides may contribute to the pathophysiology of PD. However, the mechanisms mediating PQ and MB developmental neurotoxicity are not yet understood. Therefore, we investigated the neurotoxic effect of low concentrations of PQ and MB in primary cultures of rat embryonic neural stem cells (NSCs), with particular focus on cell proliferation and oxidative stress. Exposure to PQ alone or in combination with MB (PQ + MB) led to a significant decrease in cell proliferation, while the cell death rate was not affected. Consistently, PQ + MB exposure altered the expression of major genes regulating the cell cycle, namely cyclin D1, cyclin D2, Rb1, and p19. Moreover, PQ and PQ + MB exposures increased the reactive oxygen species (ROS) production that could be neutralized upon N-acetylcysteine (NAC) treatment. Notably, in the presence of NAC, Rb1 expression was normalized and a normal cell proliferation pattern could be restored. These findings suggest that exposure to PQ + MB impairs NSCs proliferation by mechanisms involving alterations in the redox state.

Paraquat poisoning: an experimental model of dose-dependent acute lung injury due to surfactant dysfunction

Directory of Open Access Journals (Sweden)

M.F.R. Silva

1998-03-01

Full Text Available Since the most characteristic feature of paraquat poisoning is lung damage, a prospective controlled study was performed on excised rat lungs in order to estimate the intensity of lesion after different doses. Twenty-five male, 2-3-month-old non-SPF Wistar rats, divided into 5 groups, received paraquat dichloride in a single intraperitoneal injection (0, 1, 5, 25, or 50 mg/kg body weight 24 h before the experiment. Static pressure-volume (PV curves were performed in air- and saline-filled lungs; an estimator of surface tension and tissue works was computed by integrating the area of both curves and reported as work/ml of volume displacement. Paraquat induced a dose-dependent increase of inspiratory surface tension work that reached a significant two-fold order of magnitude for 25 and 50 mg/kg body weight (P<0.05, ANOVA, sparing lung tissue. This kind of lesion was probably due to functional abnormalities of the surfactant system, as was shown by the increase in the hysteresis of the paraquat groups at the highest doses. Hence, paraquat poisoning provides a suitable model of acute lung injury with alveolar instability that can be easily used in experimental protocols of mechanical ventilation

Possible Appearance of Degradation Products of Paraquat in Crops

Energy Technology Data Exchange (ETDEWEB)

Slade, P. [Imperial Chemical Industries LTD., Jealott' s Hill Research Station, Bracknell, Berks. (United Kingdom)

1966-05-15

Chemical analysis has established that residue levels of paraquat in crops harvested after use of the chemical are at such a low level as to constitute no hazard to the consuming public. (Paraquat dichloride is 1,1'-dimethyl-4,4'-bipyridylium dichloride). There remained the possibility that toxic metabolites or other conversion products of paraquat might appear in crops. This paper is concerned with attempts to evaluate this possibility, and demonstrates that no hazard arises from the formation of degradation products. It has been shown, using paraquat labelled with {sup 14}C in the methyl groups and in the pyridine nuclei, that the chemical is not metabolically degraded in plants. However, photochemical degradation of paraquat can occur on the surface of leaves in sunlight. In vitro experiments involving ultra-violet irradiation of aqueous solutions of {sup 14}C-paraquat have shown that 4-carboxy-1-methylpyridinium chloride and methylamine hydrochloride are the only products formed in significant amount in the photochemical degradation. Paper chromatography and isotope dilution have shown that these products are formed on leaves of plants treated with {sup 14}C-paraquat (mostly after the plants are dead). Whole plant radioautography has established that 4-carboxy-1-{sup 14}C methylpyridinium chloride is not translocated at all from the dead leaves on which it is formed and certainly this compound will not appear in harvested crops. This has been confirmed in an experiment in which {sup 14}C-paraquat was used to desiccate the tops of potato plants before harvesting the tubers. All the radioactivity subsequently found in the tubers could be accounted for as paraquat (level 0.08 ppm). There was no evidence for the presence of significant amounts of other radioactive compounds in the tubers, even though chromatography of extracts of the desiccated plants showed that photochemical degradation products were formed on the leaves: these were not translocated into the

The Protective Effect of Minocycline in a Paraquat-Induced Parkinson's Disease Model in Drosophila is Modified in Altered Genetic Backgrounds

Directory of Open Access Journals (Sweden)

Arati A. Inamdar

2012-01-01

Full Text Available Epidemiological studies link the herbicide paraquat to increased incidence of Parkinson's disease (PD. We previously reported that Drosophila exposed to paraquat recapitulate PD symptoms, including region-specific degeneration of dopaminergic neurons. Minocycline, a tetracycline derivative, exerts ameliorative effects in neurodegenerative disease models, including Drosophila. We investigated whether our environmental toxin-based PD model could contribute to an understanding of cellular and genetic mechanisms of minocycline action and whether we could assess potential interference with these drug effects in altered genetic backgrounds. Cofeeding of minocycline with paraquat prolonged survival, rescued mobility defects, blocked generation of reactive oxygen species, and extended dopaminergic neuron survival, as has been reported previously for a genetic model of PD in Drosophila. We then extended this study to identify potential interactions of minocycline with genes regulating dopamine homeostasis that might modify protection against paraquat and found that deficits in GTP cyclohydrolase adversely affect minocycline rescue. We further performed genetic studies to identify signaling pathways that are necessary for minocycline protection against paraquat toxicity and found that mutations in the Drosophila genes that encode c-Jun N-terminal kinase (JNK and Akt/Protein kinase B block minocycline rescue.

Clinical features and prognosis of paraquat poisoning in French Guiana

Science.gov (United States)

Elenga, Narcisse; Merlin, Caroline; Le Guern, Rémi; Kom-Tchameni, Rémi; Ducrot, Yves-Marie; Pradier, Maxime; Ntab, Balthazar; Dinh-Van, Kim-Anh; Sobesky, Milko; Mathieu, Daniel; Dueymes, Jean-Marc; Egmann, Gérald; Kallel, Hatem; Mathieu-Nolf, Monique

2018-01-01

Abstract Paraquat is a nonselective contact herbicide of great toxicological importance, being associated with high mortality rates. Because of its high toxicity, the European Union withdrew it from its market in 2007. The aim of this study is to analyze all cases of paraquat poisoning hospitalized in French Guiana in order to assess their incidence and main characteristics. Medical records of all paraquat intoxicated patients hospitalized from 2008 until 2015 were reviewed in this retrospective study. Demographics, clinical presentation, and laboratory data were evaluated. A total of 62 cases were reviewed. The incidence of paraquat poisoning was 3.8/100,000 inhabitants/year. There were 44 adults and 18 children younger than 16 years of age. The median ages were 31 years [18.08–75.25] in adults and 13.4 years [0.75–15.08] in children, respectively. The median duration of hospitalization was longer in children [15.5 days (1–24)] than in adults [2 days (1–30)], P < .01. The majority of cases was due to self-poisoning (84%). Children had ingested a lower quantity of paraquat [48.8 mg/kg (10–571.1)] than adults [595.8 mg/kg (6–3636.4), P = .03]. There were more deaths among adults (65%) than in children (22%), P = .004. The severity and outcome was determined primarily by the amount of paraquat ingested. In conclusion, French Guiana has the largest cohort of paraquat poisonings in the European Union. The major factor affecting the prognosis of patients was the ingested amount of paraquat. The administration of activated charcoal or Pemba, in situ, within the first hour after ingestion of paraquat is essential. PMID:29642226

Acute kidney injury from Paraquat poisoning: a case report. | Slater ...

African Journals Online (AJOL)

Acute kidney injury from Paraquat poisoning: a case report. H. E. Slater, O.C.A. Okoye, O. Okperi, N. Rajora. Abstract. Paraquat is a salt widely used as a herbicide. Although paraquat poisoning is rare in the general population, it may be considered as one of the most toxic poisons frequently used for suicide attempts, and is ...

Autoradiography of [14C]paraquat or [14C]diquat in frogs and mice: accumulation in neuromelanin

International Nuclear Information System (INIS)

Lindquist, N.G.; Larsson, B.S.; Lyden-Sokolowski, A.

1988-01-01

The herbicide paraquat has been suggested as a causative agent for Parkinson's disease because of its structural similarity to a metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which may induce a parkinsonism-like condition. MPTP as well as its metabolite 1-methyl-4-phenylpyridine have melanin affinity, and the parkinsonism-inducing potency of MPTP is much stronger in species with melanin in the nerve cells. Autoradiography of [ 3 H]MPTP in experimental animals has shown accumulation in melanin-containing tissues, including pigmented neurons. In the present whole body autoradiographic study accumulation and retention was seen in neuromelanin in frogs after i.p. injection of [ 14 C]paraquat or[ 14 C]diquat. By means of whole body autoradiography of [ 14 C]diquat in mice (a species with no or very limited amounts of neuromelanin) a low, relatively uniformly distributed level of radioactivity was observed in brain tissue. Accumulation of toxic chemical compounds, such as paraquat, in neuromelanin may ultimately cause lesions in the pigmented nerve cells, leading to Parkinson's disease

Triptolide suppresses paraquat induced idiopathic pulmonary fibrosis by inhibiting TGFB1-dependent epithelial mesenchymal transition.

Science.gov (United States)

Chen, Hong; Chen, Qun; Jiang, Chun-Ming; Shi, Guang-Yue; Sui, Bo-Wen; Zhang, Wei; Yang, Li-Zhen; Li, Zhu-Ying; Liu, Li; Su, Yu-Ming; Zhao, Wen-Cheng; Sun, Hong-Qiang; Li, Zhen-Zi; Fu, Zhou

2018-03-01

Idiopathic pulmonary fibrosis (IPF) and tumor are highly similar to abnormal cell proliferation that damages the body. This malignant cell evolution in a stressful environment closely resembles that of epithelial-mesenchymal transition (EMT). As a popular EMT-inducing factor, TGFβ plays an important role in the progression of multiple diseases. However, the drugs that target TGFB1 are limited. In this study, we found that triptolide (TPL), a Chinese medicine extract, exerts an anti-lung fibrosis effect by inhibiting the EMT of lung epithelial cells. In addition, triptolide directly binds to TGFβ and subsequently increase E-cadherin expression and decrease vimentin expression. In in vivo studies, TPL improves the survival state and inhibits lung fibrosis in mice. In summary, this study revealed the potential therapeutic effect of paraquat induced TPL in lung fibrosis by regulating TGFβ-dependent EMT progression. Copyright © 2017 Elsevier B.V. All rights reserved.

Studies of the occupational exposure of Malaysian plantation workers to paraquat

Energy Technology Data Exchange (ETDEWEB)

Chester, G; Woollen, B H

1982-02-01

Studies carried out on the occupational exposure to paraquat of plantation workers in Malaysia comprised quantitative estimates of dermal and respiratory exposure of knapsack spray operators, carriers, and rubber tappers operating under their normal working conditions. Spray operators have been shown to be dermally exposed to paraquat by walking through recently sprayed vegetation and into their own spray, regular adjustment and unblocking of spray nozzles and leakage, and overfilling of knapsack spray tanks. Carriers also received measurable dermal exposure from walking through recently sprayed vegetation and accidental spillage when carrying and loading. The infrequent and negligible dermal exposure of tappers resulted from walking through recently sprayed vegetation. Determinations of the total airborne paraquat concentrations in the breathing zone show that spray operators and carriers are exposed to an order of 1% or less of the current TLV for respirable paraquat. No paraquat was detected in the breathing zones of tappers working in simultaneously sprayed blocks. The calculated ranges of dermal and respiratory exposures, when compared with published data on both the exposure to, and the toxicity of, paraquat, indicate that there should be no toxicological risk to any of the three groups studied as a result of using paraquat.

Directed-spray application of paraquat and diuron in physic nut plants

OpenAIRE

Costa,N.V.; Neunfeld,T.H.; Ohland,T.; Piano,J.T.; Klein,J.

2013-01-01

There is little information about the selectivity of herbicides in physic nut (Jatropha curcas) in Brazil. Therefore, this study aimed to evaluate the selectivity of different doses and mixtures of paraquat and diuron in direted-spray applications in physic nut plants in greenhouse conditions. The study used a randomized block design, with five replicates. The treatments were: paraquat (200 and 600 g ha-1), diuron (1,000 and 2,000 g ha-1), paraquat + diuron (200 + 1,000 g ha-1), paraquat + di...

Aspectos gerais e diagnóstico clinicolaboratorial da intoxicação por paraquat General aspects and clinical laboratorial diagnostic of poisoning by paraquat

Directory of Open Access Journals (Sweden)

Gabriela Cristina Schmitt

2006-08-01

very toxic product, fatally poisoning mainly by the lack of an efficient antidote to revert the clinical state. FISIOPATHOLOGY: Toxicological effects are decurrent of oxidative stress. The most important target organ is the lung, which can display edema, hemorrhage, interstitial inflammation and fibroses, culminating in serious respiratory failure and death. Moreover, it is nephrotoxic, hepatotoxic, miotoxic and neurotoxic. TREATMENT: Besides aiming the decrease of absorption and stimulating the excretion of absorbed paraquat, the poisoning treatment nowadays is based on measures that decrease oxidative stress using antioxidants, consequently reverting clinical state, mainly the pulmonary. Diagnostic methods: Among the available quantitative methods, the chromatographic are the most reported ones for biological samples. However, capillary electrophoresis and immunoassay methods can be used. Immunoassays stand out for being typically found in hospital laboratories, while chromatographic and electrophoretic methods are not. On the other hand, a simple and fast urinary reaction with sodium dithionite is very utilized because it is predictive in acute poisoning suspect. CONCLUSION: In the presence of high morbimortality potential in paraquat intoxications, the reversion of pulmonary toxicity with antioxidants is extensively studied, but a specific antidote is not established. In laboratorial diagnostic, chromatographic, electrophoretic and immunologic techniques are applied to paraquat quantification, although in clinical toxicology the sodium dithionite reaction is still significant.

Glucose Metabolism and AMPK Signaling Regulate Dopaminergic Cell Death Induced by Gene (α-Synuclein)-Environment (Paraquat) Interactions.

Science.gov (United States)

Anandhan, Annadurai; Lei, Shulei; Levytskyy, Roman; Pappa, Aglaia; Panayiotidis, Mihalis I; Cerny, Ronald L; Khalimonchuk, Oleh; Powers, Robert; Franco, Rodrigo

2017-07-01

While environmental exposures are not the single cause of Parkinson's disease (PD), their interaction with genetic alterations is thought to contribute to neuronal dopaminergic degeneration. However, the mechanisms involved in dopaminergic cell death induced by gene-environment interactions remain unclear. In this work, we have revealed for the first time the role of central carbon metabolism and metabolic dysfunction in dopaminergic cell death induced by the paraquat (PQ)-α-synuclein interaction. The toxicity of PQ in dopaminergic N27 cells was significantly reduced by glucose deprivation, inhibition of hexokinase with 2-deoxy-D-glucose (2-DG), or equimolar substitution of glucose with galactose, which evidenced the contribution of glucose metabolism to PQ-induced cell death. PQ also stimulated an increase in glucose uptake, and in the levels of glucose transporter type 4 (GLUT4) and Na + -glucose transporters isoform 1 (SGLT1) proteins, but only inhibition of GLUT-like transport with STF-31 or ascorbic acid reduced PQ-induced cell death. Importantly, while autophagy protein 5 (ATG5)/unc-51 like autophagy activating kinase 1 (ULK1)-dependent autophagy protected against PQ toxicity, the inhibitory effect of glucose deprivation on cell death progression was largely independent of autophagy or mammalian target of rapamycin (mTOR) signaling. PQ selectively induced metabolomic alterations and adenosine monophosphate-activated protein kinase (AMPK) activation in the midbrain and striatum of mice chronically treated with PQ. Inhibition of AMPK signaling led to metabolic dysfunction and an enhanced sensitivity of dopaminergic cells to PQ. In addition, activation of AMPK by PQ was prevented by inhibition of the inducible nitric oxide syntase (iNOS) with 1400W, but PQ had no effect on iNOS levels. Overexpression of wild type or A53T mutant α-synuclein stimulated glucose accumulation and PQ toxicity, and this toxic synergism was reduced by inhibition of glucose metabolism

Multiple pathways for uptake of paraquat, methylglyoxal bis(guanylhydrazone), and polyamines

Energy Technology Data Exchange (ETDEWEB)

Byers, T.L.; Kameji, R.; Rannels, D.E.; Pegg, A.E.

1987-06-01

The uptake of polyamines, methylglyoxal bis(guanylhydrazone) (MGBG), and paraquat (N,N-dimethyl-4,4'-bipyridylium) into control Chinese hamster ovary (CHO) cells and a mutant CHO cell line selected for resistance to the toxicity of MGBG was examined. In contrast to control CHO cells, the mutant cells had no detectable uptake of (/sup 14/C)-MGBG or any of the polyamines. There was no difference between the two cell lines in the uptake of ..cap alpha..-aminoisobutyric (/sup 3/H-AIB), which indicates that there was no general change in membrane transport processes. The mutant cells were also found to be resistant to the toxicity of paraquat and to have a reduced capability to take up the herbicide. This finding confirms that the uptake of paraquat is necessary for the toxicity of this compound and that the paraquat is taken up by a transport system that also transports MGBG. Competition experiments showed that an excess of unlabeled paraquat inhibited uptake of MGBG and, to a lesser extent, uptake of putrescine and spermidine, but no inhibitory action on spermine uptake could be detected. Studies with type II cells isolated from rat lung also demonstrated uptake of paraquat and spermidine, but paraquat was only a weak inhibitor of spermidine uptake in this system. These results suggest that there may be multiple systems for the uptake of MGBG and polyamines and that paraquat is taken up by at least one but not by all of these systems.

Multiple pathways for uptake of paraquat, methylglyoxal bis(guanylhydrazone), and polyamines

International Nuclear Information System (INIS)

Byers, T.L.; Kameji, R.; Rannels, D.E.; Pegg, A.E.

1987-01-01

The uptake of polyamines, methylglyoxal bis(guanylhydrazone) (MGBG), and paraquat [N,N-dimethyl-4,4'-bipyridylium] into control Chinese hamster ovary (CHO) cells and a mutant CHO cell line selected for resistance to the toxicity of MGBG was examined. In contrast to control CHO cells, the mutant cells had no detectable uptake of [ 14 C]-MGBG or any of the polyamines. There was no difference between the two cell lines in the uptake of α-aminoisobutyric ( 3 H-AIB), which indicates that there was no general change in membrane transport processes. The mutant cells were also found to be resistant to the toxicity of paraquat and to have a reduced capability to take up the herbicide. This finding confirms that the uptake of paraquat is necessary for the toxicity of this compound and that the paraquat is taken up by a transport system that also transports MGBG. Competition experiments showed that an excess of unlabeled paraquat inhibited uptake of MGBG and, to a lesser extent, uptake of putrescine and spermidine, but no inhibitory action on spermine uptake could be detected. Studies with type II cells isolated from rat lung also demonstrated uptake of paraquat and spermidine, but paraquat was only a weak inhibitor of spermidine uptake in this system. These results suggest that there may be multiple systems for the uptake of MGBG and polyamines and that paraquat is taken up by at least one but not by all of these systems

Clinical features and prognosis of paraquat poisoning: a review of 41 cases

OpenAIRE

Delirrad, Mohammad; Majidi, Mohammad; Boushehri, Behzad

2015-01-01

Purpose: Paraquat is a contact herbicide which is highly toxic to human. Deliberate self-poisoning with paraquat continues to be a major public health concern in many developing countries. This study aimed to evaluate the data on cases of acute paraquat poisoning and to compare different variables between survivors and non-survivors. Methods: In this cross sectional study, medical records of all paraquat intoxicated patients were reviewed at Taleghani hospital of Urmia, Iran, from 2007 to 201...

Effect of acute paraquat poisoning on CYP450 isoforms activity in rats by cocktail method

OpenAIRE

Wang, Shuanghu; Wang, Zhiyi; Chen, Dongxin; Chen, Mengchun; Lin, Yingying; Liu, Zezheng; Zhang, Lijing; Wen, Congcong; Wang, Xianqin; Ma, Jianshe

2015-01-01

Paraquat is a highly effective contact herbicide that is marketed worldwide as a fantastical, non-selective compound for broadleaf weed control. As compared to most pesticides, paraquat is extremely toxic to humans and the lack of strategies to manage paraquat poisoning has resulted in high fatality rates. The rats were randomly divided into acute paraquat poisoning group and control group. The paraquat group rats were given 36 mg/kg paraquat by intragastric administration. The influence of a...

Effects of paraquat on Escherichia coli: Differences between B and K-12 strains

International Nuclear Information System (INIS)

Kitzler, J.W.; Minakami, H.; Fridovich, I.

1990-01-01

Escherichia coli B and K-12 are equally susceptible to the bacteriostatic effects of aerobic paraquat, but they differed strikingly when the lethality of paraquat was evaluated. E. coli B suffered an apparent loss of viability when briefly exposed to paraquat, whereas E. coli K-12 did not. This difference depended on the ability of the B-strain, but not the K-12 strain, to retain internalized paraquat; the B strain was killed on aerobic tryptic soy-yeast extract plates during the incubation which preceded the counting of colonies. This difference in retention of paraquat between strains was demonstrated by delayed loss of viability, by growth inhibition, and by cyanide-resistant respiration after brief exposure to paraquat, washing, and testing in fresh medium. This difference was also shown by using [ 14 C]paraquat. This previously unrecognized difference between E. coli B and K-12 has been the cause of apparently contradictory reports and should lead to some reevaluation of the pertinent literature

Paraquat Exposure of Pregnant Women and Neonates in Agricultural Areas in Thailand

Directory of Open Access Journals (Sweden)

Pajaree Konthonbut

2018-06-01

Full Text Available This study aimed to assess paraquat concentrations in the urine of women at 28 weeks of pregnancy, delivery and 2 months postpartum and in the meconium of neonates. In all, 79 pregnant women were recruited from three hospitals located in agricultural areas in Thailand. The subjects were interviewed about personal characteristics, agricultural activities and pesticide use patterns. Paraquat was analyzed in urine and meconium using high performance liquid chromatography equipped with a fluorescence detector. The geometric mean (GSD of urinary paraquat concentrations at 28 weeks of pregnancy, delivery and 2 months postpartum were 2.04 (4.22, 2.06 (5.04 and 2.42 (5.33 ng/mL, respectively. The urinary paraquat concentrations at 28 weeks of pregnancy, delivery and 2 months postpartum between agriculturist and non-agriculturist were not significantly different (p = 0.632, p = 0.915, p = 0.57 respectively. The geometric mean (GSD of paraquat concentration in the meconium was 33.31 (4.59 ng/g. The factors predicting paraquat exposures among pregnant women and neonates included working outside, living near farmland, having family members who work on a farm, drinking well water and using herbicides or paraquat.

[Clinical analysis of lower limb thrombosis caused by paraquat poisoning].

Science.gov (United States)

Yu, L J; Jian, X D; Zhang, Z C; Ren, Y L; Ning, Q; Wang, K; Gao, B J; Jia, J E

2018-01-20

Objective: To investigate the causes of peripheral vascular thrombosis in patients with paraquat poisoning. Methods: The patients with paraquat poisoning who were admitted to our department in recent two years were observed to screen out the patients with large vessel thrombosis. The data on toxic exposure history, clinical features, and treatment were collected to analyze the causes of thrombosis in the patients with paraquat poisoning. Results: Three patients had typical lower limb thrombosis. There was one case of right common femoral vein thrombosis, one case of bilateral calf muscle vein thrombosis, and one case of right calf superficial vein thrombosis and right calf muscle vein thrombosis. Conclusions: After paraquat poisoning, the blood is in a hypercoagulable state and prolonged bed rest may increase the risk of thrombosis.

Magnetic Hybrid Nanosorbents for the Uptake of Paraquat from Water

Directory of Open Access Journals (Sweden)

Tiago Fernandes

2017-03-01

Full Text Available Although paraquat has been banned in European countries, this herbicide is still used all over the world, thanks to its low-cost, high-efficiency, and fast action. Because paraquat is highly toxic to humans and animals, there is interest in mitigating the consequences of its use, namely by implementing removal procedures capable of curbing its environmental and health risks. This research describes new magnetic nanosorbents composed of magnetite cores functionalized with bio-hybrid siliceous shells, that can be used to uptake paraquat from water using magnetically-assisted procedures. The biopolymers κ-carrageenan and starch were introduced into the siliceous shells, resulting in two hybrid materials, Fe3O4@SiO2/SiCRG and Fe3O4@SiO2/SiStarch, respectively, that exhibit a distinct surface chemistry. The Fe3O4@SiO2/SiCRG biosorbents displayed a superior paraquat removal performance, with a good fitting to the Langmuir and Toth isotherm models. The maximum adsorption capacity of paraquat for Fe3O4@SiO2/SiCRG biosorbents was 257 mg·g−1, which places this sorbent among the best systems for the removal of this herbicide from water. The interesting performance of the κ-carrageenan hybrid, along with its magnetic properties and good regeneration capacity, presents a very efficient way for the remediation of water contaminated with paraquat.

Autoradiography of ( sup 14 C)paraquat or ( sup 14 C)diquat in frogs and mice: accumulation in neuromelanin

Energy Technology Data Exchange (ETDEWEB)

Lindquist, N G; Larsson, B S; Lyden-Sokolowski, A [Uppsala Univ., Biomedical Center, (Sweden). Dept. of Toxicology

1988-10-31

The herbicide paraquat has been suggested as a causative agent for Parkinson's disease because of its structural similarity to a metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), which may induce a parkinsonism-like condition. MPTP as well as its metabolite 1-methyl-4-phenylpyridine have melanin affinity, and the parkinsonism-inducing potency of MPTP is much stronger in species with melanin in the nerve cells. Autoradiography of ({sup 3}H)MPTP in experimental animals has shown accumulation in melanin-containing tissues, including pigmented neurons. In the present whole body autoradiographic study accumulation and retention was seen in neuromelanin in frogs after i.p. injection of ({sup 14}C)paraquat or({sup 14}C)diquat. By means of whole body autoradiography of ({sup 14}C)diquat in mice (a species with no or very limited amounts of neuromelanin) a low, relatively uniformly distributed level of radioactivity was observed in brain tissue. Accumulation of toxic chemical compounds, such as paraquat, in neuromelanin may ultimately cause lesions in the pigmented nerve cells, leading to Parkinson's disease.

Viral-toxin interactions and Parkinson’s disease: poly(I:C priming enhanced the neurodegenerative effects of paraquat

Directory of Open Access Journals (Sweden)

Bobyn Jessica

2012-05-01

Full Text Available Abstract Background Parkinson’s disease (PD has been linked with exposure to a variety of environmental and immunological insults (for example, infectious pathogens in which inflammatory and oxidative processes seem to be involved. In particular, epidemiological studies have found that pesticide exposure and infections may be linked with the incidence of PD. The present study sought to determine whether exposure to a viral mimic prior to exposure to pesticides would exacerbate PD-like pathology. Methods Mice received a supra-nigral infusion of 5 μg of the double-stranded RNA viral analog, polyinosinic: polycytidylic acid (poly(I:C, followed 2, 7 or 14 days later by administration of the pesticide, paraquat (nine 10 mg/kg injections over three weeks. Results As hypothesized, poly(I:C pre-treatment enhanced dopamine (DA neuron loss in the substantia nigra pars compacta elicited by subsequent paraquat treatment. The augmented neuronal loss was accompanied by robust signs of microglial activation, and by increased expression of the catalytic subunit (gp91 of the NADPH oxidase oxidative stress enzyme. However, the paraquat and poly(I:C treatments did not appreciably affect home-cage activity, striatal DA terminals, or subventricular neurogenesis. Conclusions These findings suggest that viral agents can sensitize microglial-dependent inflammatory responses, thereby rendering nigral DA neurons vulnerable to further environmental toxin exposure.

Paraquat: A fatal poison

Directory of Open Access Journals (Sweden)

J Shashibhushan

2015-01-01

Full Text Available Paraquat (1, 1′-dimethyl-4, 4′-dipyridylium is a bipyridilium herbicide used widely in our country and is a highly toxic compound. This compound is very notorious to cause rapid development of renal, liver, and respiratory failure with very high mortality due to lack of specific antidote and dearth of high-quality evidence-based treatment. Respiratory system involvement is the most common cause of death in these people. We hereby report a fatal case of a 30-year-old male with a history of paraquat consumption. The patient developed oliguric renal failure, deterioration of liver function, and acute respiratory distress syndrome over next few days. Different treatment modalities were tried to manage patient′s condition. In this case, none of the strategies worked well, and death ensued due to multi-organ dysfunction syndrome.

Clinical screening of paraquat in plasma samples using capillary electrophoresis with contactless conductivity detection: Towards rapid diagnosis and therapeutic treatment of acute paraquat poisoning in Vietnam.

Science.gov (United States)

Vu, Anh Phuong; Nguyen, Thi Ngan; Do, Thi Trang; Doan, Thu Ha; Ha, Tran Hung; Ta, Thi Thao; Nguyen, Hung Long; Hauser, Peter C; Nguyen, Thi Anh Huong; Mai, Thanh Duc

2017-08-15

The employment of a purpose-made capillary electrophoresis (CE) instrument with capacitively coupled contactless conductivity detection (C 4 D) as a simple and cost-effective solution for clinical screening of paraquat in plasma samples for early-stage diagnosis of acute herbicide poisoning is reported. Paraquat was determined using an electrolyte composed of 10mM histidine adjusted to pH 4 with acetic acid. A detection limit of 0.5mg/L was achieved. Good agreement between results from CE-C 4 D and the confirmation method (HPLC-UV) was obtained, with relative errors for the two pairs of data better than 20% for 31 samples taken from paraquat-intoxicated patients. The results were used by medical doctors for identification and prognosis of acute paraquat poisoning cases. The objective of the work is the deployment of the developed approach in rural areas in Vietnam as a low-cost solution to reduce the mortality rate due to accidental or suicidal ingestion of paraquat. Copyright © 2017. Published by Elsevier B.V.

Effect of low doses of herbicide paraquat on antioxidant defense in Drosophila

Czech Academy of Sciences Publication Activity Database

Krůček, Tomáš; Korandová, Michala; Szakosová, K.; Šerý, Michal; Čapková Frydrychová, Radmila

2015-01-01

Roč. 88, č. 4 (2015), s. 235-248 ISSN 0739-4462 R&D Projects: GA ČR GA14-07172S Grant - others:GA JU(CZ) 038/2014/P; GA JU(CZ) 052/2013/P; European Union Seventh Framework Programme(CZ) 316304 Program:FP7 Institutional support: RVO:60077344 Keywords : Drosophila * oxidative stress * paraquat Subject RIV: CE - Biochemistry Impact factor: 1.357, year: 2015 http://onlinelibrary.wiley.com/doi/10.1002/arch.21222/epdf

Investigating global trends in paraquat intoxication research from 1962 to 2015 using bibliometric analysis.

Science.gov (United States)

Zyoud, Sa'ed H

2018-06-01

Paraquat is considered to be the main pesticide involved in accidental and intentional poisoning, and is responsible for a high rate of morbidity and mortality. The aim of this study is to present a comprehensive bibliometric analysis of paraquat intoxication-related research. Data was retrieved in March 2017 from the Scopus database. An overview of the research on paraquat intoxication was presented alongside the information related to several bibliometric indicators, such as research trends, countries with their h-index, collaboration, hot issues, top-cited publications, journals, and institutions. There were 1971 publications related to paraquat intoxication in the Scopus database that were published between 1966 and 2015. There was increasing research output in the field of paraquat intoxication during the period 2006-2015. The USA published the highest number of publications (n = 338), followed by Japan with 228 publications, and China with 159 publications. The USA and the UK achieved the greatest h-index values (h-index values of 49 and 31, respectively). The USA also achieved the highest number of publications involving international collaboration, with 55 publications, followed by the UK, with 18 publications. The most prevalent topics in this field were "acute paraquat intoxication," "toxic effects of paraquat to the lung," and "mechanism of paraquat toxicity." Although a substantial amount of research has been produced on paraquat intoxication for most developed countries, there are research gaps regarding the international research agenda in this research area. The findings could be applied for prioritizing and organizing future research efforts related to paraquat toxicity. © 2018 Wiley Periodicals, Inc.

Activation of apoptosis signal-regulating kinase 1 is a key factor in paraquat-induced cell death: modulation by the Nrf2/Trx axis.

Science.gov (United States)

Niso-Santano, Mireia; González-Polo, Rosa A; Bravo-San Pedro, José M; Gómez-Sánchez, Rubén; Lastres-Becker, Isabel; Ortiz-Ortiz, Miguel A; Soler, Germán; Morán, José M; Cuadrado, Antonio; Fuentes, José M

2010-05-15

Although oxidative stress is fundamental to the etiopathology of Parkinson disease, the signaling molecules involved in transduction after oxidant exposure to cell death are ill-defined, thus making it difficult to identify molecular targets of therapeutic relevance. We have addressed this question in human dopaminergic neuroblastoma SH-SY5Y cells exposed to the parkinsonian toxin paraquat (PQ). This toxin elicited a dose-dependent increase in reactive oxygen species and cell death that correlated with activation of ASK1 and the stress kinases p38 and JNK. The relevance of these kinases in channeling PQ neurotoxicity was demonstrated with the use of interference RNA for ASK1 and two well-established pharmaceutical inhibitors for JNK and p38. The toxic effect of PQ was substantially attenuated by preincubation with vitamin E, blocking ASK1 pathways and preventing oxidative stress and cell death. In a search for a physiological pathway that might counterbalance PQ-induced ASK1 activation, we analyzed the role of the transcription factor Nrf2, master regulator of redox homeostasis, and its target thioredoxin (Trx), which binds and inhibits ASK1. Trx levels were undetectable in Nrf2-deficient mouse embryo fibroblasts (MEFs), whereas they were constitutively high in Keap1-deficient MEFs as well as in SH-SY5Y cells treated with sulforaphane (SFN). Consistent with these data, Nrf2-deficient MEFs were more sensitive and Keap1-deficient MEFs and SH-SY5Y cells incubated with SFN were more resistant to PQ-induced cell death. This study identifies ASK1/JNK and ASK1/p38 as two critical pathways involved in the activation of cell death under oxidative stress conditions and identifies the Nrf2/Trx axis as a new target to block these pathways and protect from oxidant exposure such as that found in Parkinson and other neurodegenerative diseases. Copyright 2010 Elsevier Inc. All rights reserved.

Chest radiographic findings in acute paraquat poisoning

Energy Technology Data Exchange (ETDEWEB)

Na, Gyeong Gyun; Lee, Mi Sook; Kim, Hee Jun; Sun, In O [Presbyterian Medical Center, Jeonju (Korea, Republic of)

2016-01-15

To describe the chest radiographic findings of acute paraquat poisoning. 691 patients visited the emergency department of our hospital between January 2006 and October 2012 for paraquat poisoning. Of these 691, we identified 56 patients whose initial chest radiographs were normal but who developed radiographic abnormalities within one week. We evaluated their radiographic findings and the differences in imaging features based on mortality. The most common finding was diffuse consolidation (29/56, 52%), followed by consolidation with linear and nodular opacities (18/56, 32%), and combined consolidation and pneumomediastinum (7/56, 13%). Pleural effusion was noted in 17 patients (30%). The two survivors (4%) showed peripheral consolidations, while the 54 patients (96%) who died demonstrated bilateral (42/54, 78%) or unilateral (12/54, 22%) diffuse consolidations. Rapidly progressing diffuse pulmonary consolidation was observed within one week on follow-up radiographs after paraquat ingestion in the deceased, but the survivors demonstrated peripheral consolidation.

Complexation between Methyl Viologen (Paraquat) Bis(Hexafluorophosphate) and Dibenzo[24]Crown-8 Revisited

DEFF Research Database (Denmark)

Gasa, Travis B.; Spruell, Jason M.; Dichtel, William R.

2009-01-01

Paraquat bis(hexafluorophosphate) undergoes stepwise dissociation in acetone. All three species - the neutral molecule, and the mono- and dications - are represented significantly under the experimental conditions typically used in host-guest binding studies. Paraquat forms at least four host...... toward dibenzo[24]crown-8. Thus, the relative abundance of neutral, singly, and doubly charged pseudorotaxanes is identical to the relative abundance of neutral, singly, and doubly charged paraquat unbound with respect to the crown ether in acetone. In the specific case of paraquat/dibenzo[24]crown-8...

Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure.

Science.gov (United States)

Tang, Suk Peng; Kuttulebbai Nainamohamed Salam, Sirajudeen; Jaafar, Hasnan; Gan, Siew Hua; Muzaimi, Mustapha; Sulaiman, Siti Amrah

2017-01-01

Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2 mL/kg/day), Tualang honey (1.0 g/kg/day), or ubiquinol (0.2 g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week) or PQ (10 mg/kg/week) once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ ( p honey ameliorated the toxic effects observed in the midbrain and lungs. The beneficial effects of Tualang honey were comparable to those of ubiquinol, which was used as a positive control. These findings suggest that treatment with Tualang honey may protect against PQ-induced toxicity in the rat midbrain and lung.

Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure

Science.gov (United States)

Sulaiman, Siti Amrah

2017-01-01

Paraquat (PQ) is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2 mL/kg/day), Tualang honey (1.0 g/kg/day), or ubiquinol (0.2 g/kg/day) throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week) or PQ (10 mg/kg/week) once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ (p honey ameliorated the toxic effects observed in the midbrain and lungs. The beneficial effects of Tualang honey were comparable to those of ubiquinol, which was used as a positive control. These findings suggest that treatment with Tualang honey may protect against PQ-induced toxicity in the rat midbrain and lung. PMID:28127418

Removal of paraquat and linuron from water by continuous flow adsorption/ ultrafiltration membrane processes

International Nuclear Information System (INIS)

Zahoor, M.

2013-01-01

The magnetic activated carbon (MAC) was prepared, characterized and compared with powdered activated carbon (PAC) for its adsorptive parameters. Both adsorbents were then used in combination ultrafiltration (UF) membrane as pretreatment for the removal of paraquat and linuron from water. The comparison of membrane parameters like percent retention, permeate flux and backwash times for PAC/UF and MAC/UF hybrid processes showed that percent retention of paraquat and linuron was high for PAC due to its high surface area. However due to cake formation over membrane surface the decline permeate fluxes and long backwash times for PAC were observed. PAC also caused blackening of pipes and flow meter. MAC (an iron oxide and PAC composite) was removed from slurry through magnet thus no cake formation and secondary problems observed for PAC was not encountered. Also the backwash times were minimum for MAC/UF process. (author)

Paraquat prohibition and change in the suicide rate and methods in South Korea.

Directory of Open Access Journals (Sweden)

Woojae Myung

Full Text Available The annual suicide rate in South Korea is the highest among the developed countries. Paraquat is a highly lethal herbicide, commonly used in South Korea as a means for suicide. We have studied the effect of the 2011 paraquat prohibition on the national suicide rate and method of suicide in South Korea. We obtained the monthly suicide rate from 2005 to 2013 in South Korea. In our analyses, we adjusted for the effects of celebrity suicides, and economic, meteorological, and seasonal factors on suicide rate. We employed change point analysis to determine the effect of paraquat prohibition on suicide rate over time, and the results were verified by structural change analysis, an alternative statistical method. After the paraquat prohibition period in South Korea, there was a significant reduction in the total suicide rate and suicide rate by poisoning with herbicides or fungicides in all age groups and in both genders. The estimated suicide rates during this period decreased by 10.0% and 46.1% for total suicides and suicides by poisoning of herbicides or fungicides, respectively. In addition, method substitution effect of paraquat prohibition was found in suicide by poisoning by carbon monoxide, which did not exceed the reduction in the suicide rate of poisoning with herbicides or fungicides. In South Korea, paraquat prohibition led to a lower rate of suicide by paraquat poisoning, as well as a reduction in the overall suicide rate. Paraquat prohibition should be considered as a national suicide prevention strategy in developing and developed countries alongside careful observation for method substitution effects.

Paraquat prohibition and change in the suicide rate and methods in South Korea.

Science.gov (United States)

Myung, Woojae; Lee, Geung-Hee; Won, Hong-Hee; Fava, Maurizio; Mischoulon, David; Nyer, Maren; Kim, Doh Kwan; Heo, Jung-Yoon; Jeon, Hong Jin

2015-01-01

The annual suicide rate in South Korea is the highest among the developed countries. Paraquat is a highly lethal herbicide, commonly used in South Korea as a means for suicide. We have studied the effect of the 2011 paraquat prohibition on the national suicide rate and method of suicide in South Korea. We obtained the monthly suicide rate from 2005 to 2013 in South Korea. In our analyses, we adjusted for the effects of celebrity suicides, and economic, meteorological, and seasonal factors on suicide rate. We employed change point analysis to determine the effect of paraquat prohibition on suicide rate over time, and the results were verified by structural change analysis, an alternative statistical method. After the paraquat prohibition period in South Korea, there was a significant reduction in the total suicide rate and suicide rate by poisoning with herbicides or fungicides in all age groups and in both genders. The estimated suicide rates during this period decreased by 10.0% and 46.1% for total suicides and suicides by poisoning of herbicides or fungicides, respectively. In addition, method substitution effect of paraquat prohibition was found in suicide by poisoning by carbon monoxide, which did not exceed the reduction in the suicide rate of poisoning with herbicides or fungicides. In South Korea, paraquat prohibition led to a lower rate of suicide by paraquat poisoning, as well as a reduction in the overall suicide rate. Paraquat prohibition should be considered as a national suicide prevention strategy in developing and developed countries alongside careful observation for method substitution effects.

Toxicological responses on cytochrome P450 and metabolic transferases in liver of goldfish (Carassius auratus) exposed to lead and paraquat.

Science.gov (United States)

Xu, Xiaoming; Cui, Zhaojie; Wang, Xinlei; Wang, Xixin; Zhang, Su

2018-04-30

As the producer of reactive oxygen species (ROS), both lead (Pb) and paraquat (PQ) can generate serious oxidative stress in target organs which result in irreversible toxic effects on organisms. They can disturb the normal catalytic activities of many enzymes by means of different toxicity mechanism. The changed responses of enzymes are frequently used as the biomarkers for indicating the relationship between toxicological effects and exposure levels. In this work, goldfish was exposed to a series of test groups containing lead and paraquat in the range of 0.05-10mg/L, respectively. Four hepatic enzyme activities, including 7-ethoxyresorufinO-deethylase (EROD), 7-benzyloxy-4-trifluoromethyl-coumarin-O-debenzyloxylase (BFCOD), glutathione S-transferase (GST) and UDP-glucuronosyltransferase (UGT) were determined after 1, 7, 14, 28 days exposure. The results showed that the activities of EROD and BFCOD in fish were significantly inhibited in response to paraquat at all exposure levels during the whole experiment. Similarly, the inhibitory effects of lead exposure on BFCOD activity were found in our study, while different responses of lead on EROD were observed. There were no significant differences on EROD activity under lower concentrations of lead (less than 0.1mg/L) before 14 days until an obvious increase was occurred for the 0.5mg/L lead treatment group at day 14. Furthermore, lead showed stronger inhibition on GST activity than paraquat when the concentrations of the two toxicants were more than 0.5mg/L. However, the similar dose and time-dependent manners of UGT activity were found under lead and paraquat exposure. Our results indicated that higher exposure levels and longer accumulations caused inhibitory effects on the four enzymes regardless of lead or paraquat stress. In addition, the responses of phase I enzymes were more sensitive than that of phase II enzymes and they may be served as the acceptable biomarkers for evaluating the toxicity effects of both

Qualidade de tubérculos de batatas-semente tratados com paraquat e o desenvolvimento de uma metodologia simplificada de detecção de resíduo do herbicida Quality of seed potato tubers treated with paraquat and the development of a simplified methodology for paraquat residue detection

Directory of Open Access Journals (Sweden)

Welington Pereira

1995-01-01

Full Text Available O objetivo desse trabalho foi avaliar a qualidade de tubérculos de batatas-semente (Solanum tuberosum tratados com paraquat e desenvolver uma metodologia simplificada de detecção de resíduos de herbicida. Dois ensaios foram realizados no Laboratório da Ciência das Plantas Daninhas do Centro Nacional de Pesquisa de hortaliças, Brasília, DF. No experimento, tubérculos das cultivares Achat e Baronesa foram submersos em soluções de 0 e 200 ppm de paraquat ou injetados com 0,5 ml de soluções de 0 e 200 ppm do herbicida. O delineamento experimental foi inteiramente casualizado com 8 repetições e 12 tubérculos por parcela. Os tubérculos foram colocados em câmara fria, após a aplicação com paraquat, para quebra da dormência. Após a brotação dos tubérculos avaliou-se a qualidade interna dos mesmos, amostrando, posteriormente, 2 tubérculos de cada parcela para o plantio em vasos, sob condições de telado, para verificar possíveis danos no crescimento das plantas oriundas dos tubérculos tratados. Os tratamentos de imersão não provocaram, aparentemente, nenhum dano interno nos tubérculos, ou nem mesmo afetaram a nova geração, entretanto, os tubérculos injetados com paraquat foram severamente deteriorados e carbonizados, originando plantas bastante debilitadas. Esses resultados indicam que quando o paraquat for aplicado sob condições que favoreçam sua penetração ou translocação para o interior do tubérculo, atingindo os vasos e a polpa, pode danificá-lo severamente, prejudicar sua aparência, qualidade de produção e reduzir o desenvolvimento da nova geração de plantas oriundas dos tubérculos contaminados . No segundo experimento, desenvolveu-se uma metodologia simplificada para detectar resíduos de paraquat nos tubérculos através de colorimetria, visto que o paraquat é reduzido a um radical de cor azul na presença de ditionito de sódio (Na2S2O4 a 1% em meio básico, a qual se intensifica à medida que a

Differential Effects of Methyl-4-Phenylpyridinium Ion, Rotenone, and Paraquat on Differentiated SH-SY5Y Cells

Directory of Open Access Journals (Sweden)

João Barbosa Martins

2013-01-01

Full Text Available Paraquat (PQ, a cationic nonselective bipyridyl herbicide, has been used as neurotoxicant to modulate Parkinson’s disease in laboratory settings. Other compounds like rotenone (ROT, a pesticide, and 1-methyl-4-phenylpyridinium ion (MPP+ have been widely used as neurotoxicants. We compared the toxicity of these three neurotoxicants using differentiated dopaminergic SH-SY5Y human cells, aiming to elucidate their differential effects. PQ-induced neurotoxicity was shown to be concentration and time dependent, being mitochondrial dysfunction followed by neuronal death. On the other hand, cells exposure to MPP+ induced mitochondrial dysfunction, but not cellular lyses. Meanwhile, ROT promoted both mitochondrial dysfunction and neuronal death, revealing a biphasic pattern. To further elucidate PQ neurotoxic mechanism, several protective agents were used. SH-SY5Y cells pretreatment with tiron (TIR and 2-hydroxybenzoic acid sodium salt (NaSAL, both antioxidants, and Nω-nitro-L-arginine methyl ester hydrochloride (L-NAME, a nitric oxide synthase inhibitor, partially protected against PQ-induced cell injury. Additionally, 1-(2-[bis(4-fluorophenylmethoxy]ethyl-4-(3-phenyl-propylpiperazine (GBR 12909, a dopamine transporter inhibitor, and cycloheximide (CHX, a protein synthesis inhibitor, also partially protected against PQ-induced cell injury. In conclusion, we demonstrated that PQ, MPP+, and ROT exerted differential toxic effects on dopaminergic cells. PQ neurotoxicity occurred through exacerbated oxidative stress, with involvement of uptake through the dopamine transporter and protein synthesis.

Characterization and comprehension of zeolite NaY/mesoporous SBA-15 composite as adsorbent for paraquat

Energy Technology Data Exchange (ETDEWEB)

Osakoo, Nattawut, E-mail: natawut.work@gmail.com [School of Chemistry, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima, 30000 (Thailand); Pansakdanon, Chaianun [School of Chemistry, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima, 30000 (Thailand); Department of Chemistry, Faculty of Science, Ubon Ratchathani University, Ubon Ratchathani, 34190 (Thailand); Sosa, Narongrit; Deekamwong, Krittanun; Keawkumay, Chalermpan; Rongchapo, Wina [School of Chemistry, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima, 30000 (Thailand); Chanlek, Narong [Synchrotron Light Research Institute, Nakhon Ratchasima, 30000 (Thailand); Jitcharoen, Juthamas [Department of Chemistry, Faculty of Science, Ubon Ratchathani University, Ubon Ratchathani, 34190 (Thailand); Prayoonpokarach, Sanchai [School of Chemistry, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima, 30000 (Thailand); Wittayakun, Jatuporn, E-mail: jatuporn@g.sut.ac.th [School of Chemistry, Institute of Science, Suranaree University of Technology, Nakhon Ratchasima, 30000 (Thailand)

2017-06-01

NaY was synthesized from fumed silica and further modified to form a composite with SBA-15. Textural properties and basicity of the composite NaY-SBA-15 were between those of the parent materials. Paraquat adsorption on NaY was 204.1 mg/g, higher than that on NaY synthesized with rice husk silica from the previous work. SBA-15 was a poor adsorbent for paraquat. Based on the weight of NaY, the adsorption capacity of analytical-grade paraquat on the NaY-SBA-15 composite was 241.5 mg/g-NaY. Moreover, the composite adsorbed blue dye from a commercial grade paraquat. Interaction between the NaY-SBA-15 and paraquat could be from C and N atoms in paraquat with oxygen atom on NaY-SBA-15. - Highlights: • Zeolite NaY/mesoporous SBA-15 composite was synthesized with a simple method. • NaY and SBA-15 coexisted in the composite confirmed by FTIR, CO{sub 2}-TPD and XPS. • Adsorption capacity of paraquat (mg/g-NaY) was improved by NaY and SBA-15 composite. • C and N atoms in paraquat could interact with oxygen atom on NaY-SBA-15 composite.

DNaseI Protects against Paraquat-Induced Acute Lung Injury and Pulmonary Fibrosis Mediated by Mitochondrial DNA

Directory of Open Access Journals (Sweden)

Guo Li

2015-01-01

Full Text Available Background. Paraquat (PQ poisoning is a lethal toxicological challenge that served as a disease model of acute lung injury and pulmonary fibrosis, but the mechanism is undetermined and no effective treatment has been discovered. Methods and Findings. We demonstrated that PQ injures mitochondria and leads to mtDNA release. The mtDNA mediated PBMC recruitment and stimulated the alveolar epithelial cell production of TGF-β1 in vitro. The levels of mtDNA in circulation and bronchial alveolar lavage fluid (BALF were elevated in a mouse of PQ-induced lung injury. DNaseI could protect PQ-induced lung injury and significantly improved survival. Acute lung injury markers, such as TNFα, IL-1β, and IL-6, and marker of fibrosis, collagen I, were downregulated in parallel with the elimination of mtDNA by DNaseI. These data indicate a possible mechanism for PQ-induced, mtDNA-mediated lung injury, which may be shared by other causes of lung injury, as suggested by the same protective effect of DNaseI in bleomycin-induced lung injury model. Interestingly, increased mtDNA in the BALF of patients with amyopathic dermatomyositis-interstitial lung disease can be appreciated. Conclusions. DNaseI targeting mtDNA may be a promising approach for the treatment of PQ-induced acute lung injury and pulmonary fibrosis that merits fast tracking through clinical trials.

Clinical features and prognosis of paraquat poisoning: a review of 41 cases

Science.gov (United States)

Delirrad, Mohammad; Majidi, Mohammad; Boushehri, Behzad

2015-01-01

Purpose: Paraquat is a contact herbicide which is highly toxic to human. Deliberate self-poisoning with paraquat continues to be a major public health concern in many developing countries. This study aimed to evaluate the data on cases of acute paraquat poisoning and to compare different variables between survivors and non-survivors. Methods: In this cross sectional study, medical records of all paraquat intoxicated patients were reviewed at Taleghani hospital of Urmia, Iran, from 2007 to 2013, retrospectively. Demographics, clinical features and laboratory findings were evaluated. The variables compared between survivors and non-survivors were the amount of paraquat ingested, occurrence of vomiting after ingestion, time and place of hospital admission, length of hospital stay, leukocytosis, serum creatinine level and the outcomes. Results: A total of 41 patients were evaluated. The mean ± standard deviation of patients’ age were 31.6±16.9 years. The Length of hospital stay was 5.75±4.6 days. Most poisonings occurred in spring and summer. The in-hospital fatality rate was 46.3%. Statistically significant associations were found between the outcome of patients and the amount ingested (P=0.001), vomiting (P=0.004), early need to intensive cares (P=0.009), leukocytosis (P=0.001), serum creatinine levels (P=0.001), manifestations of acute hepatic (P<0.001) and respiratory failure (P=0.007). Conclusion: Ingestion of more than 30 ml, prompt vomiting, early need to intensive cares, leukocytosis, and multi-organ failures are major determinants for fatal outcome of paraquat poisoning. It may be useful to educate health professionals and the general population about the serious consequences of exposure to paraquat. PMID:26221379

Effets combinés du compost, du Paraquat et de la ...

African Journals Online (AJOL)

Ce-PC

aimed at evaluating the synergistic effects of Paraquat and Lambdacyhalothrin in the presence of the compost .... Paraquat (200 g/l) et la Lambda super 2.5 EC, ..... Enhanced microbial degradation implicated in rapid loss of chlorpyrifos from the controlled release formulation susucon(R) Blue in soil. Crop. Protection,. 17:.

Clinical features and prognosis of paraquat poisoning in French Guiana: A review of 62 cases.

Science.gov (United States)

Elenga, Narcisse; Merlin, Caroline; Le Guern, Rémi; Kom-Tchameni, Rémi; Ducrot, Yves-Marie; Pradier, Maxime; Ntab, Balthazar; Dinh-Van, Kim-Anh; Sobesky, Milko; Mathieu, Daniel; Dueymes, Jean-Marc; Egmann, Gérald; Kallel, Hatem; Mathieu-Nolf, Monique

2018-04-01

Paraquat is a nonselective contact herbicide of great toxicological importance, being associated with high mortality rates. Because of its high toxicity, the European Union withdrew it from its market in 2007. The aim of this study is to analyze all cases of paraquat poisoning hospitalized in French Guiana in order to assess their incidence and main characteristics.Medical records of all paraquat intoxicated patients hospitalized from 2008 until 2015 were reviewed in this retrospective study.Demographics, clinical presentation, and laboratory data were evaluated.A total of 62 cases were reviewed. The incidence of paraquat poisoning was 3.8/100,000 inhabitants/year. There were 44 adults and 18 children younger than 16 years of age. The median ages were 31 years [18.08-75.25] in adults and 13.4 years [0.75-15.08] in children, respectively. The median duration of hospitalization was longer in children [15.5 days (1-24)] than in adults [2 days (1-30)], P < .01. The majority of cases was due to self-poisoning (84%).Children had ingested a lower quantity of paraquat [48.8 mg/kg (10-571.1)] than adults [595.8 mg/kg (6-3636.4), P = .03]. There were more deaths among adults (65%) than in children (22%), P = .004. The severity and outcome was determined primarily by the amount of paraquat ingested.In conclusion, French Guiana has the largest cohort of paraquat poisonings in the European Union. The major factor affecting the prognosis of patients was the ingested amount of paraquat. The administration of activated charcoal or Pemba, in situ, within the first hour after ingestion of paraquat is essential.

Standardized extracts of Bacopa monniera protect against MPP+- and paraquat-induced toxicity by modulating mitochondrial activities, proteasomal functions, and redox pathways.

Science.gov (United States)

Singh, Manjeet; Murthy, Ven; Ramassamy, Charles

2012-01-01

Parkinson's disease (PD) is one of the most common age-related neurodegenerative diseases and affects millions of people worldwide. Strong evidence supports the role of free radicals, oxidative stress, mitochondrial, and proteasomal dysfunctions underlying neuronal death in PD. Environmental factors, especially pesticides, represent one of the primary classes of neurotoxic agents associated with PD, and several epidemiological studies have identified the exposure of the herbicide paraquat (PQ) as a potential risk factor for the onset of PD. The objective of our study was to investigate the neuroprotective effects of the standardized extracts of Bacopa monniera (BM) against PQ-induced and 1-methyl-4-phenyl-pyridinium iodide (MPP(+))-induced toxicities and to elucidate the mechanisms underlying this protection. Our results show that a pretreatment with the BM extract from 50 μg/ml protected the dopaminergic SK-N-SH cell line against MPP(+)- and PQ-induced toxicities in various cell survival assays. We demonstrate that BM pretreatment prevented the depletion of glutathione (GSH) besides preserving the mitochondrial membrane potential and maintaining the mitochondrial complex I activity. BM pretreatment from 10.0 μg/ml also prevented the generation of intracellular reactive oxygen species and decreased the mitochondrial superoxide level. BM treatment activated the nuclear factor erythroid 2-related factor 2 pathway by modulating the expression of Keap1, thereby upregulating the endogenous GSH synthesis. The effect of BM on the phosphorylation of Akt further strengthens its role in the promotion of cell survival. By preserving the cellular redox homeostasis and mitochondrial activities and by promoting cell survival pathways, BM extract may have therapeutic uses in various age-related neurodegenerative diseases such as PD.

Paraquat-loaded alginate/chitosan nanoparticles: Preparation, characterization and soil sorption studies

Energy Technology Data Exchange (ETDEWEB)

Santos Silva, Mariana dos; Sgarbi Cocenza, Daniela [Department of Environmental Engineering, Sao Paulo State University - UNESP, Avenida Tres de Marco, No. 511, CEP 18087-180, Sorocaba, SP (Brazil); Grillo, Renato; Silva de Melo, Nathalie Ferreira [Department of Environmental Engineering, Sao Paulo State University - UNESP, Avenida Tres de Marco, No. 511, CEP 18087-180, Sorocaba, SP (Brazil); Department of Biochemistry, Institute of Biology, State University of Campinas - UNICAMP, Campinas, SP (Brazil); Tonello, Paulo Sergio [Department of Environmental Engineering, Sao Paulo State University - UNESP, Avenida Tres de Marco, No. 511, CEP 18087-180, Sorocaba, SP (Brazil); Camargo de Oliveira, Luciana [Department of Chemistry, UFSCAr, Campus Sorocaba, SP (Brazil); Lopes Cassimiro, Douglas [Institute of Chemistry, Sao Paulo State University - UNESP, Araraquara, SP (Brazil); Rosa, Andre Henrique [Department of Environmental Engineering, Sao Paulo State University - UNESP, Avenida Tres de Marco, No. 511, CEP 18087-180, Sorocaba, SP (Brazil); Fernandes Fraceto, Leonardo, E-mail: leonardo@sorocaba.unesp.br [Department of Environmental Engineering, Sao Paulo State University - UNESP, Avenida Tres de Marco, No. 511, CEP 18087-180, Sorocaba, SP (Brazil); Department of Biochemistry, Institute of Biology, State University of Campinas - UNICAMP, Campinas, SP (Brazil)

2011-06-15

Agrochemicals are amongst the contaminants most widely encountered in surface and subterranean hydrological systems. They comprise a variety of molecules, with properties that confer differing degrees of persistence and mobility in the environment, as well as different toxic, carcinogenic, mutagenic and teratogenic potentials, which can affect non-target organisms including man. In this work, alginate/chitosan nanoparticles were prepared as a carrier system for the herbicide paraquat. The preparation and physico-chemical characterization of the nanoparticles was followed by evaluation of zeta potential, pH, size and polydispersion. The techniques employed included transmission electron microscopy, differential scanning calorimetry and Fourier transform infrared spectroscopy. The formulation presented a size distribution of 635 {+-} 12 nm, polydispersion of 0.518, zeta potential of -22.8 {+-} 2.3 mV and association efficiency of 74.2%. There were significant differences between the release profiles of free paraquat and the herbicide associated with the alginate/chitosan nanoparticles. Tests showed that soil sorption of paraquat, either free or associated with the nanoparticles, was dependent on the quantity of organic matter present. The results presented in this work show that association of paraquat with alginate/chitosan nanoparticles alters the release profile of the herbicide, as well as its interaction with the soil, indicating that this system could be an effective means of reducing negative impacts caused by paraquat.

Paraquat Induced Changes in Reserve Carbohydrates, Fatty Acids and Oleoresin Content of Young Slash Pines

Science.gov (United States)

Claud L. Brown; Terry R. Clason; Jerry L. Michael

1976-01-01

Paraquat was fed into the terminal leaders of five-year-old slash pine trees and collected at weekly intervals for 4 weeks.Cytological observations showed a decrease in starch levels and a corresponding increase in content of oleoresin. Quantitative analysis indicated a decrease in starch accompanying increases in fatty acids, monoterpenes, and resin acids.

Tualang Honey Protects the Rat Midbrain and Lung against Repeated Paraquat Exposure

Directory of Open Access Journals (Sweden)

Suk Peng Tang

2017-01-01

Full Text Available Paraquat (PQ is a dopaminergic neurotoxin and a well-known pneumotoxicant that exerts its toxic effect via oxidative stress-mediated cellular injuries. This study investigated the protective effects of Tualang honey against PQ-induced toxicity in the midbrain and lungs of rats. The rats were orally treated with distilled water (2 mL/kg/day, Tualang honey (1.0 g/kg/day, or ubiquinol (0.2 g/kg/day throughout the experimental period. Two weeks after the respective treatments, the rats were injected intraperitoneally with saline (1 mL/kg/week or PQ (10 mg/kg/week once per week for four consecutive weeks. After four weekly exposures to PQ, the glutathione peroxidase activity and the number of tyrosine-hydroxylase immunopositive neurons in the midbrain were significantly decreased in animals from group PQ (p<0.05. The lungs of animals from group PQ showed significantly decreased activity of superoxide dismutase and glutathione-S-transferase. Treatment with Tualang honey ameliorated the toxic effects observed in the midbrain and lungs. The beneficial effects of Tualang honey were comparable to those of ubiquinol, which was used as a positive control. These findings suggest that treatment with Tualang honey may protect against PQ-induced toxicity in the rat midbrain and lung.

Degradation of Paraquat in Gramoxone Pesticide with Addition of ZnO

Directory of Open Access Journals (Sweden)

Febrina Arfi

2017-11-01

Full Text Available Paraquat is the most toxic herbicide, the main agricultural crops and plantations that use them are cloves, cocoa, oil palm, rubber, coffee, and pepper. Therefore, it is necessary to study to degrade paraquat compounds by photolysis method with using ZnO. Photolysis is a process of UV irradiation with a wavelength of 200-400 nm. In this study Photolysis method used UV light with λ = 365 nm. Degradation of paraquat compound was done with the influence of variation of time without the addition ZnO, the influence of ZnO additional variations, and the effect of combination between variations of time and optimization of ZnO addition. The result of the study shows that photolysis degradation product without the addition of ZnO for 120 minutes has been degraded by 12.56%. While the optimum addition of 0.1 grams ZnO increased the percentage of degradation which is about 57.64%. This is proved that the addition of ZnO with photolysis method can degrade more paraquat compounds.

Honey bee (Apis mellifera) drones survive oxidative stress due to increased tolerance instead of avoidance or repair of oxidative damage.

Science.gov (United States)

Li-Byarlay, Hongmei; Huang, Ming Hua; Simone-Finstrom, Michael; Strand, Micheline K; Tarpy, David R; Rueppell, Olav

2016-10-01

Oxidative stress can lead to premature aging symptoms and cause acute mortality at higher doses in a range of organisms. Oxidative stress resistance and longevity are mechanistically and phenotypically linked; considerable variation in oxidative stress resistance exists among and within species and typically covaries with life expectancy. However, it is unclear whether stress-resistant, long-lived individuals avoid, repair, or tolerate molecular damage to survive longer than others. The honey bee (Apis mellifera L.) is an emerging model system that is well-suited to address this question. Furthermore, this species is the most economically important pollinator, whose health may be compromised by pesticide exposure, including oxidative stressors. Here, we develop a protocol for inducing oxidative stress in honey bee males (drones) via Paraquat injection. After injection, individuals from different colony sources were kept in common social conditions to monitor their survival compared to saline-injected controls. Oxidative stress was measured in susceptible and resistant individuals. Paraquat drastically reduced survival but individuals varied in their resistance to treatment within and among colony sources. Longer-lived individuals exhibited higher levels of lipid peroxidation than individuals dying early. In contrast, the level of protein carbonylation was not significantly different between the two groups. This first study of oxidative stress in male honey bees suggests that survival of an acute oxidative stressor is due to tolerance, not prevention or repair, of oxidative damage to lipids. It also demonstrates colony differences in oxidative stress resistance that might be useful for breeding stress-resistant honey bees. Copyright © 2016 Elsevier Inc. All rights reserved.

Prediction of paraquat exposure and toxicity in clinically ill poisoned patients: a model based approach.

Science.gov (United States)

Wunnapuk, Klintean; Mohammed, Fahim; Gawarammana, Indika; Liu, Xin; Verbeeck, Roger K; Buckley, Nicholas A; Roberts, Michael S; Musuamba, Flora T

2014-10-01

Paraquat poisoning is a medical problem in many parts of Asia and the Pacific. The mortality rate is extremely high as there is no effective treatment. We analyzed data collected during an ongoing cohort study on self-poisoning and from a randomized controlled trial assessing the efficacy of immunosuppressive therapy in hospitalized paraquat-intoxicated patients. The aim of this analysis was to characterize the toxicokinetics and toxicodynamics of paraquat in this population. A non-linear mixed effects approach was used to perform a toxicokinetic/toxicodynamic population analysis in a cohort of 78 patients. The paraquat plasma concentrations were best fitted by a two compartment toxicokinetic structural model with first order absorption and first order elimination. Changes in renal function were used for the assessment of paraquat toxicodynamics. The estimates of toxicokinetic parameters for the apparent clearance, the apparent volume of distribution and elimination half-life were 1.17 l h(-1) , 2.4 l kg(-1) and 87 h, respectively. Renal function, namely creatinine clearance, was the most significant covariate to explain between patient variability in paraquat clearance.This model suggested that a reduction in paraquat clearance occurred within 24 to 48 h after poison ingestion, and afterwards the clearance was constant over time. The model estimated that a paraquat concentration of 429 μg l(-1) caused 50% of maximum renal toxicity. The immunosuppressive therapy tested during this study was associated with only 8% improvement of renal function. The developed models may be useful as prognostic tools to predict patient outcome based on patient characteristics on admission and to assess drug effectiveness during antidote drug development. © 2014 The British Pharmacological Society.

Transcriptome profiling to discover putative genes associated with paraquat resistance in goosegrass (Eleusine indica L..

Directory of Open Access Journals (Sweden)

Jing An

Full Text Available BACKGROUND: Goosegrass (Eleusine indica L., a serious annual weed in the world, has evolved resistance to several herbicides including paraquat, a non-selective herbicide. The mechanism of paraquat resistance in weeds is only partially understood. To further study the molecular mechanism underlying paraquat resistance in goosegrass, we performed transcriptome analysis of susceptible and resistant biotypes of goosegrass with or without paraquat treatment. RESULTS: The RNA-seq libraries generated 194,716,560 valid reads with an average length of 91.29 bp. De novo assembly analysis produced 158,461 transcripts with an average length of 1153.74 bp and 100,742 unigenes with an average length of 712.79 bp. Among these, 25,926 unigenes were assigned to 65 GO terms that contained three main categories. A total of 13,809 unigenes with 1,208 enzyme commission numbers were assigned to 314 predicted KEGG metabolic pathways, and 12,719 unigenes were categorized into 25 KOG classifications. Furthermore, our results revealed that 53 genes related to reactive oxygen species scavenging, 10 genes related to polyamines and 18 genes related to transport were differentially expressed in paraquat treatment experiments. The genes related to polyamines and transport are likely potential candidate genes that could be further investigated to confirm their roles in paraquat resistance of goosegrass. CONCLUSION: This is the first large-scale transcriptome sequencing of E. indica using the Illumina platform. Potential genes involved in paraquat resistance were identified from the assembled sequences. The transcriptome data may serve as a reference for further analysis of gene expression and functional genomics studies, and will facilitate the study of paraquat resistance at the molecular level in goosegrass.

Transcriptome profiling to discover putative genes associated with paraquat resistance in goosegrass (Eleusine indica L.).

Science.gov (United States)

An, Jing; Shen, Xuefeng; Ma, Qibin; Yang, Cunyi; Liu, Simin; Chen, Yong

2014-01-01

Goosegrass (Eleusine indica L.), a serious annual weed in the world, has evolved resistance to several herbicides including paraquat, a non-selective herbicide. The mechanism of paraquat resistance in weeds is only partially understood. To further study the molecular mechanism underlying paraquat resistance in goosegrass, we performed transcriptome analysis of susceptible and resistant biotypes of goosegrass with or without paraquat treatment. The RNA-seq libraries generated 194,716,560 valid reads with an average length of 91.29 bp. De novo assembly analysis produced 158,461 transcripts with an average length of 1153.74 bp and 100,742 unigenes with an average length of 712.79 bp. Among these, 25,926 unigenes were assigned to 65 GO terms that contained three main categories. A total of 13,809 unigenes with 1,208 enzyme commission numbers were assigned to 314 predicted KEGG metabolic pathways, and 12,719 unigenes were categorized into 25 KOG classifications. Furthermore, our results revealed that 53 genes related to reactive oxygen species scavenging, 10 genes related to polyamines and 18 genes related to transport were differentially expressed in paraquat treatment experiments. The genes related to polyamines and transport are likely potential candidate genes that could be further investigated to confirm their roles in paraquat resistance of goosegrass. This is the first large-scale transcriptome sequencing of E. indica using the Illumina platform. Potential genes involved in paraquat resistance were identified from the assembled sequences. The transcriptome data may serve as a reference for further analysis of gene expression and functional genomics studies, and will facilitate the study of paraquat resistance at the molecular level in goosegrass.

Regulation by SoxR of mfsA, Which Encodes a Major Facilitator Protein Involved in Paraquat Resistance in Stenotrophomonas maltophilia.

Directory of Open Access Journals (Sweden)

Kriangsuk Srijaruskul

Full Text Available Stenotrophomonas maltophilia MfsA (Smlt1083 is an efflux pump in the major facilitator superfamily (MFS. Deletion of mfsA renders the strain more susceptible to paraquat, but no alteration in the susceptibility levels of other oxidants is observed. The expression of mfsA is inducible upon challenge with redox cycling/superoxide-generating drug (paraquat, menadione and plumbagin treatments and is directly regulated by SoxR, which is a transcription regulator and sensor of superoxide-generating agents. Analysis of mfsA expression patterns in wild-type and a soxR mutant suggests that oxidized SoxR functions as a transcription activator of the gene. soxR (smlt1084 is located in a head-to-head fashion with mfsA, and these genes share the -10 motif of their promoter sequences. Purified SoxR specifically binds to the putative mfsA promoter motifs that contain a region that is highly homologous to the consensus SoxR binding site, and mutation of the SoxR binding site abolishes binding of purified SoxR protein. The SoxR box is located between the putative -35 and -10 promoter motifs of mfsA; and this position is typical for a promoter in which SoxR acts as a transcriptional activator. At the soxR promoter, the SoxR binding site covers the transcription start site of the soxR transcript; thus, binding of SoxR auto-represses its own transcription. Taken together, our results reveal for the first time that mfsA is a novel member of the SoxR regulon and that SoxR binds and directly regulates its expression.

HFE Genotype Restricts the Response to Paraquat in a Mouse Model of Neurotoxicity.

Science.gov (United States)

Nixon, Anne M; Meadowcroft, Mark D; Neely, Elizabeth B; Snyder, Amanda M; Purnell, Carson J; Wright, Justin; Lamendella, Regina; Nandar, Wint; Huang, Xuemei; Connor, James R

2018-05-01

Parkinson's disease is marked clinically by motor dysfunction and pathologically by dopaminergic cell loss in the substantia nigra and iron accumulation in the substantia nigra. The driver underlying iron accumulation remains unknown and could be genetic or environmental. The HFE protein is critical for the regulation of cellular iron uptake. Mutations within this protein are associated with increased iron accumulation including in the brain. We have focused on the commonly occurring H63D variant of the HFE gene as a disease modifier in a number of neurodegenerative diseases. To investigate the role of H63D HFE genotype, we generated a mouse model in which the wild-type (WT) HFE gene is replaced by the H67D gene variant (mouse homolog of the human H63D gene variant). Using paraquat toxicity as the model for Parkinson's disease, we found that WT mice responded as expected with significantly greater motor function, loss of tyrosine hydroxylase staining and increase microglial staining in the substantia nigra, and an increase in R 2 relaxation rate within the substantia nigra of the paraquat-treated mice compared to their saline-treated counterparts. In contrast, the H67D mice showed a remarkable resistance to paraquat treatment; specifically differing from the WT mice with no changes in motor function or changes in R 2 relaxation rates following paraquat exposure. At baseline, there were differences between the H67D HFE mice and WT mice in gut microbiome profile and increased L-ferritin staining in the substantia nigra that could account for the resistance to paraquat. Of particular note, the H67D HFE mice regardless of whether or not they were treated with paraquat had significantly less tyrosine hydroxylase immunostaining than WT. Our results clearly demonstrate that the HFE genotype impacts the expression of tyrosine hydroxylase in the substantia nigra, the gut microbiome and the response to paraquat providing additional support that the HFE genotype is a disease

Severe paraquat poisoning: clinical and radiological findings in a survivor

Energy Technology Data Exchange (ETDEWEB)

Neves, Fabio Fernandes; Sousa, Romualdo Barroso; Pazin-Filho, Antonio; Cupo, Palmira; Elias Junior, Jorge; Nogueira-Barbosa, Marcello Henrique, E-mail: fabioneves@hcrp.usp.b [University of Sao Paulo (USP), Sao Paulo, SP (Brazil). Medical School

2010-07-01

Paraquat is a nonselective contact herbicide of great toxicological importance, being associated with high mortality rates, mainly due to respiratory failure. We report the case of a 22-year-old male admitted to the emergency room with a sore throat, dysphagia, hemoptysis, and retrosternal pain after the ingestion of 50 mL of a paraquat solution, four days prior to admission. Chest CT scans revealed pulmonary opacities, pneumomediastinum, pneumothorax, and subcutaneous emphysema. The patient was submitted to two cycles of immunosuppressive therapy with cyclophosphamide, methylprednisolone, and dexamethasone. The pulmonary gas exchange parameters gradually improved, and the patient was discharged four weeks later. The clinical and tomographic follow-up evaluations performed at four months after discharge showed that there had been further clinical improvement. We also present a brief review of the literature, as well as a discussion of the therapeutic algorithm for severe paraquat poisoning. (author)

A simple high performance liquid chromatography method for analyzing paraquat in soil solution samples.

Science.gov (United States)

Ouyang, Ying; Mansell, Robert S; Nkedi-Kizza, Peter

2004-01-01

A high performance liquid chromatography (HPLC) method with UV detection was developed to analyze paraquat (1,1'-dimethyl-4,4'-dipyridinium dichloride) herbicide content in soil solution samples. The analytical method was compared with the liquid scintillation counting (LSC) method using 14C-paraquat. Agreement obtained between the two methods was reasonable. However, the detection limit for paraquat analysis was 0.5 mg L(-1) by the HPLC method and 0.05 mg L(-1) by the LSC method. The LSC method was, therefore, 10 times more precise than the HPLC method for solution concentrations less than 1 mg L(-1). In spite of the high detection limit, the UC (nonradioactive) HPLC method provides an inexpensive and environmentally safe means for determining paraquat concentration in soil solution compared with the 14C-LSC method.

Maneb and Paraquat-Mediated Neurotoxicity: Involvement of Peroxiredoxin/Thioredoxin System

Science.gov (United States)

Roede, James R.; Hansen, Jason M.; Go, Young-Mi; Jones, Dean P.

2011-01-01

Epidemiological and in vivo studies have demonstrated that exposure to the pesticides paraquat (PQ) and maneb (MB) increase the risk of developing Parkinson’s disease (PD) and cause dopaminergic cell loss, respectively. PQ is a well-recognized cause of oxidative toxicity; therefore, the purpose of this study was to determine if MB potentiates oxidative stress caused by PQ, thus providing a mechanism for enhanced neurotoxicity by the combination. The results show that PQ alone at a moderately toxic dose (20–30% cell death in 24 h) caused increased reactive oxygen species (ROS) generation, oxidation of mitochondrial thioredoxin-2 and peroxiredoxin-3, lesser oxidation of cytoplasmic thioredoxin-1 and peroxiredoxin-1, and no oxidation of cellular GSH/GSSG. In contrast, MB alone at a similar toxic dose resulted in no ROS generation, no oxidation of thioredoxin and peroxiredoxin, and an increase in cellular GSH after 24 h. Together, MB increased GSH and inhibited ROS production and thioredoxin/peroxiredoxin oxidation observed with PQ alone, yet resulted in more extensive (> 50%) cell death. MB treatment resulted in increased abundance of nuclear Nrf2 and mRNA for phase II enzymes under the control of Nrf2, indicating activation of cell protective responses. The results show that MB potentiation of PQ neurotoxicity does not occur by enhancing oxidative stress and suggests that increased toxicity occurs by a combination of divergent mechanisms, perhaps involving alkylation by MB and oxidation by PQ. PMID:21402726

Paraquat toxicity. (Latest citations from the Life Sciences Collection database). Published Search

Energy Technology Data Exchange (ETDEWEB)

1993-05-01

The bibliography contains citations concerning the toxic effects of the herbicide paraquat on humans and animals. Topics include clinical and pathological findings, biochemical mechanisms, effects of oxygen, pulmonary effects of exposure, and effects on freshwater and marine organisms. The contamination of marijuana plants with paraquat is also considered. (Contains 250 citations and includes a subject term index and title list.)

Eficiência dos dessecantes paraquat e diquat na antecipação da colheita do milho Effectiveness of the desiccants paraquat and diquat in anticipating maize harvesting

Directory of Open Access Journals (Sweden)

P.C. Magalhães

2002-12-01

Full Text Available O uso de dessecantes na cultura do milho pode trazer benefícios para os agricultores, especialmente visando a disponibilização antecipada do solo para implantação de uma nova cultura, assim como o oferecimento antecipado do produto colhido ao mercado. Dentre os dessecantes disponíveis comercialmente, os herbicidas paraquat e diquat merecem destaque. O objetivo deste trabalho foi avaliar a eficiência dos herbicidas paraquat e diquat, aplicados como dessecantes em diversos estádios de desenvolvimento da cultura de milho, sobre parâmetros produtivos e incidência de doenças nos grãos de milho. O ensaio foi conduzido na Embrapa Milho e Sorgo, Sete Lagoas, MG, utilizando-se os seguintes tratamentos: aplicação de paraquat e diquat aos 14 e 7 dias antes e aos 7 dias depois do ponto de maturação fisiológica (MF, assim como na própria MF. Ambos os produtos foram aplicados na dosagem de 400 g ha-1. O cultivar de milho utilizado foi o BRS 3101. Aos 0, 3, 6, 9, 12 e 15 dias após a aplicação dos produtos foram coletados 30 grãos de seis espigas aleatórias, para determinação da umidade dos grãos e peso da matéria seca. Na colheita foram avaliados: altura da planta e da espiga, índice de espigas, produção de grãos e espigas e sanidade dos grãos. Os produtos testados não apresentaram diferenças de eficiência para a maioria dos parâmetros avaliados, embora visualmente tenha sido constatado que o paraquat age mais rapidamente do que o diquat na secagem do tecido foliar verde. Apesar disso, quando se detectou alguma diferença entre os dois produtos químicos, o diquat foi superior ao paraquat. Com relação às épocas de aplicação dos produtos, foi constatado que a aplicação dos dessecantes aos 14 dias antes da MF resultou em redução na produção de grãos, devido à diminuição no peso da matéria seca dos grãos, apesar de ter antecipado em dois dias a MF e em quatro dias a colheita. Esse fato ficou mais bem

Voltammetric Quantification of Paraquat and Glyphosate in Surface Waters

Directory of Open Access Journals (Sweden)

William Roberto Alza-Camacho

2016-09-01

Full Text Available The indiscriminate use of pesticides on crops has a negative environmental impact that affects organisms, soil and water resources, essential for life. Therefore, it is necessary to evaluate the residual effect of these substances in water sources. A simple, affordable and accessible electrochemical method for Paraquat and Glyphosate quantification in water was developed. The study was conducted using as supporting electrolyte Britton-Robinson buffer solution, working electrode of glassy carbon, Ag/AgCl as the reference electrode, and platinum as auxiliary electrode. Differential pulse voltammetry (VDP method for both compounds were validated. Linearity of the methods presented a correlation coefficient of 0.9949 and 0.9919 and the limits of detection and quantification were 130 and 190 mg/L for Paraquat and 40 and 50 mg/L for glyphosate. Comparison with the reference method showed that the electrochemical method provides superior results in quantification of analytes. Of the samples tested, a value of Paraquat was between 0,011 to 1,572 mg/L and for glyphosate it was between 0.201 to 2.777 mg/L, indicating that these compounds are present in water sources and that those may be causing serious problems to human health.

Genome-wide association analysis of oxidative stress resistance in Drosophila melanogaster.

Directory of Open Access Journals (Sweden)

Allison L Weber

Full Text Available Aerobic organisms are susceptible to damage by reactive oxygen species. Oxidative stress resistance is a quantitative trait with population variation attributable to the interplay between genetic and environmental factors. Drosophila melanogaster provides an ideal system to study the genetics of variation for resistance to oxidative stress.We used 167 wild-derived inbred lines of the Drosophila Genetic Reference Panel for a genome-wide association study of acute oxidative stress resistance to two oxidizing agents, paraquat and menadione sodium bisulfite. We found significant genetic variation for both stressors. Single nucleotide polymorphisms (SNPs associated with variation in oxidative stress resistance were often sex-specific and agent-dependent, with a small subset common for both sexes or treatments. Associated SNPs had moderately large effects, with an inverse relationship between effect size and allele frequency. Linear models with up to 12 SNPs explained 67-79% and 56-66% of the phenotypic variance for resistance to paraquat and menadione sodium bisulfite, respectively. Many genes implicated were novel with no known role in oxidative stress resistance. Bioinformatics analyses revealed a cellular network comprising DNA metabolism and neuronal development, consistent with targets of oxidative stress-inducing agents. We confirmed associations of seven candidate genes associated with natural variation in oxidative stress resistance through mutational analysis.We identified novel candidate genes associated with variation in resistance to oxidative stress that have context-dependent effects. These results form the basis for future translational studies to identify oxidative stress susceptibility/resistance genes that are evolutionary conserved and might play a role in human disease.

Docosahexaenoic acid prevents paraquat-induced reactive oxygen species production in dopaminergic neurons via enhancement of glutathione homeostasis

Energy Technology Data Exchange (ETDEWEB)

Lee, Hyoung Jun; Han, Jeongsu; Jang, Yunseon; Kim, Soo Jeong; Park, Ji Hoon; Seo, Kang Sik [Department of Biochemistry, College of Medicine, Chungnam National University, Daejeon (Korea, Republic of); Jeong, Soyeon; Shin, Soyeon; Lim, Kyu [Department of Biochemistry, College of Medicine, Chungnam National University, Daejeon (Korea, Republic of); Infection Signaling Network Research Center, Chungnam National University, Daejeon (Korea, Republic of); Heo, Jun Young, E-mail: junyoung3@gmail.com [Brainscience Institute, Chungnam National University, Daejeon (Korea, Republic of); Kweon, Gi Ryang, E-mail: mitochondria@cnu.ac.kr [Department of Biochemistry, College of Medicine, Chungnam National University, Daejeon (Korea, Republic of); Infection Signaling Network Research Center, Chungnam National University, Daejeon (Korea, Republic of)

2015-01-30

Highlights: • DHA prevents PQ-induced dopaminergic neuronal loss via decreasing of excessive ROS. • DHA increases GR and GCLm derivate GSH pool by enhancement of Nrf2 expression. • Protective mechanism is removal of PQ-induced ROS via DHA-dependent GSH pool. • DHA may be a good preventive strategy for Parkinson’s disease (PD) therapy. - Abstract: Omega-3 polyunsaturated fatty acid levels are reduced in the substantia nigra area in Parkinson’s disease patients and animal models, implicating docosahexaenoic acid (DHA) as a potential treatment for preventing Parkinson’s disease and suggesting the need for investigations into how DHA might protect against neurotoxin-induced dopaminergic neuron loss. The herbicide paraquat (PQ) induces dopaminergic neuron loss through the excessive production of reactive oxygen species (ROS). We found that treatment of dopaminergic SN4741 cells with PQ reduced cell viability in a dose-dependent manner, but pretreatment with DHA ameliorated the toxic effect of PQ. To determine the toxic mechanism of PQ, we measured intracellular ROS content in different organelles with specific dyes. As expected, all types of ROS were increased by PQ treatment, but DHA pretreatment selectively decreased cytosolic hydrogen peroxide content. Furthermore, DHA treatment-induced increases in glutathione reductase and glutamate cysteine ligase modifier subunit (GCLm) mRNA expression were positively correlated with glutathione (GSH) content. Consistent with this increase in GCLm mRNA levels, Western blot analysis revealed that DHA pretreatment increased nuclear factor-erythroid 2 related factor 2 (Nrf2) protein levels. These findings indicate that DHA prevents PQ-induced neuronal cell loss by enhancing Nrf2-regulated GSH homeostasis.

Docosahexaenoic acid prevents paraquat-induced reactive oxygen species production in dopaminergic neurons via enhancement of glutathione homeostasis

International Nuclear Information System (INIS)

Lee, Hyoung Jun; Han, Jeongsu; Jang, Yunseon; Kim, Soo Jeong; Park, Ji Hoon; Seo, Kang Sik; Jeong, Soyeon; Shin, Soyeon; Lim, Kyu; Heo, Jun Young; Kweon, Gi Ryang

2015-01-01

Highlights: • DHA prevents PQ-induced dopaminergic neuronal loss via decreasing of excessive ROS. • DHA increases GR and GCLm derivate GSH pool by enhancement of Nrf2 expression. • Protective mechanism is removal of PQ-induced ROS via DHA-dependent GSH pool. • DHA may be a good preventive strategy for Parkinson’s disease (PD) therapy. - Abstract: Omega-3 polyunsaturated fatty acid levels are reduced in the substantia nigra area in Parkinson’s disease patients and animal models, implicating docosahexaenoic acid (DHA) as a potential treatment for preventing Parkinson’s disease and suggesting the need for investigations into how DHA might protect against neurotoxin-induced dopaminergic neuron loss. The herbicide paraquat (PQ) induces dopaminergic neuron loss through the excessive production of reactive oxygen species (ROS). We found that treatment of dopaminergic SN4741 cells with PQ reduced cell viability in a dose-dependent manner, but pretreatment with DHA ameliorated the toxic effect of PQ. To determine the toxic mechanism of PQ, we measured intracellular ROS content in different organelles with specific dyes. As expected, all types of ROS were increased by PQ treatment, but DHA pretreatment selectively decreased cytosolic hydrogen peroxide content. Furthermore, DHA treatment-induced increases in glutathione reductase and glutamate cysteine ligase modifier subunit (GCLm) mRNA expression were positively correlated with glutathione (GSH) content. Consistent with this increase in GCLm mRNA levels, Western blot analysis revealed that DHA pretreatment increased nuclear factor-erythroid 2 related factor 2 (Nrf2) protein levels. These findings indicate that DHA prevents PQ-induced neuronal cell loss by enhancing Nrf2-regulated GSH homeostasis

Literatuuronderzoek naar de bepalingsmetboden an paraquat en diquat in groenten, fruit en andere plantaardige produkten

NARCIS (Netherlands)

Lagerwey, W.; Tuinstra, L.G.M.Th.

1981-01-01

De resultaten van de literatuurstudie worden samengevat in een overzicht van de bepalingsmetboden van paraquat en diquat in groenten en fruit e.d. Naast de toepassingsgebieden, chemische en fysische eigenschappen van paraquat en diquat werden de bepalingsmethoden bestudeerd. Spektrofotometrische,

Finding of CT and clinical in paraquat poisoning pulmonary injury

International Nuclear Information System (INIS)

He Zaifang; Li Hongbing; Cheng Shoulin; Li Qixiang; Huang Zhen; Zeng Jianguo

2012-01-01

Objective: To investigate the CT features of pulmonary injury in paraquat poisoning. Methods: The chest CT image of lung injury in 6 cases of paraquat poisoning were analyzed retrospectively. According to different period of poisoning, the 6 cases were divided into 3 types:the early stage of poisoning (within 2 d), the middle stage of poisoning (3-14 d), the late stage of poisoning (>14 d). A comparison between CT signs and the pathological features of patients was made. Results: Among this 6 cases, 3 cases died, 2 cases pulmonary fibrosis was noted, 1 cases recovered. According to different period of poisoning, the 6 cases were divided into 3 stages: in the early stage of poisoning (within 2 d), 3 cases of all patients showed nothing remarkable, 2 cases showed ground-glass opacity, 1 case showed fuzzy lung-marking.In the middle stage of poisoning (3-14 d), all 6 cases showed ground-glass opacity, mosaic attenuation; 6 cases showed pulmonary consolidation; 4 cases showed subpleural lines; 4 cases showed bronchiectasis; 2 cases showed mid-lower pleural effusion. In the late stage of poisoning (>14 d), 4 cases showed pulmonary consolidation and pulmonary fibrosis, 3 cases showed ground-glass opacity and mosaic attenuation, 1 case showed mid-lower pleural effusion; 1 case showed mediastinal emphysema. Conclusion: The clinical pathology process of paraquat poisoning was in line with CT finding which was related with clinical stage and was helpful for clinical assessment of paraquat poisoning promptly and to guide the clinical treatment. (authors)

Intoxicação grave por paraquat: achados clínicos e radiológicos em um sobrevivente Severe paraquat poisoning: clinical and radiological findings in a survivor

Directory of Open Access Journals (Sweden)

Fábio Fernandes Neves

2010-08-01

Full Text Available O paraquat é um herbicida não seletivo que possui grande importância toxicológica, sendo associado a altas taxas de letalidade, devidas principalmente à insuficiência respiratória. Este é o relato do caso de um homem de 22 anos admitido no departamento de emergência com queixa de dor de garganta, disfagia, hemoptise e dor retroesternal. Ele relatava a ingestão de cerca de 50 mL de uma solução de paraquat quatro dias antes da admissão hospitalar. A TC de tórax exibia opacidades pulmonares, pneumomediastino, pneumotórax e enfisema subcutâneo. O paciente foi submetido a dois ciclos de terapia imunossupressora com ciclofosfamida, metilprednisolona e dexametasona. Os parâmetros gasométricos progressivamente melhoraram, e o paciente recebeu alta hospitalar após quatro semanas. Decorridos quatro meses da alta, o paciente foi submetido a controles clínico e tomográfico, os quais confirmaram a melhora clínica. Apresentamos também uma revisão sucinta da literatura, bem como uma discussão do processo de decisão terapêutica para intoxicação grave por paraquat.Paraquat is a nonselective contact herbicide of great toxicological importance, being associated with high mortality rates, mainly due to respiratory failure. We report the case of a 22-year-old male admitted to the emergency room with a sore throat, dysphagia, hemoptysis, and retrosternal pain after the ingestion of 50 mL of a paraquat solution, four days prior to admission. Chest CT scans revealed pulmonary opacities, pneumomediastinum, pneumothorax, and subcutaneous emphysema. The patient was submitted to two cycles of immunosuppressive therapy with cyclophosphamide, methylprednisolone, and dexamethasone. The pulmonary gas exchange parameters gradually improved, and the patient was discharged four weeks later. The clinical and tomographic follow-up evaluations performed at four months after discharge showed that there had been further clinical improvement. We also

Paraquat adsorption on NaX and Al-MCM-41.

Science.gov (United States)

Rongchapo, Wina; Deekamwong, Krittanun; Loiha, Sirinuch; Prayoonpokarach, Sanchai; Wittayakun, Jatuporn

2015-01-01

The aim of this work is to determine paraquat adsorption capacity of zeolite NaX and Al-MCM-41. All adsorbents were synthesized by hydrothermal method using rice husk silica. For Al-MCM-41, aluminum (Al) was added to the synthesis gel of MCM-41 with Al content of 10, 15, 20 and 25 wt%. The faujasite framework type of NaX and mesoporous characteristic of Al-MCM-41 were confirmed by X-ray diffraction. Surface area of all adsorbents determined by N2 adsorption-desorption analysis was higher than 650 m2/g. Al content and geometry were determined by X-ray fluorescence and 27Al nuclear magnetic resonance, respectively. Morphology of Al-MCM-41 were studied by transmission electron microscopy; macropores and defects were observed. The paraquat adsorption experiments were conducted using a concentration range of 80-720 mg/L for NaX and 80-560 mg/L for Al-MCM-41. The paraquat adsorption isotherms from all adsorbents fit well with the Langmuir model. The adsorption capacity of NaX was 120 mg/g-adsorbent. Regarding Al-MCM-41, the 10% Al-MCM-41 exhibited the lowest capacity of 52 mg/g-adsorbent while the other samples had adsorption capacity of 66 mg/g-adsorbent.

Modified poisoning severity score for early prognostic evaluation in acute paraquat poisoning

Directory of Open Access Journals (Sweden)

Feng-lin SONG

2018-04-01

Full Text Available Objective To study the applied value of modified poisoning severity score (PSS for early prognostic evaluation in acute paraquat poisoning. Methods Thirty-seven patients with acute paraquat poisoning from June 2013 to June 2016 were enrolled. The PSS score, the modified PSS score, the acute physiology and the chronic health status Ⅱ score (APACHE Ⅱ of the patients were calculated. The relationship between modified PSS and APACHE Ⅱ was analyzed. Also the factors that affect outcome were analyzed by logistic regression analysis. The work characteristic curve (ROC curve of the PSS, the modified PSS and the APECH Ⅱ were drawn and compared. Results There was a positive correlation between the risk of death and admission time, poisonous dose, the concentration of urine paraquat, and white blood cell count (P<0.05. There was a significant correlation between the modified PSS and the APACHE Ⅱ(P<0.0001. The immediate PSS score, the modified PSS score, and the APACHE Ⅱ score were significant for the prognosis of patients with acute paraquat poisoning. The area under the curve (AUC was in turn 0.774, 0.788, 0.799. Among them, the best bound of the modified PSS score was 6.5 (when the score is greater than 6.5, the risk of death is higher. Further comparison of the area under the three curves showed that there was no significant difference in the area under the ROC curve between the three scores in predicting the prognosis of death [P=0.7633(PSS-DPSS, P=0.7791(PSS-APACHE Ⅱ, P=0.8918(DPSS-APACHE Ⅱ]. Conclusion Modified PSS is helpful in early predicting the prognosis of acute paraquat poisoning. DOI: 10.11855/j.issn.0577-7402.2018.04.13

Adiponectin attenuates lung fibroblasts activation and pulmonary fibrosis induced by paraquat.

Directory of Open Access Journals (Sweden)

Rong Yao

Full Text Available Pulmonary fibrosis is one of the most common complications of paraquat (PQ poisoning, which demands for more effective therapies. Accumulating evidence suggests adiponectin (APN may be a promising therapy against fibrotic diseases. In the current study, we determine whether the exogenous globular APN isoform protects against pulmonary fibrosis in PQ-treated mice and human lung fibroblasts, and dissect the responsible underlying mechanisms. BALB/C mice were divided into control group, PQ group, PQ + low-dose APN group, and PQ + high-dose APN group. Mice were sacrificed 3, 7, 14, and 21 days after PQ treatment. We compared pulmonary histopathological changes among different groups on the basis of fibrosis scores, TGF-β1, CTGF and α-SMA pulmonary content via Western blot and real-time quantitative fluorescence-PCR (RT-PCR. Blood levels of MMP-9 and TIMP-1 were determined by ELISA. Human lung fibroblasts WI-38 were divided into control group, PQ group, APN group, and APN receptor (AdipoR 1 small-interfering RNA (siRNA group. Fibroblasts were collected 24, 48, and 72 hours after PQ exposure for assay. Cell viability and apoptosis were determined via Kit-8 (CCK-8 and fluorescein Annexin V-FITC/PI double labeling. The protein and mRNA expression level of collagen type III, AdipoR1, and AdipoR2 were measured by Western blot and RT-PCR. APN treatment significantly decreased the lung fibrosis scores, protein and mRNA expression of pulmonary TGF-β1, CTGF and α-SMA content, and blood MMP-9 and TIMP-1 in a dose-dependent manner (p<0.05. Pretreatment with APN significantly attenuated the reduced cell viability and up-regulated collagen type III expression induced by PQ in lung fibroblasts, (p<0.05. APN pretreatment up-regulated AdipoR1, but not AdipoR2, expression in WI-38 fibroblasts. AdipoR1 siRNA abrogated APN-mediated protective effects in PQ-exposed fibroblasts. Taken together, our data suggests APN protects against PQ-induced pulmonary fibrosis in a

Psychiatric comorbidity and its impact on mortality in patients who attempted suicide by paraquat poisoning during 2000-2010.

Directory of Open Access Journals (Sweden)

Chemin Lin

Full Text Available Paraquat poisoning is a lethal method of suicide used around the world. Although restricting its accessibility had been widely discussed, the underlying psychopathological mechanism of paraquat self-poisoning and its association with mortality have not yet been explicitly evaluated.We included all patients admitted to a tertiary general hospital in Taiwan between 2000 and 2010 following a suicide attempt by paraquat self-administration. Diagnoses were made upon psychiatric consultation based on the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition (DSM-IV criteria. The risk of mortality was calculated by logistic regression with various psychiatric or medical covariates.The consultation-liaison psychiatry team assessed 157 patients who attempted suicide by paraquat poisoning. Mood disorders (54.0%, including dysthymic (26.7% and major depressive disorders (24.7%, were the most common psychiatric diagnoses among the self-poisoning patients. Among those who attempted suicide, 87 patients (58.0% died and dysthymic disorder (OR = 5.58, 95% CI: 1.13-27.69; p < 0.05 significantly increased the mortality risk after adjustment for relevant medical variables, including age, gender, severity index of paraquat poisoning (SIPP, and risk for respiratory failure.Awareness of comorbid psychiatric illnesses, especially dysthymic disorder, is vital in the prevention and treatment of suicide by paraquat poisoning.

Developmental exposure to paraquat and maneb can impair cognition, learning and memory in Sprague-Dawley rats.

Science.gov (United States)

Li, Bai; He, Xi; Sun, Yan; Li, Baixiang

2016-10-20

Paraquat and maneb are identified environmental pollutants. Combined exposure to paraquat and maneb is a latent risk factor for many diseases, particularly those of the central nervous system, including Parkinson's disease and Alzheimer's disease. Hippocampus is the key structure in memory formation and babies are more sensitive to environmental stimuli than adults, so we investigated the neurotoxicity of paraquat and maneb on the hippocampi of rat pups. Female and male Sprague-Dawley rats were mated (female : male = 2 : 1) every night for a week. The gravid rats were randomly divided into three groups (one control and two experimental groups). A mixed solution of paraquat-maneb was administered twice a week by lavage at a dose of 10 or 15 mg kg(-1) bodyweight (containing 30 or 45 mg kg(-1) bodyweight maneb, respectively) from day 6 after pregnancy till ablactation. Maternal weight gain and offspring bodyweights were not affected by the drugs. However, behavioral tests showed that reaction latency and mistake frequency increased after treatment. Intuitively, we found significant changes in the hippocampal neurons in the morphological observation. Taking into account the interaction of the related genes in the cAMP-PKA-CREB pathway, we used a variety of methods to detect the gene and protein levels. Reduced expression of cAMP and related genes and proteins in the hippocampus and serum was also observed. These results indicate that PQ-MB stimulates cAMP to reduce the production of PKA, thus reducing the phosphorylation of CREB and inhibiting the activation of other elements (BDNF, C-JUN, and C-FOS). These changes lead to hippocampal damage and impaired abilities (learning, cognition, and memory). Our results demonstrate that PQ-MB induces hippocampal toxicity in the early life of rats, and they thus provide a theoretical foundation for further investigation of the bathypelagic mechanism involved and measures that can be taken to avoid PQ-MB neurotoxicity.

Paraquat-induced reactive oxygen species inhibit neutrophil apoptosis via a p38 MAPK/NF-κB-IL-6/TNF-α positive-feedback circuit.

Directory of Open Access Journals (Sweden)

Xiaolong Wang

Full Text Available Paraquat (PQ, a widely used herbicide and potent reactive oxygen species (ROS inducer, can injure multiple tissues and organs, especially the lung. However, the underlying mechanism is still poorly understood. According to previous reports, neutrophil aggregation and excessive ROS production might play pivotal pathogenetic roles. In the present study, we found that PQ could prolong neutrophil lifespan and induce ROS generation in a concentration-independent manner. Activated nuclear factor-κB (NF-κB, p38 mitogen-activated kinase (p38 MAPK, and myeloid cell leukemia sequence 1 (Mcl-1 but not Akt signaling pathways were involved in this process, as well as increasing levels of interleukin-6 (IL-6, tumor necrosis factor-α (TNF-α, and IL-1β. Furthermore, the proinflammatory mediators IL-6 and TNF-α could in turn promote ROS generation, creating a vicious cycle. The existence of such a feedback loop is supported by our finding that neutrophil apoptosis is attenuated by PQ in a concentration-independent manner and could partially explain the clinical dilemma why oxygen therapy will exacerbate PQ induced tissue injury.

Connective tissue growth factor stimulates the proliferation, migration and differentiation of lung fibroblasts during paraquat-induced pulmonary fibrosis.

Science.gov (United States)

Yang, Zhizhou; Sun, Zhaorui; Liu, Hongmei; Ren, Yi; Shao, Danbing; Zhang, Wei; Lin, Jinfeng; Wolfram, Joy; Wang, Feng; Nie, Shinan

2015-07-01

It is well established that paraquat (PQ) poisoning can cause severe lung injury during the early stages of exposure, finally leading to irreversible pulmonary fibrosis. Connective tissue growth factor (CTGF) is an essential growth factor that is involved in tissue repair and pulmonary fibrogenesis. In the present study, the role of CTGF was examined in a rat model of pulmonary fibrosis induced by PQ poisoning. Histological examination revealed interstitial edema and extensive cellular thickening of interalveolar septa at the early stages of poisoning. At 2 weeks after PQ administration, lung tissue sections exhibited a marked thickening of the alveolar walls with an accumulation of interstitial cells with a fibroblastic appearance. Masson's trichrome staining revealed a patchy distribution of collagen deposition, indicating pulmonary fibrogenesis. Western blot analysis and immunohistochemical staining of tissue samples demonstrated that CTGF expression was significantly upregulated in the PQ-treated group. Similarly, PQ treatment of MRC-5 human lung fibroblast cells caused an increase in CTGF in a dose-dependent manner. Furthermore, the addition of CTGF to MRC-5 cells triggered cellular proliferation and migration. In addition, CTGF induced the differentiation of fibroblasts to myofibroblasts, as was evident from increased expression of α-smooth muscle actin (α-SMA) and collagen. These findings demonstrate that PQ causes increased CTGF expression, which triggers proliferation, migration and differentiation of lung fibroblasts. Therefore, CTGF may be important in PQ-induced pulmonary fibrogenesis, rendering this growth factor a potential pharmacological target for reducing lung injury.

Complexation of triptycene-derived macrotricyclic polyether with paraquat derivatives, diquat, and a 2,7-diazapyrenium salt: guest-induced conformational changes of the host.

Science.gov (United States)

Han, Ying; Cao, Jing; Li, Peng-Fei; Zong, Qian-Shou; Zhao, Jian-Min; Guo, Jia-Bin; Xiang, Jun-Feng; Chen, Chuan-Feng

2013-04-05

Complexation between a triptycene-derived macrotricyclic polyether containing two dibenzo-[30]-crown-10 cavities and different functionalized paraquat derivatives, diquat, and a 2,7-diazapyrenium salt in both solution and solid state was investigated in detail. It was found that depending on the guests with different terminal functional groups and structures, the macrotricyclic polyether could form 1:1 or 1:2 complexes with the guests in different complexation modes in solution and also in the solid state. Especially, the conformation of the macrotricyclic polyether was efficiently adjusted by the encapsulated guests, which was to some extent similar to substrate-induced fit of enzymes. Moreover, the binding and releasing of the guests in the complexes could be controlled by potassium ions.

Reversible oxidative modification: a key mechanism of Na+-K+ pump regulation.

Science.gov (United States)

Figtree, Gemma A; Liu, Chia-Chi; Bibert, Stephanie; Hamilton, Elisha J; Garcia, Alvaro; White, Caroline N; Chia, Karin K M; Cornelius, Flemming; Geering, Kaethi; Rasmussen, Helge H

2009-07-17

Angiotensin II (Ang II) inhibits the cardiac sarcolemmal Na(+)-K(+) pump via protein kinase (PK)C-dependent activation of NADPH oxidase. We examined whether this is mediated by oxidative modification of the pump subunits. We detected glutathionylation of beta(1), but not alpha(1), subunits in rabbit ventricular myocytes at baseline. beta(1) Subunit glutathionylation was increased by peroxynitrite (ONOO(-)), paraquat, or activation of NADPH oxidase by Ang II. Increased glutathionylation was associated with decreased alpha(1)/beta(1) subunit coimmunoprecipitation. Glutathionylation was reversed after addition of superoxide dismutase. Glutaredoxin 1, which catalyzes deglutathionylation, coimmunoprecipitated with beta(1) subunit and, when included in patch pipette solutions, abolished paraquat-induced inhibition of myocyte Na(+)-K(+) pump current (I(p)). Cysteine (Cys46) of the beta(1) subunit was the likely candidate for glutathionylation. We expressed Na(+)-K(+) pump alpha(1) subunits with wild-type or Cys46-mutated beta(1) subunits in Xenopus oocytes. ONOO(-) induced glutathionylation of beta(1) subunit and a decrease in Na(+)-K(+) pump turnover number. This was eliminated by mutation of Cys46. ONOO(-) also induced glutathionylation of the Na(+)-K(+) ATPase beta(1) subunit from pig kidney. This was associated with a approximately 2-fold decrease in the rate-limiting E(2)-->E(1) conformational change of the pump, as determined by RH421 fluorescence. We propose that kinase-dependent regulation of the Na(+)-K(+) pump occurs via glutathionylation of its beta(1) subunit at Cys46. These findings have implications for pathophysiological conditions characterized by neurohormonal dysregulation, myocardial oxidative stress and raised myocyte Na(+) levels.

Paraquat initially damages cochlear support cells leading to anoikis-like hair cell death.

Science.gov (United States)

Zhang, Jianhui; Sun, Hong; Salvi, Richard; Ding, Dalian

2018-07-01

Paraquat (PQ), one of the most widely used herbicides, is extremely dangerous because it generates the highly toxic superoxide radical. When paraquat was applied to cochlear organotypic cultures, it not only damaged the outer hair cells (OHCs) and inner hair cells (IHCs), but also caused dislocation of the hair cell rows. We hypothesized that the dislocation arose from damage to the support cells (SCs) that anchors hair cells within the epithelium. To test this hypothesis, rat postnatal cochlear cultures were treated with PQ. Shortly after PQ treatment, the rows of OHCs separated from one another and migrated radially away from IHCs suggesting loss of cell-cell adhesion that hold the hair cells in proper alignment. Hair cells dislocation was associated with extensive loss of SCs in the organ of Corti, loss of tympanic border cells (TBCs) beneath the basilar membrane, the early appearance of superoxide staining and caspase-8 labeling in SCs below the OHCs and disintegration of E-cadherin and β-catenin in the organ of Corti. Damage to the TBCs and SCs occurred prior to loss of OHC or IHC loss suggesting a form of detachment-induced apoptosis referred to as anoikis. Copyright © 2018 Elsevier B.V. All rights reserved.

Oxidative stress provokes distinct transcriptional responses in the stress-tolerant atr7 and stress-sensitive loh2 Arabidopsis thaliana mutants as revealed by multi-parallel quantitative real-time PCR analysis of ROS marker and antioxidant genes

NARCIS (Netherlands)

Mehterov, Nikolay; Balazadeh, Salma; Hille, Jacques; Toneva, Valentina; Mueller-Roeber, Bernd; Gechev, Tsanko

2012-01-01

The Arabidopsis thaliana atr7 mutant is tolerant to oxidative stress induced by paraquat (PQ) or the catalase inhibitor aminotriazole (AT), while its original background loh2 and wild-type plants are sensitive. Both, AT and PQ which stimulate the intracellular formation of H2O2 or superoxide anions,

Proteomics of the oxidative stress response induced by hydrogen peroxide and paraquat reveals a novel AhpC-like protein in Pseudomonas aeruginosa

DEFF Research Database (Denmark)

Hare, Nathan J; Scott, Nichollas E; Shin, Eun Hye H

2011-01-01

hypothetical antioxidant protein (PA3450) that shares sequence similarity with 1-Cys peroxiredoxins. Other induced proteins included known oxidative stress proteins (superoxide dismutase and catalase), as well as those involved in iron acquisition (siderophore biosynthesis and receptor proteins FpvA and Fpt...

[Intensive hemoperfusion and long-term hemofiltration for treatment of paraquat poisoning: a case report].

Science.gov (United States)

Peng, Zhi-Yun; Chang, Ping; Wang, Hua; Cen, Zhong-Ran; Zhou, Jian; Liu, Zhan-Guo

2015-10-01

A 20-year-old male patient was admitted in our department 14 h after paraquat poisoning at the dose of about 50 mL. The patient underwent intensive hemoperfusion for 2 h (3 times a day) for 9 consecutive days and received continuous renal replacement therapy (CRRT) in the mode of continuous veno-venous hemofiltration (CVVH) for 10 consecutive days in addition to routine medications. The biochemical indexes were monitored during the therapy. After the treatment, paraquat concentrations in the blood and urine were decreased, and the patient's urine volume (UV) increased, serum creatinine (Cr) level decreased, and the oxygenation index became normal. Dynamic CT scan showed no obvious pulmonary fibrosis. The patient was followed up for 6 months after discharge and no complaint of discomforts was reported. This case suggests that early intensive hemoperfusion and long-term CVVH may help improve the prognosis after paraquat poisoning.

Predictive values of urine paraquat concentration, dose of poison, arterial blood lactate and APACHE II score in the prognosis of patients with acute paraquat poisoning.

Science.gov (United States)

Liu, Xiao-Wei; Ma, Tao; Li, Lu-Lu; Qu, Bo; Liu, Zhi

2017-07-01

The present study investigated the predictive values of urine paraquat (PQ) concentration, dose of poison, arterial blood lactate and Acute Physiology and Chronic Health Evaluation (APACHE) II score in the prognosis of patients with acute PQ poisoning. A total of 194 patients with acute PQ poisoning, hospitalized between April 2012 and January 2014 at the First Affiliated Hospital of P.R. China Medical University (Shenyang, China), were selected and divided into survival and mortality groups. Logistic regression analysis, receiver operator characteristic (ROC) curve analysis and Kaplan-Meier curve were applied to evaluate the values of urine paraquat (PQ) concentration, dose of poison, arterial blood lactate and (APACHE) II score for predicting the prognosis of patients with acute PQ poisoning. Initial urine PQ concentration (C0), dose of poison, arterial blood lactate and APACHE II score of patients in the mortality group were significantly higher compared with the survival group (all Ppoison and arterial blood lactate correlated with mortality risk of acute PQ poisoning (all Ppoison, arterial blood lactate and APACHE II score in predicting the mortality of patients within 28 days were 0.921, 0.887, 0.808 and 0.648, respectively. The AUC of C0 for predicting early and delayed mortality were 0.890 and 0.764, respectively. The AUC values of urine paraquat concentration the day after poisoning (Csec) and the rebound rate of urine paraquat concentration in predicting the mortality of patients within 28 days were 0.919 and 0.805, respectively. The 28-day survival rate of patients with C0 ≤32.2 µg/ml (42/71; 59.2%) was significantly higher when compared with patients with C0 >32.2 µg/ml (38/123; 30.9%). These results suggest that the initial urine PQ concentration may be the optimal index for predicting the prognosis of patients with acute PQ poisoning. Additionally, dose of poison, arterial blood lactate, Csec and rebound rate also have referential significance.

Mucuna pruriens reduces inducible nitric oxide synthase expression in Parkinsonian mice model.

Science.gov (United States)

Yadav, Satyndra Kumar; Rai, Sachchida Nand; Singh, Surya Pratap

2017-03-01

Parkinson's disease is one of the most common neurodegenerative disease found in aged peoples. Plentiful studies are being conducted to find a suitable and effective cure for this disease giving special impetus on use of herbal plants. The study aimed at investigating the effect of ethanolic extract of Mucuna pruriens (Mp) on level of nitric oxide (NO) in paraquat (PQ) induced Parkinson's disease (PD) mouse model and its subsequent contribution to lipid peroxidation. Twenty four Swiss albino mice were divided into three groups; Control, PQ and PQ+Mp. PQ doses were given intraperitoneally, twice in a week and oral dose of ethanolic extract of Mp seed was given for 9 weeks. Nitrite content and lipid peroxidation was measured in all treated groups along with respective controls. RNA was isolated from the nigrostriatal tissue of control and the treated mice and was reverse transcribed into cDNA. PCR was performed to amplify iNOS mRNA and western blot analysis was performed to check its protein level. We had also perfused the mice in all treated group and performed Tyrosine hydroxylase (TH) and iNOS immunoreactivity in substantia nigra region of mice brain. PQ-treatment increased nitrite content, expression of iNOS and lipid peroxidation compared to respective controls. Mp treatment resulted in a significant attenuation of iNOS expression, nitrite content and lipid peroxidation demonstrating that it reduces nitric oxide in PQ-induced Parkinson's disease. Interestingly; we also observed that mRNA, protein expression and immunoreactivity of iNOS was significantly decreased after Mp treatment and TH immunoreactivity was significantly improved after the treatment of Mp. Our results demonstrated that Mp protects the dopaminergic neurons from the NO injury in substantia nigra. Copyright © 2016 Elsevier B.V. All rights reserved.

Impact of paraquat regulation on suicide in South Korea.

Science.gov (United States)

Cha, Eun Shil; Chang, Shu-Sen; Gunnell, David; Eddleston, Michael; Khang, Young-Ho; Lee, Won Jin

2016-04-01

Ingestion of pesticides (mainly paraquat) accounted for one-fifth of suicides in South Korea in 2006-10. We investigated the effect on suicide mortality of regulatory action, culminating in a ban on paraquat in South Korea in 2011-12. We calculated age-standardized method-specific suicide mortality rates among people aged ≥15 in South Korea (1983-2013) using registered death data. Negative binomial regression was used to estimate changes in the rate and number of pesticide suicides in 2013, compared with those expected based on previous trends (2003-11). Pesticide suicide mortality halved from 5.26 to 2.67 per 100 000 population between 2011 and 2013. Compared with the number expected based on previous trends, the regulations were followed by an estimated 847 [95% confidence interval (CI) -1180 to -533] fewer pesticide suicides, a 37% reduction in rates (rate ratio = 0.63, 95% CI 0.55 to 0.73) in 2013. The decline in pesticide suicides after the regulations was seen in all age/sex/geographical groups. The absolute reduction in the number of suicides was greatest among men, the elderly and in rural areas. The reduction in pesticide suicides contributed to 56% of the decline in overall suicides that occurred between 2011 and 2013. There was no impact of the regulations on crop yield. The regulation of paraquat in South Korea in 2011-12 was associated with a reduction in pesticide suicide. Further legislative interventions to prevent the easy availability of highly lethal suicide methods are recommended for reducing the number of suicides worldwide. © The Author 2015; all rights reserved. Published by Oxford University Press on behalf of the International Epidemiological Association.

Parameters affecting the determination of paraquat at silver rotating electrodes using differential pulse voltammetry

Directory of Open Access Journals (Sweden)

A. Farahi

2014-08-01

Full Text Available The electrochemical determination of aqueous paraquat PQ(II by differential pulse voltammetry at a solid rotating silver electrode (RSE is described. The aim of this work is to optimize all factors that can influence this determination. Potential wave forms, potential scan parameters and deposition time were examined for their effect on the paraquat peak shape and intensity. The best responses were obtained with differential pulse voltammetry in 0.1 mol L−1 Na2SO4 as supporting electrolyte using amplitude 50 mV, scan increment 5 mV, deposition time 120 s, frequency 50 s−1 and step amplitude 0.05 V. Electrochemical and mechanical surface cleaning, aimed at removing the amount of paraquat deposited onto the silver surface, were necessary for obtaining a good performance of the electrode. Response linearity, repeatability, accuracy and detection limit were also evaluated. The obtained detection limits were 7.1 × 10−9 mol L−1 and 2.8 × 10−9 mol L−1 for peak 1 and peak 2 respectively. The relative standard deviation (RSD was found to be 1.19% in 1.0 × 10−4 mol L−1 paraquat. The applicability of the RSE for PQ(II determination in milk samples, without any sample pretreatment, was successfully demonstrated.

Paraquat poisoning: Acute lung injury – a missed diagnosis

African Journals Online (AJOL)

Paraquat poisoning is frequent in rural and agricultural regions around the world owing to the agricultural use of this compound as a herbicide.[1] It is readily available in agricultural areas of South. Africa (SA), as evident in the case described below. Making a timeous diagnosis and administering appropriate stepwise ...

Paraquat poisoning: Acute lung injury – a missed diagnosis ...

African Journals Online (AJOL)

Paraquat is a herbicide of great toxicological importance because it is associated with high mortality rates, mainly due to respiratory failure. We report the case of a 28-year-old man admitted to the casualty department at Ngwelezana Hospital, Empangeni, KwaZulu- Natal, South Africa, with a history of vomiting and ...

A facile fluorescent "turn-off" method for sensing paraquat based on pyranine-paraquat interaction

Science.gov (United States)

Zhao, Zuzhi; Zhang, Fengwei; Zhang, Zipin

2018-06-01

Development of a technically simple yet effective method for paraquat (PQ) detection is of great importance due to its high clinical and environmental relevance. In this study, we developed a pyranine-based fluorescent "turn-off" method for PQ sensing based on pyranine-PQ interaction. We investigated the dependence of analytical performance of this method on the experimental conditions, such as the ion strength, medium pH, and so on. Under the optimized conditions, the method is sensitive and selective, and could be used for PQ detection in real-world sample. This study essentially provides a readily accessible fluorescent system for PQ sensing which is cheap, robust, and technically simple, and it is envisaged to find more interesting clinical and environmental applications.

ADSORPTION OF PARAQUAT DICHLORIDE TO KAOLIN PARTICLES AND TO MIXTURES OF KAOLIN AND HEMATITE PARTICLES

Directory of Open Access Journals (Sweden)

Dina Alexandra Martins

2015-03-01

Full Text Available Deliberate contamination with pesticides is a potential risk to water security, due to the availability of these contaminants and the fact that they do not need special expertise to handle or apply. Adsorption of the herbicide paraquat from an aqueous solution to suspended particles of kaolin and kaolin/hematite mixture was investigated by kinetic and equilibrium assays, taking into consideration several parameters such as initial pH, sorbent dosage and agitation speed. The results showed that the adsorption process is quite fast, reaching an 18% reduction in paraquat concentration in a very short period of time. The addition of hematite particles to kaolin suspension had no apparent effect on the maximum amount of paraquat adsorbed. Kinetic parameters were determined by fitting the pseudo-second order model to the experimental data (correlation coefficients close to 1. Isotherm studies indicate an inhibitory effect, promoted by hematite particles, that was not detected in the adsorption assays. Equilibrium data was best adjusted using the Langmuir model which yielded higher correlation coefficient values and smaller normalized standard deviations.

Oxidative stress contributes to outcome severity in a Drosophila melanogaster model of classic galactosemia

Directory of Open Access Journals (Sweden)

Patricia P. Jumbo-Lucioni

2013-01-01

Classic galactosemia is a genetic disorder that results from profound loss of galactose-1P-uridylyltransferase (GALT. Affected infants experience a rapid escalation of potentially lethal acute symptoms following exposure to milk. Dietary restriction of galactose prevents or resolves the acute sequelae; however, many patients experience profound long-term complications. Despite decades of research, the mechanisms that underlie pathophysiology in classic galactosemia remain unclear. Recently, we developed a Drosophila melanogaster model of classic galactosemia and demonstrated that, like patients, GALT-null Drosophila succumb in development if exposed to galactose but live if maintained on a galactose-restricted diet. Prior models of experimental galactosemia have implicated a possible association between galactose exposure and oxidative stress. Here we describe application of our fly genetic model of galactosemia to the question of whether oxidative stress contributes to the acute galactose sensitivity of GALT-null animals. Our first approach tested the impact of pro- and antioxidant food supplements on the survival of GALT-null and control larvae. We observed a clear pattern: the oxidants paraquat and DMSO each had a negative impact on the survival of mutant but not control animals exposed to galactose, and the antioxidants vitamin C and α-mangostin each had the opposite effect. Biochemical markers also confirmed that galactose and paraquat synergistically increased oxidative stress on all cohorts tested but, interestingly, the mutant animals showed a decreased response relative to controls. Finally, we tested the expression levels of two transcripts responsive to oxidative stress, GSTD6 and GSTE7, in mutant and control larvae exposed to galactose and found that both genes were induced, one by more than 40-fold. Combined, these results implicate oxidative stress and response as contributing factors in the acute galactose sensitivity of GALT-null Drosophila and, by

Use of Cdse/ZnS quantum dots for sensitive detection and quantification of paraquat in water samples

Energy Technology Data Exchange (ETDEWEB)

Durán, Gema M. [Department of Analytical Chemistry and Food Technology, University of Castilla – La Mancha, Avenida Camilo José Cela, 10, 13004 Ciudad Real (Spain); IRICA (Regional Institute of Applied Scientific Research), Avenida Camilo José Cela, s/n., 13071 Ciudad Real (Spain); Contento, Ana M. [Department of Analytical Chemistry and Food Technology, University of Castilla – La Mancha, Avenida Camilo José Cela, 10, 13004 Ciudad Real (Spain); Ríos, Ángel, E-mail: Angel.Rios@uclm.es [Department of Analytical Chemistry and Food Technology, University of Castilla – La Mancha, Avenida Camilo José Cela, 10, 13004 Ciudad Real (Spain)

2013-11-01

Graphical abstract: -- Highlights: •Analytical use of CdSe/ZnS quantum dots. •Methodology for water solubilization of CdSe/ZnS QDs. •Sensitive and selective reaction with paraquat herbicide. •Application to water samples. -- Abstract: Based on the highly sensitive fluorescence change of water-soluble CdSe/ZnS core-shell quantum dots (QD) by paraquat herbicide, a simple, rapid and reproducible methodology was developed to selectively determine paraquat (PQ) in water samples. The methodology enabled the use of simple pretreatment procedure based on the simple water solubilization of CdSe/ZnS QDs with hydrophilic heterobifunctional thiol ligands, such as 3-mercaptopropionic acid (3-MPA), using microwave irradiation. The resulting water-soluble QDs exhibit a strong fluorescence emission at 596 nm with a high and reproducible photostability. The proposed analytical method thus satisfies the need for a simple, sensible and rapid methodology to determine residues of paraquat in water samples, as required by the increasingly strict regulations for health protection introduced in recent years. The sensitivity of the method, expressed as detection limits, was as low as 3.0 ng L{sup −1}. The lineal range was between 10–5 × 10{sup 3} ng L{sup −1}. RSD values in the range of 71–102% were obtained. The analytical applicability of proposed method was demonstrated by analyzing water samples from different procedence.

Use of Cdse/ZnS quantum dots for sensitive detection and quantification of paraquat in water samples

International Nuclear Information System (INIS)

Durán, Gema M.; Contento, Ana M.; Ríos, Ángel

2013-01-01

Graphical abstract: -- Highlights: •Analytical use of CdSe/ZnS quantum dots. •Methodology for water solubilization of CdSe/ZnS QDs. •Sensitive and selective reaction with paraquat herbicide. •Application to water samples. -- Abstract: Based on the highly sensitive fluorescence change of water-soluble CdSe/ZnS core-shell quantum dots (QD) by paraquat herbicide, a simple, rapid and reproducible methodology was developed to selectively determine paraquat (PQ) in water samples. The methodology enabled the use of simple pretreatment procedure based on the simple water solubilization of CdSe/ZnS QDs with hydrophilic heterobifunctional thiol ligands, such as 3-mercaptopropionic acid (3-MPA), using microwave irradiation. The resulting water-soluble QDs exhibit a strong fluorescence emission at 596 nm with a high and reproducible photostability. The proposed analytical method thus satisfies the need for a simple, sensible and rapid methodology to determine residues of paraquat in water samples, as required by the increasingly strict regulations for health protection introduced in recent years. The sensitivity of the method, expressed as detection limits, was as low as 3.0 ng L −1 . The lineal range was between 10–5 × 10 3 ng L −1 . RSD values in the range of 71–102% were obtained. The analytical applicability of proposed method was demonstrated by analyzing water samples from different procedence

Preparation of methacrylic acid-modified rice husk improved by an experimental design and application for paraquat adsorption

International Nuclear Information System (INIS)

Hsu, Shih-Tong; Chen, Lung-Chuan; Lee, Cheng-Chieh; Pan, Ting-Chung; You, Bing-Xuan; Yan, Qi-Feng

2009-01-01

Methacrylic acid (MAA) grafted rice husk was synthesized using graft copolymerization with Fenton's reagent as the redox initiator and applied to the adsorption of paraquat. The highest grafting percentage of 44.3% was obtained using the traditional kinetic method. However, a maximum grafting percentage of 65.3% was calculated using the central composite design. Experimental results based on the recipes predicted from the statistical analysis are consistent with theoretical calculations. A representative polymethacrylic acid-g-rice husk (PMAA-g-rice husk) copolymer was hydrolyzed to a salt type and applied to the adsorption of paraquat. The adsorption equilibrium data correlate more closely with the Langmuir isotherm than with the Freundlich equation. The maximum adsorption capacity of modified rice husk is 292.5 mg/g-adsorbent. This value exceeds those for Fuller's earth and activated carbon, which are the most common binding agents used for paraquat. The samples at various stages were characterized by solid-state 13 C NMR spectroscopy.

Preparation of methacrylic acid-modified rice husk improved by an experimental design and application for paraquat adsorption

Energy Technology Data Exchange (ETDEWEB)

Hsu, Shih-Tong, E-mail: shihtong@mail.ksu.edu.tw [Department of Polymer Materials, Kun Shan University, No. 949 Da-Wan Rd., Yung-Kang City, Tainan Hsien, Taiwan (China); Chen, Lung-Chuan, E-mail: lcchen@mail.ksu.edu.tw [Department of Polymer Materials, Kun Shan University, No. 949 Da-Wan Rd., Yung-Kang City, Tainan Hsien, Taiwan (China); Lee, Cheng-Chieh, E-mail: etmediagoing@yahoo.com.tw [Department of Environmental Engineering, Kun Shan University, No. 949 Da-Wan Rd., Yung-Kang City 710, Tainan Hsien, Taiwan (China); Pan, Ting-Chung, E-mail: tcpan@mail.ksu.edutw [Department of Environmental Engineering, Kun Shan University, No. 949 Da-Wan Rd., Yung-Kang City 710, Tainan Hsien, Taiwan (China); You, Bing-Xuan, E-mail: kp2681@yahoo.com.tw [Department of Polymer Materials, Kun Shan University, No. 949 Da-Wan Rd., Yung-Kang City, Tainan Hsien, Taiwan (China); Yan, Qi-Feng, E-mail: rsrs0938@yahoo.com.tw [Department of Polymer Materials, Kun Shan University, No. 949 Da-Wan Rd., Yung-Kang City, Tainan Hsien, Taiwan (China)

2009-11-15

Methacrylic acid (MAA) grafted rice husk was synthesized using graft copolymerization with Fenton's reagent as the redox initiator and applied to the adsorption of paraquat. The highest grafting percentage of 44.3% was obtained using the traditional kinetic method. However, a maximum grafting percentage of 65.3% was calculated using the central composite design. Experimental results based on the recipes predicted from the statistical analysis are consistent with theoretical calculations. A representative polymethacrylic acid-g-rice husk (PMAA-g-rice husk) copolymer was hydrolyzed to a salt type and applied to the adsorption of paraquat. The adsorption equilibrium data correlate more closely with the Langmuir isotherm than with the Freundlich equation. The maximum adsorption capacity of modified rice husk is 292.5 mg/g-adsorbent. This value exceeds those for Fuller's earth and activated carbon, which are the most common binding agents used for paraquat. The samples at various stages were characterized by solid-state {sup 13}C NMR spectroscopy.

Preparation of methacrylic acid-modified rice husk improved by an experimental design and application for paraquat adsorption.

Science.gov (United States)

Hsu, Shih-Tong; Chen, Lung-Chuan; Lee, Cheng-Chieh; Pan, Ting-Chung; You, Bing-Xuan; Yan, Qi-Feng

2009-11-15

Methacrylic acid (MAA) grafted rice husk was synthesized using graft copolymerization with Fenton's reagent as the redox initiator and applied to the adsorption of paraquat. The highest grafting percentage of 44.3% was obtained using the traditional kinetic method. However, a maximum grafting percentage of 65.3% was calculated using the central composite design. Experimental results based on the recipes predicted from the statistical analysis are consistent with theoretical calculations. A representative polymethacrylic acid-g-rice husk (PMAA-g-rice husk) copolymer was hydrolyzed to a salt type and applied to the adsorption of paraquat. The adsorption equilibrium data correlate more closely with the Langmuir isotherm than with the Freundlich equation. The maximum adsorption capacity of modified rice husk is 292.5mg/g-adsorbent. This value exceeds those for Fuller's earth and activated carbon, which are the most common binding agents used for paraquat. The samples at various stages were characterized by solid-state (13)C NMR spectroscopy.

Paraquat Exposure of Knapsack Spray Operators on Banana Plantations in Costa Rica

NARCIS (Netherlands)

Van Wendel de Joode BN, [No Value; De Graaf IA, [No Value; Wesseling, B; Kromhout, S.B.; de Graaf, Inge

1996-01-01

A study of occupational exposure to paraquat was performed among 11 knapsack spray operators at banana plantations in Costa Rica. External and internal exposures were quantified and determinants of exposure identified by measurements, observations, and interviews. Dermal exposure was measured with

A Study on the Quality and Identity of Brazilian Pampa Biome Honey: Evidences for Its Beneficial Effects against Oxidative Stress and Hyperglycemia.

Science.gov (United States)

Cruz, L C; Batista, J E S; Zemolin, A P P; Nunes, M E M; Lippert, D B; Royes, L F F; Soares, F A; Pereira, A B; Posser, T; Franco, J L

2014-01-01

We characterized, for the first time, the quality and identity of Brazilian Pampa biome honey and its antioxidant properties in vitro (FRAP, DDPH and ABTS). The potential protective effect of honey against oxidative stress induced by iron (Fe) and paraquat, (PQ) in a Drosophila melanogaster model (in vivo) was also tested. The results indicated that all honey samples tested showed antioxidant activity in vitro. Flies treated with honey showed increased lifespan and were protected against oxidative stress induced by Fe and PQ. Despite the high concentration of sugars in honey (approximately 70-80%), our results demonstrate a hypoglycemic-like effect of honey in Drosophila. Thus, this study demonstrates the high quality of Brazilian Pampa biome honey as well as its significant antioxidant activity in vitro and in vivo, pointing to the potential use of this natural product as an alternative in the therapy of oxidative stress-associated diseases.

Synthesis, solid and solution studies of paraquat dichloride calixarene complexes. Molecular modelling

International Nuclear Information System (INIS)

Garcia S, I.; Ramirez, F. M.

2010-01-01

The interaction of the herbicide paraquat dichloride (P Q, substrate) with p-tert-butylcalix arenas (L, receptor) was investigated in both the solution and solid states. The isolated paraquat calixarene complexes were characterised by UV-visible, 1 H NMR, ESI-Ms, Luminescence and IR spectroscopies and elemental analysis. The stoichiometry of complexes 1 and 2 was 1:1 (1 herbicide: 1 calixarene) and both revealed a biexponential luminescence decay with lifetimes depending on the size and the conformational particularity of the calixarenes. Molecular modelling suggested that both calixarenes interact with the herbicide through cation-π interaction. P Q in included in the p-tert butylcalix a rene cavity, a situation favoured by its pinched conformation in polar solvent while it is partially included in the p-tert butylcalix a rene cavity because of its in-out cone conformation. The theoretical results, in particular using Mopac procedures, were in agreement with the experimental findings. (Author)

Synthesis, solid and solution studies of paraquat dichloride calixarene complexes. Molecular modelling

Energy Technology Data Exchange (ETDEWEB)

Garcia S, I.; Ramirez, F. M., E-mail: flor.ramirez@inin.gob.m [ININ, Departamento de Quimica, Carretera Mexico-Toluca s/n, 52750 Ocoyoacac, Estado de Mexico (Mexico)

2010-07-01

The interaction of the herbicide paraquat dichloride (P Q, substrate) with p-tert-butylcalix arenas (L, receptor) was investigated in both the solution and solid states. The isolated paraquat calixarene complexes were characterised by UV-visible, {sup 1}H NMR, ESI-Ms, Luminescence and IR spectroscopies and elemental analysis. The stoichiometry of complexes 1 and 2 was 1:1 (1 herbicide: 1 calixarene) and both revealed a biexponential luminescence decay with lifetimes depending on the size and the conformational particularity of the calixarenes. Molecular modelling suggested that both calixarenes interact with the herbicide through cation-{pi} interaction. P Q in included in the p-tert butylcalix a rene cavity, a situation favoured by its pinched conformation in polar solvent while it is partially included in the p-tert butylcalix a rene cavity because of its in-out cone conformation. The theoretical results, in particular using Mopac procedures, were in agreement with the experimental findings. (Author)

Traditional chinese medicine Xuebijing treatment is associated with decreased mortality risk of patients with moderate paraquat poisoning.

Science.gov (United States)

Gong, Ping; Lu, Zhidan; Xing, Jing; Wang, Na; Zhang, Yu

2015-01-01

Paraquat poisoning causes multiple organ injury and high mortality due to severe toxicity and lack of effective treatment. Xuebijing (XBJ) injection, a traditional Chinese medicine preparation of five Chinese herbs (Radix Salviae Miltiorrhiae, Rhizoma Chuanxiong, Flos Carthami, Angelica Sinensis and Radix Paeoniae Rubra), has an anti-inflammatory effect and is widely used in the treatment of sepsis. This retrospective study was designed to evaluate the effects of XBJ combined with conventional therapy on mortality risk of patients with acute paraquat poisoning. Out of 68 patients, 27 were treated with conventional therapy (control group) and 41 were treated with intravenous administration of XBJ (100 ml, twice a day, up to 7 days) plus conventional therapy (XBJ group). Vital organ function, survival time within 28 days and adverse events during the treatment were reviewed. Results indicated that XBJ treatment significantly increased median survival time among patients ingesting 10-30 ml of paraquat (P=0.02) compared with the control group. After adjustment for covariates, XBJ treatment was associated significantly with a lower mortality risk (adjusted HR 0.242, 95% CI 0.113 to 0.516, P=0.001) compared with the control group. Additionally, compared with Day 1, on Day 3 the value of PaO2/FiO2 was significantly decreased, and the values of serum alanine aminotransferase, creatinine and troponin T were significantly increased in the control group (all Ptreatment is associated with decreased mortality risk of patients with moderate paraquat poisoning, which may be attributed to improved function of vital organs with no severe adverse events.

Multiwall carbon nanotubes modulate paraquat toxicity in Arabidopsis thaliana.

Science.gov (United States)

Fan, Xiaoji; Xu, Jiahui; Lavoie, Michel; Peijnenburg, W J G M; Zhu, Youchao; Lu, Tao; Fu, Zhengwei; Zhu, Tingheng; Qian, Haifeng

2018-02-01

Carbon nanotubes can be either toxic or beneficial to plant growth and can also modulate toxicity of organic contaminants through surface sorption. The complex interacting toxic effects of carbon nanotubes and organic contaminants in plants have received little attention in the literature to date. In this study, the toxicity of multiwall carbon nanotubes (MWCNT, 50 mg/L) and paraquat (MV, 0.82 mg/L), separately or in combination, were evaluated at the physiological and the proteomic level in Arabidopsis thaliana for 7-14 days. The results revealed that the exposure to MWCNT had no inhibitory effect on the growth of shoots and leaves. Rather, MWCNT stimulated the relative electron transport rate and the effective photochemical quantum yield of PSII value as compared to the control by around 12% and lateral root production up to nearly 4-fold as compared to the control. The protective effect of MWCNT on MV toxicity on the root surface area could be quantitatively explained by the extent of MV adsorption on MWCNT and was related to stimulation of photosynthesis, antioxidant protection and number and area of lateral roots which in turn helped nutrient assimilation. The influence of MWCNT and MV on photosynthesis and oxidative stress at the physiological level was consistent with the proteomics analysis, with various over-expressed photosynthesis-related proteins (by more than 2 folds) and various under-expressed oxidative stress related proteins (by about 2-3 folds). This study brings new insights into the interactive effects of two xenobiotics (MWCNT and MV) on the physiology of a model plant. Copyright © 2017 Elsevier Ltd. All rights reserved.

A Study on the Quality and Identity of Brazilian Pampa Biome Honey: Evidences for Its Beneficial Effects against Oxidative Stress and Hyperglycemia

Directory of Open Access Journals (Sweden)

L. C. Cruz

2014-01-01

Full Text Available We characterized, for the first time, the quality and identity of Brazilian Pampa biome honey and its antioxidant properties in vitro (FRAP, DDPH and ABTS. The potential protective effect of honey against oxidative stress induced by iron (Fe and paraquat, (PQ in a Drosophila melanogaster model (in vivo was also tested. The results indicated that all honey samples tested showed antioxidant activity in vitro. Flies treated with honey showed increased lifespan and were protected against oxidative stress induced by Fe and PQ. Despite the high concentration of sugars in honey (approximately 70–80%, our results demonstrate a hypoglycemic-like effect of honey in Drosophila. Thus, this study demonstrates the high quality of Brazilian Pampa biome honey as well as its significant antioxidant activity in vitro and in vivo, pointing to the potential use of this natural product as an alternative in the therapy of oxidative stress-associated diseases.

Egyptian Journal of Biochemistry and Molecular Biology - Vol 24, No ...

African Journals Online (AJOL)

Protective role of green tea polyphenols against paraquat induced oxidative stress in rat liver · EMAIL FULL TEXT EMAIL FULL TEXT DOWNLOAD FULL ... Role of reduced glutathione, nitric oxide and some trace elements in Alzheimer's disease and vascular dementia · EMAIL FULL TEXT EMAIL FULL TEXT DOWNLOAD ...

Serum paraquat concentration detected by spectrophotometry in patients with paraquat poisoning

Science.gov (United States)

Li, Chang-bin; Li, Xin-hua; Wang, Zhen; Jiang, Cheng-hua; Peng, Ai

2011-01-01

BACKGROUND: Paraquat (PQ) is a world-wide used herbicide and also a type of common poison for suicide and accidental poisoning. Numerous studies have proved that the concentration of serum PQ plays an important role in prognosis. Spectrophotometry, including common spectrophotometry and second-derivative spectrophotometry, is commonly used for PQ detection in primary hospitals. So far, lack of systematic research on the reliability of the method and the correlation between clinical features of patients with PQ poisoning and the test results has restricted the clinical use of spectrophotometry. This study aimed to evaluate the reliability and value of spectrophotometry in detecting the concentration of serum PQ. METHODS: The wavelengths for detecting the concentration of serum PQ by common and second-derivative spectrophotometry were determined. Second-derivative spectrophotometry was applied to detect the concentration of serum PQ. The linear range and precision for detection of PQ concentration by this method were confirmed. The concentration of serum PQ shown by second-derivative spectrophotometry and HPLC were compared in 8 patients with PQ poisoning. Altogether 21 patients with acute poisoning 4 hours after PQ ingestion treated in the period of October 2008 to September 2010 were retrospectively reviewed. The patients were divided into higher and lower than 1.8 μg/mL groups based on their concentrations of serum PQ measured by second-derivative spectrophotometry on admission. The severity of clinical manifestations between the two groups were analyzed with Student's t test or Fisher's exact test. RESULTS: The absorption peak of 257 nm could not be found when common spectrophotometry was used to detect the PQ concentration in serum. The calibration curve in the 0.4–8.0 μg/mL range for PQ concentration shown by second-derivative spectrophotometry obeyed Beer's law with r=0.996. The average recovery rates of PQ were within a range of 95.0% to 99.5%, relative

Addition of immunosuppressive treatment to hemoperfusion is associated with improved survival after paraquat poisoning: a nationwide study.

Directory of Open Access Journals (Sweden)

Wen-Pyng Wu

Full Text Available Paraquat poisoning associates very high mortality rate. Early treatment with hemoperfusion is strongly suggested by animal and human studies. Although the survival benefit of additional immunosuppressive treatment (IST in combination with hemoperfusion is also reported since 1971, the large-scale randomized control trials to confirm the effects of IST is difficult to be executed. Therefore, we designed this nationwide large-scale population-based retrospective cohort study to investigate the outcome of paraquat poisoning with hemoperfusion and the additional effects of IST combined with hemoperfusion. This nationwide retrospective cohort study utilized data retrieved from the National Health Insurance Research Database (NHIRD of Taiwan. A total of 1811 hospitalized patients with a diagnosis of paraquat poisoning who received hemoperfusion between 1997 and 2009 were enrolled. The mean age of all 1811 study subjects was 47.3 years. 70% was male. The overall survival rate was only 26.4%. Respiratory failure and renal failure were diagnosed in 56.2% and 36% patients. The average frequency of hemoperfusion was twice. IST was added in 42.2% patients. IST significantly increases survival rate (from 24.3% to 29.3%, P<0.001. The combined IST with methylprednisolone, cyclophosphamide and dexamethasone associates with the highest survival rate (48%, P<0.001. Moreover, patients younger than 45 years of age in the IST group had the best survival (41.0% vs. 33.7%, p<0.001. Our results support the use of IST with hemoperfusion for paraquat-poisoned patients. The best survival effect of IST is the combination of methylprednisolone, cyclophosphamide and daily dexamethasone, especially in patients with younger age.

Toxicity of paraquat in nestling birds: effects on plasma and tissue biochemistry in American kestrels

Science.gov (United States)

Hoffman, Daivd J.; Franson, J. Christian; Pattee, Oliver H.; Bunck, Christine M.; Murray, Helen C.

1987-01-01

Beginning the day after hatching, American kestrel (Falco sparverius) nestlings were orally dosed daily for 10 days with 5 μL/g of distilled water (controls), 10 mg/kg, 25 mg/kg, or 60 mg/kg of paraquat dichloride (1,1′-dimethyl-4,4′-bipyridinium dichloride) in distilled water. Forty-four percent of the nestlings receiving 60 mg/kg died after 4 days. Plasma LDH activity and total protein concentration were elevated, and plasma alkaline phosphatase activity was lower in survivors of the 60 mg/kg group at 10 days. Lung total sulfhydryl (TSH) and protein-bound sulfhydryl (PBSH) concentrations were significantly higher in the 10 mg/kg, 25 mg/kg, or 60 mg/kg groups. Lung DNA, RNA, protein, and hydroxyproline (collagen) concentrations were not significantly affected by treatment. Liver NPSH was lower in the 60 mg/kg group while liver glycogen concentration was not affected by treatment. Kidney DNA, RNA, and RNA to protein concentration ratio were higher in the 25 mg/kg or 60 mg/kg groups. These findings in combination with recently reported effects on growth and histopathology suggest that altricial nestling kestrels are more sensitive to paraquat exposure than young or adult birds of precocial species. From a comparative viewpoint, lungs of nestling kestrels are less sensitive to paraquat than mammalian lungs.

Testing the effect of paraquat exposure on genomic recombination rates in queens of the western honey bee, Apis mellifera.

Science.gov (United States)

Langberg, Kurt; Phillips, Matthew; Rueppell, Olav

2018-04-01

The rate of genomic recombination displays evolutionary plasticity and can even vary in response to environmental factors. The western honey bee (Apis mellifera L.) has an extremely high genomic recombination rate but the mechanistic basis for this genome-wide upregulation is not understood. Based on the hypothesis that meiotic recombination and DNA damage repair share common mechanisms in honey bees as in other organisms, we predicted that oxidative stress leads to an increase in recombination rate in honey bees. To test this prediction, we subjected honey bee queens to oxidative stress by paraquat injection and measured the rates of genomic recombination in select genome intervals of offspring produced before and after injection. The evaluation of 26 genome intervals in a total of over 1750 offspring of 11 queens by microsatellite genotyping revealed several significant effects but no overall evidence for a mechanistic link between oxidative stress and increased recombination was found. The results weaken the notion that DNA repair enzymes have a regulatory function in the high rate of meiotic recombination of honey bees, but they do not provide evidence against functional overlap between meiotic recombination and DNA damage repair in honey bees and more mechanistic studies are needed.

Traditional chinese medicine Xuebijing treatment is associated with decreased mortality risk of patients with moderate paraquat poisoning.

Directory of Open Access Journals (Sweden)

Ping Gong

Full Text Available Paraquat poisoning causes multiple organ injury and high mortality due to severe toxicity and lack of effective treatment. Xuebijing (XBJ injection, a traditional Chinese medicine preparation of five Chinese herbs (Radix Salviae Miltiorrhiae, Rhizoma Chuanxiong, Flos Carthami, Angelica Sinensis and Radix Paeoniae Rubra, has an anti-inflammatory effect and is widely used in the treatment of sepsis. This retrospective study was designed to evaluate the effects of XBJ combined with conventional therapy on mortality risk of patients with acute paraquat poisoning. Out of 68 patients, 27 were treated with conventional therapy (control group and 41 were treated with intravenous administration of XBJ (100 ml, twice a day, up to 7 days plus conventional therapy (XBJ group. Vital organ function, survival time within 28 days and adverse events during the treatment were reviewed. Results indicated that XBJ treatment significantly increased median survival time among patients ingesting 10-30 ml of paraquat (P=0.02 compared with the control group. After adjustment for covariates, XBJ treatment was associated significantly with a lower mortality risk (adjusted HR 0.242, 95% CI 0.113 to 0.516, P=0.001 compared with the control group. Additionally, compared with Day 1, on Day 3 the value of PaO2/FiO2 was significantly decreased, and the values of serum alanine aminotransferase, creatinine and troponin T were significantly increased in the control group (all P<0.05, but these values were significant improved in the XBJ group (all P<0.05. Only one patient had skin rash with itch within 30 minutes after injection and no severe adverse events were found in the XBJ group. In conclusion, XBJ treatment is associated with decreased mortality risk of patients with moderate paraquat poisoning, which may be attributed to improved function of vital organs with no severe adverse events.

The effect of paraquat inhalation on parkinsonism, organ morphology and anatomy of mice and its recovery with the application of etliringea hemisphaerica (blume, r.m. smith) crude extract

Science.gov (United States)

Muslim, Choirul; Nurul Kamila, Santi

2018-03-01

This research is aimed to understand the effect of paraquat herbicide inhalation on Parkinsonism, morphology and anatomy change in mice, and its recovery with Etliringea hemisphaerica crude extract application. Sixty mice were placed into three following groups: group R0 were mice receiving standard food ransom, R1 were a group of mice receiving the regular food ransom plus inhalation of 1% paraquat, and R2 were a group of R1 plus obtaining 0,39mg/bw extract E. hemisphaerica (Bl.) R.M. Smith). After 2 X 7 days of sub-sequential application of both paraquat and “helani tulip” extract, we observed the effects. The examination included bradikinesia attitude, postural instability and rigidity, morphology and anatomy of brain, liver, blood, lung, and kidney. The data were tabulated and analyzed qualitative and semi quantitative description on the behavioural disorder, the alteration of morphology and anatomy, and their remedy based on Sander 2004, Junqueira and Carneiro, 2007. The results showed that the application of paraquat caused strong bradikinesia, postural instability and rigidity. The treatment of the extract was only resulting in the bradikinesia removal but was minor improving the consequence of postural instability and rigidity. Paraquat was not affecting the morphology of neural brain but was altering the morphology and anatomy of lung, liver, blood, and the kidney. In general, the negative impact of the paraquat was weakly eliminated by the treatment of “helani tulip” extract.

Paraquat induces extrinsic pathway of apoptosis in A549 cells by induction of DR5 and repression of anti-apoptotic proteins, DDX3 and GSK3 expression.

Science.gov (United States)

Hathaichoti, Sasiphen; Visitnonthachai, Daranee; Ngamsiri, Pronrumpa; Niyomchan, Apichaya; Tsogtbayar, Oyu; Wisessaowapak, Churaibhon; Watcharasit, Piyajit; Satayavivad, Jutamaad

2017-08-01

Paraquat (PQ) is a bipyridyl derivative herbicide known to cause lung toxicity partly through induction of apoptosis. Here we demonstrated that PQ caused apoptosis in A549 cells. PQ increased cleavage of caspase-8 and Bid, indicating caspase-8 activation and truncated Bid, the two key mediators of extrinsic apoptosis. Additionally, PQ treatment caused an increase in DR5 (death receptor-5) and caspase-8 interaction, indicating formation of DISC (death-inducing signaling complex). These results indicate that PQ induces apoptosis through extrinsic pathway in A549 cells. Moreover, PQ drastically increased DR5 expression and membrane localization. Furthermore, PQ caused prominent concentration dependent reductions of DDX3 (the DEAD box protein-3) and GSK3 (glycogen synthase kinase-3) which can associate with DR5 and prevent DISC formation. Additionally, PQ decreased DR5-DDX3 interaction, suggesting a reduction of DDX3/GSK3 anti-apoptotic complex. Inhibition of GSK3, which is known to promote extrinsic apoptosis by its pharmacological inhibitor, BIO accentuated PQ-induced apoptosis. Moreover, GSK3 inhibition caused a further decrease in PQ-reduced DR5-DDX3 interaction. Taken together, these results suggest that PQ may induce extrinsic pathway of apoptosis in A549 cells through upregulation of DR5 and repression of anti-apoptotic proteins, DDX3/GSK3 leading to reduction of anti-apoptotic complex. Copyright © 2017 Elsevier Ltd. All rights reserved.

Electrochemical impedance spectroscopy for analytical determination of paraquat in meconium samples using an immunosensor modified with fullerene, ferrocene and ionic liquid

Energy Technology Data Exchange (ETDEWEB)

Sun Xiulan [State Key Laboratory of Food Science and Technology, Wuxi 214122 (China); Li Zaijun, E-mail: zaijunli@263.ne [School of Chemical and Materials Engineering, Jiangnan University, Lihu Road 1800, Wuxi 214122 (China); Cai, Yan; Wei, Zhilei [School of Chemical and Materials Engineering, Jiangnan University, Lihu Road 1800, Wuxi 214122 (China); Fang Yinjun; Ren Guoxiao; Huang Yaru [Zhejiang Zanyu Technology Limited Corporation, Hangzhou 311215 (China)

2011-01-01

The paper reports a highly sensitive electrochemical immunosensor for the detection of paraquat. The immunosensor bases on glassy carbon electrode modified with a composite made from fullerene, ferrocene and the ionic liquid. The components were immobilized on the electrode surface by chitosan. The antibody of paraquat was covalently conjugated to the surface which was then blocked with bovine serum albumin. Analytical characteristics of the immunosensor were investigated by electrochemical impedance spectroscopy. It offers good repeatability (RSD = 1.5%), a stability of more than 150 days, an impedimetric response to paraquat in the range from 3.89 x 10{sup -11} to 4.0 x 10{sup -8} mol L{sup -1}, and a detection limit (S/N = 3) of 9.0 x 10{sup -12} mol L{sup -1}. The effects of omitting fullerene and the ionic liquid were well tested. The results indicated that sensitivity of the immunosensor is 3.7-fold better if fullerene and ionic liquid are used. This demonstrates that fullerene facilitates electron transfer on surface of the electrode due to unique electrochemical properties, while the ionic liquid provides biocompatible microenvironment for the antibody, which results in the enhanced sensitivity and stability. Moreover, surface morphology feature and electrochemical properties of the electrode were also examined. The method was satisfactorily applied to the determination of paraquat in meconium.

Browse Title Index

African Journals Online (AJOL)

Items 101 - 150 of 187 ... ... NMR and Solvent Effect Study on the Thymine-Adenine-Thymine ... animal model of schistosoma mansoni treated with myrrh or praziquantel, Abstract ... On In Vivo Paraquat Induced Oxidative Damage In Rats, Abstract.

Addition of immunosuppressive treatment to hemoperfusion is associated with improved survival after paraquat poisoning: a nationwide study.

Science.gov (United States)

Wu, Wen-Pyng; Lai, Ming-Nan; Lin, Ching-Heng; Li, Yu-Fen; Lin, Ching-Yuang; Wu, Ming-Ju

2014-01-01

Paraquat poisoning associates very high mortality rate. Early treatment with hemoperfusion is strongly suggested by animal and human studies. Although the survival benefit of additional immunosuppressive treatment (IST) in combination with hemoperfusion is also reported since 1971, the large-scale randomized control trials to confirm the effects of IST is difficult to be executed. Therefore, we designed this nationwide large-scale population-based retrospective cohort study to investigate the outcome of paraquat poisoning with hemoperfusion and the additional effects of IST combined with hemoperfusion. This nationwide retrospective cohort study utilized data retrieved from the National Health Insurance Research Database (NHIRD) of Taiwan. A total of 1811 hospitalized patients with a diagnosis of paraquat poisoning who received hemoperfusion between 1997 and 2009 were enrolled. The mean age of all 1811 study subjects was 47.3 years. 70% was male. The overall survival rate was only 26.4%. Respiratory failure and renal failure were diagnosed in 56.2% and 36% patients. The average frequency of hemoperfusion was twice. IST was added in 42.2% patients. IST significantly increases survival rate (from 24.3% to 29.3%, Ppoisoned patients. The best survival effect of IST is the combination of methylprednisolone, cyclophosphamide and daily dexamethasone, especially in patients with younger age.

[Clinical study on the treatment of acute paraquat poisoning with sequential whole gastric and bowel irrigation].

Science.gov (United States)

Zhao, Bo; Dai, Jingbin; Li, Jun; Xiao, Lei; Sun, Baoquan; Liu, Naizheng; Zhang, Yanmin; Jian, Xiangdong

2015-03-01

To explore the clinical efficacy of early application of sequential gastrointestinal lavage in patients with acute paraquat poisoning by analyzing the clinical data of 97 patients. A total of 97 eligible patients with acute paraquat poisoning were divided into conventional treatment group (n = 48) and sequential treatment group (n = 49). The conventional treatment group received routine gastric lavage with water. Then 30 g of montmorillonite powder, 30 g of activated charcoal, and mannitol were given to remove intestinal toxins once a day for five days. The sequential treatment group received 60 g of montmorillonite powder for oral administration, followed by small-volume low-pressure manual gastric lavage with 2.5%bicarbonate liquid. Then 30 g of activated charcoal, 30 g of montmorillonite powder, and polyethylene glycol electrolyte lavage solution were given one after another for gastrointestinal lavage once a day for five days. Both groups received large doses of corticosteroids, blood perfusion, and anti-oxidation treatment. The levels of serum potassium, serum amylase (AMY) alanine aminotransferase (ALT), total bilirubin (TBIL), blood urea nitrogen (BUN), creatinine (Cr), lactate (Lac), and PaO₂of patients were determined at 1, 3, 5, 7, and 10 days. Laxative time, mortality, and survival time of dead cases were evaluated in the two groups. The incidence rates of hypokalemia (110 U/L) were significantly lower in the sequential treatment group than in the conventional treatment group (P 80 U/L), TBIL (>34.2 µmol/L), BUN (>7.2 mmol/L), and Cr (>177 µmol/L) between the two groups (P>0.05). However, the highest levels of ALT, TBIL, BUN, Cr, and Lac were significantly lower in the sequential treatment group than in the conventional treatment group (P treatment group had significantly lower incidence of PaO₂(treatment group (P poisoning.

Comparative studies of the mechanisms of paraquat and 1-methyl-4-phenylpyridine (MPP+) cytotoxicity

International Nuclear Information System (INIS)

Di Monte, D.; Sandy, M.S.; Ekstroem, G.; Smith, M.T.

1986-01-01

1-Methyl-4-phenylpyridine (MPP + ) is the putative toxic metabolite of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) and is structurally similar to the herbicide paraquat (PQ ++ ). The authors have therefore compared the effects of MPP + and PQ ++ on isolated rat hepatocytes. PQ ++ generates reactive oxygen species within cells by redox cycling and its toxicity to hepatocytes was potentiated by pretreatment with 1,3-bis(2-chlorethyl)-1-nitrosourea (BCNU), an inhibitor of glutathione reductase. In BCNU-treated cells, PQ ++ caused GSH depletion, lipid peroxidation and cell death. These cytotoxic effects were prevented by the antioxidant N,N'-diphenyl-p-phenylenediamine (DPPD) and the iron-chelating agent desferrioxamine. MPP + also caused GSH depletion in BCNU-treated hepatocytes but its cytotoxicity was not markedly affected by BCNU, nor was it accompanied by significant lipid peroxidation. DPPD and desferrioxamine also failed to prevent MPP + -induced cell death

The role of paraquat (1,1-dimethyl-4,4-bipyridinium chloride) and glyphosate (n-phosphonomethyl glycine) in translocation of metal ions to subsurface soils

International Nuclear Information System (INIS)

Mbuk, R.O.; Sha'Ato, R.; Nkpa, N.N.

2009-01-01

We investigated the role of paraquat (1,1'-Dimethyl-4,4'-bipyridinium dichloride) and glyphosate (N-(phosphonomethyl) glycine), on the translocation of some metals (K, Mg(II), Mn(II), Fe(II), Pb(II), Cu(II) and Cd(II)) in soil, using a topsoil (Aquic Ustifluvent: USDA Soil Taxonomy, 2000) sampled at the University of Agriculture Makurdi Crop Farm, in Central Nigeria (7 degree 47'N, 8 degree 32'E). Employing column leaching experiments with water only on native soil and soil spiked with the metals and different levels of glyphosate or paraquat treatment, leachates were collected and analyzed for their metal contents. Results showed that in the presence of paraquat the transport of Fe(II) and Mn(II) by leaching in the soil was suppressed while that of Cu(II), K and Pb(II) was enhanced. Glyphosate, similarly suppressed Mn(II) and to some extent Fe(II) translocation in the soil; however, it enhanced the mobility of Cd(II), Cu(II), Mg(II), Pb(II) and K under similar treatment. While paraquat seemed to enhance the translocation of Mg(II) at low application rates of the herbicide, glyphosate promoted its transport only at high application rates; there was no evidence that paraquat affected the movement of Cd(II) in the soil. Our results show that the long term use of these pesticides in the field may result in the depletion of Cu(II), K and Mg(II) in agricultural soils, and that the use of glyphosate may present the additional risk of possible groundwater contamination with Cd(II) and Pb(II). (author)

Chitosan oligosaccharides attenuates oxidative-stress related retinal degeneration in rats.

Directory of Open Access Journals (Sweden)

I-Mo Fang

Full Text Available This study investigated the therapeutic potential and mechanisms of chitosan oligosaccharides (COS for oxidative stress-induced retinal diseases. Retinal oxidative damage was induced in Sprague-Dawley rats by intravitreal injection of paraquat (PQ. Low-dose (5 mg/kg or high-dose (10 mg/kg COS or PBS was intragastrically given for 14 days after PQ injection. Electroretinograms were performed to determine the functionality of the retinas. The surviving neurons in the retinal ganglion cell layer and retinal apoptosis were determined by counting Neu N-positive cells in whole-mounted retinas and TUNEL staining, respectively. The generation of reactive oxygen species (ROS was determined by lucigenin- and luminol-enhanced chemiluminescence. Retinal oxidative damages were assessed by staining with nitrotyrosine, acrolein, and 8-hydroxy-2'-deoxyguanosine (8-OHdG. Immunohistochemical studies were used to demonstrate the expression of nuclear factor-kappa B (NF-κB p65 in retinas. An in vitro study using RGC-5 cells was performed to verify the results. We demonstrated COS significantly enhanced the recovery of retinal function, preserved inner retinal thickness, and decreased retinal neurons loss in a dose-dependent manner. COS administration demonstrated anti-oxidative effects by reducing luminol- and lucigenin-dependent chemiluminenscense levels and activating superoxide dismutase and catalase, leading to decreased retinal apoptosis. COS markedly reduced retinal NF-κB p65. An in vitro study demonstrated COS increased IκB expression, attenuated the increase of p65 and thus decreased NF-κB/DNA binding activity in PQ-stimulated RGC-5 cells. In conclusion, COS attenuates oxidative stress-induced retinal damages, probably by decreasing free radicals, maintaining the activities of anti-oxidative enzymes, and inhibiting the activation of NF-κB.

Adiponectin attenuates lung fibroblasts activation and pulmonary fibrosis induced by paraquat.

Science.gov (United States)

Yao, Rong; Cao, Yu; He, Ya-rong; Lau, Wayne Bond; Zeng, Zhi; Liang, Zong-an

2015-01-01

Pulmonary fibrosis is one of the most common complications of paraquat (PQ) poisoning, which demands for more effective therapies. Accumulating evidence suggests adiponectin (APN) may be a promising therapy against fibrotic diseases. In the current study, we determine whether the exogenous globular APN isoform protects against pulmonary fibrosis in PQ-treated mice and human lung fibroblasts, and dissect the responsible underlying mechanisms. BALB/C mice were divided into control group, PQ group, PQ + low-dose APN group, and PQ + high-dose APN group. Mice were sacrificed 3, 7, 14, and 21 days after PQ treatment. We compared pulmonary histopathological changes among different groups on the basis of fibrosis scores, TGF-β1, CTGF and α-SMA pulmonary content via Western blot and real-time quantitative fluorescence-PCR (RT-PCR). Blood levels of MMP-9 and TIMP-1 were determined by ELISA. Human lung fibroblasts WI-38 were divided into control group, PQ group, APN group, and APN receptor (AdipoR) 1 small-interfering RNA (siRNA) group. Fibroblasts were collected 24, 48, and 72 hours after PQ exposure for assay. Cell viability and apoptosis were determined via Kit-8 (CCK-8) and fluorescein Annexin V-FITC/PI double labeling. The protein and mRNA expression level of collagen type III, AdipoR1, and AdipoR2 were measured by Western blot and RT-PCR. APN treatment significantly decreased the lung fibrosis scores, protein and mRNA expression of pulmonary TGF-β1, CTGF and α-SMA content, and blood MMP-9 and TIMP-1 in a dose-dependent manner (ppulmonary fibrosis in a dose-dependent manner, via suppression of lung fibroblast activation. Functional AdipoR1 are expressed by human WI-38 lung fibroblasts, suggesting potential future clinical applicability of APN against pulmonary fibrosis.

Efecto del control de malezas con paraquat y glifosato sobre la erosión y pérdida de nutrimentos del suelo en cafeto

Directory of Open Access Journals (Sweden)

Robin G\\u00F3mez G\\u00F3mez

2005-01-01

Full Text Available Efecto del control de malezas con paraquat y glifosatosobre la erosión y pérdida de nutrimentos del suelo encafeto. En Alajuela, Costa Rica, se realizó un experimento enlos años 2002 y 2003 tendiente a determinar el control de malezas, la dinámica poblacional de las malezas y la erosión ypérdida de nutrimentos del suelo debido a aplicaciones sucesivas de paraquat y glifosato. Dos parcelas de 900 m2dentrode una plantación de café fueron aplicadas con paraquat y dosmás tratadas con glifosato. En el año 2003 una parcela de ca-da tratamiento fue disturbada aplicándole materia orgánica(broza de café y carbonato de calcio. El agua de escorrentía ylos sedimentos provenientes de parcelas de 2x7m fueron recogidos en colectores de 200 litros de capacidad y se midieronlas pérdidas de nutrientes. Al inicio de los tratamientos el control de malezas con ambos herbicidas fue de 90-100%, posteriormente con las continuas aplicaciones de herbicidas, sepresentaron malezas tolerantes, haciendo necesario el controlmecánico y aumentar la dosis del herbicida para controlarlas.Durante el 2002 las pérdidas de suelo de las parcelas tratadascon glifosato fueron el doble (3,956 t/ha comparadas con lasocurridas en las parcelas aplicadas con paraquat (1,936 t/ha.En el 2003, en las parcelas no disturbadas tratadas con paraquat se determinó menos erosión (0,231 t/ha en comparacióncon 0,329 t/ha en aquellas aplicadas con glifosato. Asimismo,en las parcelas disturbadas por enmiendas las pérdidas fueronmenores en las aplicadas con paraquat: 0,170 vs. 0,187 t/ha deglifosato. Los análisis de sedimentos y agua mostraron unapérdida importante de Ca, Mg y K, similar en ambos tratamientos. El rendimiento estimado en el año 2003 fue muy similar en ambos tratamientos

[Clinical effect of compound monoammonium glycyrrhizinate combined with dandelion in treatment of acute paraquat poisoning].

Science.gov (United States)

Zhao, Y; Jian, X D

2016-07-20

Objective: To investigate the clinical effect of compound monoammonium glycyrrhizinate combined with dandelion in the treatment of acute paraquat poisoning. Methods: A total of 80 patients with acute paraquat poisoning who were admitted to our hospital were enrolled as study subjects and randomly divided into routine treatment group (38 patients) and traditional Chinese medicine (TCM) group (42 patients) . The patients in the TCM group were given compound monoammonium glycyrrhizinate and dandelion in addition to the treatment in the control group. Serum alanine aminotransferase (ALT) , total bilirubin (TBil) , blood urea nitrogen (BUN) , creatinine (Cr) , and arterial blood lactate (Lac) and partial pressure of oxygen (PaO 2 ) during different time periods on day 3, 7, and 9 of treatment were observed in both groups, and ulceration of oral mucosa, pulmonary fibrosis, multiple organ dysfunction syndrome (MODS) , and mortality were compared between the two groups. Results: On days 3, 7, and 9 of treatment, the routine treatment group had significantly higher serum ALT, TBil, BUN, Cr, and arterial blood Lac than the TCM group. The routine treatment group had significantly lower arterial blood PaO 2 than the TCM group, while the TCM group had significantly lower incidence rates of ulceration of oral mucosa, pulmonary fibrosis, and MODS and a significantly lower mortality rate than the routine treatment group ( P treatment of patients with acute paraquat poisoning, compound monoammonium glycyrrhizinate combined with dandelion can effectively improve organ function, reduce the incidence of pulmonary fibrosis and MODS, improve the healing rate of oral ulcer, improve prognosis, and reduce mortality rate.

Impact on mormortality of o one conjugated treatment in 10 paraquat intoxicated patients attended at the San Vicente de Paul University Hospital in Medellín, Colombia, from august 2002 to august 2003 Impacto en la mortalidad de un tratamiento conjugado, en pacientes intoxicados no ocupacionalmente, con paraquat en el Hospital Universitario San Vicente de Paúl de Medellín, entre agosto de 2002 y agosto de 2003

Directory of Open Access Journals (Sweden)

Luz Marina Quiceno Quiceno

2004-01-01

Full Text Available Paraquat is a frequently used herbicide in Colombia. Its ingestion produces a severe intoxication with a high lethality. Up to now there is not a successful treatment for it. The purpose of this study was to determine if a conjugated treatment with NAcetylcysteine; A, C, and E vitamins, Propranolol, Colchicine and Furosemide increased the survival of ten paraquat intoxicated patients attended at the San Vicente de Paul University Hospital in Medellín, Colombia, based on the predicted probability of survival, Paraquat plasmatic concentration and clinical assessment. Six patients died because of their intoxication severity, three of them due to multisystemic organic failure, and three from acute respiratory failure. The results had statistical significance, showing a direct proportion between the high plasma levels of paraquat and mortality; and the fact that those with a multiorganic involvement died, despite their low Paraquat plasma levels. Based on clinical data it is possible to conclude that the treatment is useful only for patients with mild to moderate intoxication; there is not an exact correlation between the clinical features and the Paraquat plasma levels; and the clinical features are a very good indicator of the prognosis in Paraquat intoxicated patients. Further experimental and clinical trials are needed. En Colombia se utiliza frecuentemente el Paraquat, herbicida que al ser ingerido en cualquier cantidad produce toxicidad grave y alta mortalidad, sin haberse encontrado un tratamiento eficaz para la recuperación de los intoxicados. El objetivo de este estudio fue establecer si un tratamiento conjugado con N-acetilcisteína, vitamina A, C, E, propranolol, colchicina y furosemida, disminuye la mortalidad en pacientes, basados en la probabilidad de supervivencia, los niveles plasmáticos y el seguimiento clínico. Resultados: De diez pacientes con intoxicaciones no ocupacionales que ingresaron al Hospital Universitario San Vicente

Acute effects of a prooxidant herbicide on the microalga Chlamydomonas reinhardtii: Screening cytotoxicity and genotoxicity endpoints

International Nuclear Information System (INIS)

Esperanza, Marta; Cid, Ángeles; Herrero, Concepción; Rioboo, Carmen

2015-01-01

Highlights: • Mitochondrial membrane potential constituted the most sensitive parameter assayed. • Several genotoxicity methods were applied for first time in ecotoxicological studies. • Oxidative DNA base damage (8-OHdG) was induced by paraquat exposure. • Cells with DNA strand breakage and subG1-nuclei increased in treated cultures. • Typical apoptosis hallmarks were observed in microalgal cells exposed to paraquat. - Abstract: Since recent evidence has demonstrated that many types of chemicals exhibit oxidative and/or genotoxic potential on living organisms, reactive oxygen species (ROS) formation and DNA damage are currently the best accepted paradigms to assess the potential hazardous biological effects of a wide range of contaminants. The goal of this study was to evaluate the sensitivity of different cytotoxicity and genotoxicity responses on the model microalga Chlamydomonas reinhardtii exposed to the prooxidant herbicide paraquat. In addition to the growth endpoint, cell viability, mitochondrial membrane potential and presence of reactive oxygen species (ROS) were assayed as potential markers of cytotoxicity using flow cytometry (FCM). To study the effects of paraquat on C. reinhardtii DNA, several genotoxicity approaches were implemented for the first time in an ecotoxicological study on microalgae. Oxidative DNA base damage was analysed by measuring the oxidative DNA lesion 8-OHdG by FCM. DNA fragmentation was analysed by different methods: comet assay, and cell cycle analysis by FCM, with a particular focus on the presence of subG1-nuclei. Finally, effects on morphology of nuclei were monitored through DAPI staining. The evaluation of these endpoints showed that several physiological and biochemical parameters reacted to oxidative stress disturbances with greater sensitivity than integrative parameters such as growth rates or cell viability. The experiments revealed concentration-dependent cytotoxicity (ROS formation, depolarization of

Acute effects of a prooxidant herbicide on the microalga Chlamydomonas reinhardtii: Screening cytotoxicity and genotoxicity endpoints

Energy Technology Data Exchange (ETDEWEB)

Esperanza, Marta; Cid, Ángeles; Herrero, Concepción; Rioboo, Carmen, E-mail: carmen.rioboo@udc.es

2015-08-15

Highlights: • Mitochondrial membrane potential constituted the most sensitive parameter assayed. • Several genotoxicity methods were applied for first time in ecotoxicological studies. • Oxidative DNA base damage (8-OHdG) was induced by paraquat exposure. • Cells with DNA strand breakage and subG1-nuclei increased in treated cultures. • Typical apoptosis hallmarks were observed in microalgal cells exposed to paraquat. - Abstract: Since recent evidence has demonstrated that many types of chemicals exhibit oxidative and/or genotoxic potential on living organisms, reactive oxygen species (ROS) formation and DNA damage are currently the best accepted paradigms to assess the potential hazardous biological effects of a wide range of contaminants. The goal of this study was to evaluate the sensitivity of different cytotoxicity and genotoxicity responses on the model microalga Chlamydomonas reinhardtii exposed to the prooxidant herbicide paraquat. In addition to the growth endpoint, cell viability, mitochondrial membrane potential and presence of reactive oxygen species (ROS) were assayed as potential markers of cytotoxicity using flow cytometry (FCM). To study the effects of paraquat on C. reinhardtii DNA, several genotoxicity approaches were implemented for the first time in an ecotoxicological study on microalgae. Oxidative DNA base damage was analysed by measuring the oxidative DNA lesion 8-OHdG by FCM. DNA fragmentation was analysed by different methods: comet assay, and cell cycle analysis by FCM, with a particular focus on the presence of subG1-nuclei. Finally, effects on morphology of nuclei were monitored through DAPI staining. The evaluation of these endpoints showed that several physiological and biochemical parameters reacted to oxidative stress disturbances with greater sensitivity than integrative parameters such as growth rates or cell viability. The experiments revealed concentration-dependent cytotoxicity (ROS formation, depolarization of

Foliar Desiccators Glyphosate, Carfentrazone, and Paraquat Affect the Technological and Chemical Properties of Cowpea Grains.

Science.gov (United States)

Lindemann, Igor da Silva; Lang, Gustavo Heinrich; Hoffmann, Jessica Fernanda; Rombaldi, Cesar Valmor; de Oliveira, Maurício; Elias, Moacir Cardoso; Vanier, Nathan Levien

2017-08-16

The effects of the use of glyphosate (GLY), glyphosate plus carfentrazone (GLY/CAR), and paraquat (PAR) as plant desiccators on the technological and chemical properties of cowpea grains were investigated. All studied desiccants provided lower cooking time to freshly harvested cowpea. However, the coat color of PAR- and GLY/CAR-treated cowpea was reddish in comparison to the control treatment. Principal component analysis (PCA) from liquid chromatography-mass spectrometry (LC-MS) data sets showed a clear distinction among cowpea from the different treatments. Catechin-3-glucoside and epicatechin significantly contributed for discriminating GLY-treated cowpea, while citric acid was responsible for discriminating GLY/CAR-treated cowpea. Quercetin derivative and gluconic acid were responsible for discriminating control treatment. Residual glyphosate and paraquat content was higher than the maximum limits allowed by Codex Alimentarius and the European Union Commission. Improvements in the technological and chemical properties of cowpea may not be overlapped by the risks that those desiccants exhibit when exceeding the maximum limits of tolerance in food.

Multiple resistance to glyphosate, paraquat and ACCase-inhibiting herbicides in Italian ryegrass populations from California: confirmation and mechanisms of resistance.

Science.gov (United States)

Tehranchian, Parsa; Nandula, Vijay; Jugulam, Mithila; Putta, Karthik; Jasieniuk, Marie

2018-04-01

Glyphosate, paraquat and acetyl CoA carboxylase (ACCase)-inhibiting herbicides are widely used in California annual and perennial cropping systems. Recently, glyphosate, paraquat, and ACCase- and acetolactate synthase (ALS)-inhibitor resistance was confirmed in several Italian ryegrass populations from the Central Valley of California. This research characterized the possible mechanisms of resistance. Multiple-resistant populations (MR1, MR2) are resistant to several herbicides from at least three modes of action. Dose-response experiments revealed that the MR1 population was 45.9-, 122.7- and 20.5-fold, and the MR2 population was 24.8-, 93.9- and 4.0-fold less susceptible to glyphosate, sethoxydim and paraquat, respectively, than the susceptible (Sus) population. Accumulation of shikimate in Sus plants was significantly greater than in MR plants 32 h after light pretreatments. Glyphosate resistance in MR plants was at least partially due to Pro106-to-Ala and Pro106-to-Thr substitutions at site 106 of 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS). EPSPS gene copy number and expression level were similar in plants from the Sus and MR populations. An Ile1781-to-Leu substitution in ACCase gene of MR plants conferred a high level of resistance to sethoxydim and cross-resistance to other ACCase-inhibitors. Radiolabeled herbicide studies and phosphorimaging indicated that MR plants had restricted translocation of 14 C-paraquat to untreated leaves compared to Sus plants. This study shows that multiple herbicide resistance in Italian ryegrass populations in California, USA, is due to both target-site and non-target-site resistance mechanisms. © 2017 Society of Chemical Industry. © 2017 Society of Chemical Industry.

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

Rotenone and paraquat perturb dopamine metabolism: a computational analysis of pesticide toxicity

OpenAIRE

Qi, Zhen; Miller, Gary W.; Voit, Eberhard O.

2013-01-01

Pesticides, such as rotenone and paraquat, are suspected in the pathogenesis of Parkinson’s disease (PD), whose hallmark is the progressive loss of dopaminergic neurons in the substantia nigra pars compacta. Thus, compounds expected to play a role in the pathogenesis of PD will likely impact the function of dopaminergic neurons. To explore the relationship between pesticide exposure and dopaminergic toxicity, we developed a custom-tailored mathematical model of dopamine metabolism and utilize...

Efeito tóxico dos praguicidas maneb e paraquat sobre a atividade da enzima antioxidante catalase em ratos

Directory of Open Access Journals (Sweden)

M. D. Arbo

2009-01-01

Full Text Available

Os radicais livres estão envolvidos em um grande número de enfermidades do ser humano. O cérebro tem níveis baixos de enzimas antioxidantes e um conteúdo lípidico elevado, tornando-se muito susceptível ao ataque de espécies reativas de oxigênio. Neste trabalho avaliou- se a lipoperoxidação em hipocampo e a atividade da enzima catalase em estriado e hipocampo de ratos tratados com o fungicida maneb (30 mg/kg e o herbicida paraquat (10 mg/kg. Não houve alteração na lipoperoxidação nem na atividade enzimática no hipocampo dos animais tratados com ambos os praguicidas, porém foi observada uma inibição da catalase no estriado dos ratos tratados com maneb e com paraquat. Com estes resultados pode-se sugerir, de forma preliminar, uma ação tóxica maior sobre centros dopaminérgicos. Estudos sobre a toxicidade destes compostos são essenciais na compreensão do papel destes praguicidas e dos radicais livres na etiologia das doenças. Palavras-chave: catalase; paraquat; maneb; estriado; hipocampo; radicais livres.

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.

Quercitrin protects skin from UVB-induced oxidative damage

International Nuclear Information System (INIS)

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

2013-01-01

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

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.

HCV-Induced Oxidative Stress: Battlefield-Winning Strategy

Directory of Open Access Journals (Sweden)

Khadija Rebbani

2016-01-01

Full Text Available 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.

Toxicidad in vitro de los herbicidas atrazina y paraquat sobre el crecimiento vegetativo y la esporulación de hongos saprobios del suelo

OpenAIRE

CHAN CUPUL, Wilberth; HEREDIA ABARCA, Gabriela; RODRÍGUEZ VÁZQUEZ, Refugio; ARIAS MOTA, Rosa María

2014-01-01

El objetivo de este estudio fue evaluar la toxicidad in vitro de los herbicidas atrazina y paraquat sobre el crecimiento vegetativo y la esporulación de hongos saprobios del suelo. Se realizaron bioensayos dosis-respuesta en trece especies con cuatro concentraciones de atrazina (468, 937, 1875 y 3750 mg/L) y paraquat (93, 187, 375 y 750 mg/L). Los hongos fueron inoculados con 2 μL de una suspensión de 1.0 x 10(6) esporas/mL en cajas de Petri con agar papa dextrosa (APD) adicionado con atrazin...

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.

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

African Journals Online (AJOL)

The effects of NO on alleviating arsenic-induced oxidative damage in tall fescue leaves were investigated. Arsenic (25 M) treatment induced significantly accumulation of reactive oxygen species (ROS) and led to serious lipid peroxidation in tall fescue leaves and the application of 100 M SNP before arsenic stress resulted ...

The role of lager beer yeast in oxidative stability of model beer

DEFF Research Database (Denmark)

Berner, Torben Sune; Arneborg, Nils

2012-01-01

that the oxidative stress resistance was strain dependent. Fermentation of model wort in European Brewing Convention tubes using three yeast strains with varying oxidative stress resistances resulted in three model beers with different rates of radical formation as measured by electron spin resonance in forced......AIMS: In this study, we investigated the relationship between the ability of lager brewing yeast strains to tolerate oxidative stress and their ability to produce oxidative stable model beer. METHODS AND RESULTS: Screening of 21 lager brewing yeast strains against diamide and paraquat showed...... in the model beers. CONCLUSIONS: A more oxidative stable beer is not obtained by a more-oxidative-stress-tolerant lager brewing yeast strain, exhibiting a higher secretion of thioredoxin, but rather by a less-oxidative-stress-tolerant strain, exhibiting a higher iron uptake. SIGNIFICANCE AND IMPACT...

Oxidative Stressors Modify the Response of Streptococcus mutans to Its Competence Signal Peptides.

Science.gov (United States)

De Furio, Matthew; Ahn, Sang Joon; Burne, Robert A; Hagen, Stephen J

2017-11-15

The dental caries pathogen Streptococcus mutans is continually exposed to several types of stress in the oral biofilm environment. Oxidative stress generated by reactive oxygen species has a major impact on the establishment, persistence, and virulence of S. mutans Here, we combined fluorescent reporter-promoter fusions with single-cell imaging to study the effects of reactive oxygen species on activation of genetic competence in S. mutans Exposure to paraquat, which generates superoxide anion, produced a qualitatively different effect on activation of expression of the gene for the master competence regulator, ComX, than did treatment with hydrogen peroxide (H 2 O 2 ), which can yield hydroxyl radical. Paraquat suppressed peptide-mediated induction of comX in a progressive and cumulative fashion, whereas the response to H 2 O 2 displayed a strong threshold behavior. Low concentrations of H 2 O 2 had little effect on induction of comX or the bacteriocin gene cipB , but expression of these genes declined sharply if extracellular H 2 O 2 exceeded a threshold concentration. These effects were not due to decreased reporter gene fluorescence. Two different threshold concentrations were observed in the response to H 2 O 2 , depending on the gene promoter that was analyzed and the pathway by which the competence regulon was stimulated. The results show that paraquat and H 2 O 2 affect the S. mutans competence signaling pathway differently, and that some portions of the competence signaling pathway are more sensitive to oxidative stress than others. IMPORTANCE Streptococcus mutans inhabits the oral biofilm, where it plays an important role in the development of dental caries. Environmental stresses such as oxidative stress influence the growth of S. mutans and its important virulence-associated behaviors, such as genetic competence. S. mutans competence development is a complex behavior that involves two different signaling peptides and can exhibit cell

Aplicação de misturas de diuron com MSMA, e com paraquat, no controle de plantas daninhas de folhas largas em cultura de algodão (Gossypium hirsutum L. Mixture of diuron whit MSMA and with paraquat for broadleaved weeds control in cotton

Directory of Open Access Journals (Sweden)

L. S. P. Cruz

1978-01-01

Full Text Available Em ensaio de campo conduzido em 1975/76 procurou-se avaliar a ação de misturas de MSMA com diuron e de paraquat com diuron, aplicadas em pós-emergência, em jato dirigido, em duas épocas diferentes, no controle de algumas plantas daninhas de folhas largas em algodão: carrapicho- do-campo (Acanthospermum australe (Loef O. Kuntze , falsa-poaia (Borreria ala ta (Aubl DC, poaia-branca (Richardia brasiliensis Gomez e guanxuma (Sida spp . A vegetação natural da área do ensaio era formada ainda pela gramínea capim-de-colchão (Digitaria sanguinalis (L. Scop . Os resultados mostraram que as misturas de 2,00 kg e 2,70 kg/ha de MSMA com, respectivamente 0,30 kg e 0,40 kg/ha de diuron, e a mistura de 0.60 kg/ha de paraquat com 0,60 kg/ ha de diuron, foram eficientes no co ntro le daquelas dicotiledôneas, e também no da gramínea. Todos os tratamentos provocaram leves sintomas de fitotoxicidade nos algodoeiros, mas desapareceram depois e não prejudicaram o desenvolvimento vegetativo das plantas, assim como a produção de algodão em caroço.In a field trial carried out in 1975/76, a diuron mixtu re with MSMA and another with paraquat was tested on broadleaved weeds in cotton crops. The applications were done in postemergence, directed-spray, in two different periods. The broadleaved weeds observed in the trial were Acanthospermum australe , Borreria alata, Richardia brasiliensis, and Sida spp, also the grass Digitaria sanguinalis. Best results were obtained with the mixture of 0,60 kg/ha of paraquat with 0,60 kg/ha of diuron, and 2,70 kg/ha of MSMA with 0,40 kg/ ha of diuron, or 2,00 kg/ha of MSMA with 0,30 kg/ha of diuron. All the treatments caused sl ight symptons of toxic ity in cotton, which disappeared later and did not damage the production.

The in vivo antioxidant effect of vitamin C on hemogram in Paraquat treated male rats (rattus norvegicus

Directory of Open Access Journals (Sweden)

Benjamin Nnamdi Okolonkwo

2013-06-01

Full Text Available Paraquat (PQ is one of the most used herbicide globally; applied around trees in orchards and between crop rows to control broad-leaved and grassy weeds. Its oxidation results in the formation of superoxides which causes damage to cellular components. In this study, we determined the antioxidant effect vitamin C has on hemograms [hemoglobin (Hb, packed cell volume (PCV and total white blood cells count] of rats under these toxic insults. The animals grouped (A-D, comprising subgroups without vitamin C (A1, B1, C1, D1 and subgroups on vitamin C (A2, B2, C2, D2, received different sub-lethal doses of PQ administered intraperitoneally monthly to the animals over a period of three months. The Hb values obtained were significantly reduced (P≤0.05 at month 1 and (P≤0.001 at months 2 and 3. These changes became more pronounced with increased dose and time. Vitamin C treated subgroups (B2, C2 and D2 had better Hb values than those without it (B1, C1 and D1 but the values were still significantly low when compared to the control subgroups (A1 and A2. This same trend was observed in the PCV results obtained. The Control subgroups showed that vitamin C treated subgroup (A2 had a more improved hemogram values than subgroup on water only (A1, but they were all higher than that of the test subgroups. These PQ induced anaemia were ameliorated by the subsequent administration of vitamin C, and continuous treatment with vitamin C restored the health status of the animals so treated.

P-glycoprotein induction in Caco-2 cells by newly synthetized thioxanthones prevents paraquat cytotoxicity.

Science.gov (United States)

Silva, Renata; Palmeira, Andreia; Carmo, Helena; Barbosa, Daniel José; Gameiro, Mariline; Gomes, Ana; Paiva, Ana Mafalda; Sousa, Emília; Pinto, Madalena; Bastos, Maria de Lourdes; Remião, Fernando

2015-10-01

The induction of P-glycoprotein (P-gp), an ATP-dependent efflux pump, has been proposed as a strategy against the toxicity induced by P-gp substrates such as the herbicide paraquat (PQ). The aim of this study was to screen five newly synthetized thioxanthonic derivatives, a group known to interact with P-gp, as potential inducers of the pump's expression and/or activity and to evaluate whether they would afford protection against PQ-induced toxicity in Caco-2 cells. All five thioxanthones (20 µM) caused a significant increase in both P-gp expression and activity as evaluated by flow cytometry using the UIC2 antibody and rhodamine 123, respectively. Additionally, it was demonstrated that the tested compounds, when present only during the efflux of rhodamine 123, rapidly induced an activation of P-gp. The tested compounds also increased P-gp ATPase activity in MDR1-Sf9 membrane vesicles, indicating that all derivatives acted as P-gp substrates. PQ cytotoxicity was significantly reduced in the presence of four thioxanthone derivatives, and this protective effect was reversed upon incubation with a specific P-gp inhibitor. In silico studies showed that all the tested thioxanthones fitted onto a previously described three-feature P-gp induction pharmacophore. Moreover, in silico interactions between thioxanthones and P-gp in the presence of PQ suggested that a co-transport mechanism may be operating. Based on the in vitro activation results, a pharmacophore model for P-gp activation was built, which will be of further use in the screening for new P-gp activators. In conclusion, the study demonstrated the potential of the tested thioxanthonic compounds in protecting against toxic effects induced by P-gp substrates through P-gp induction and activation.

Development of a sequential injection-square wave voltammetry method for determination of paraquat in water samples employing the hanging mercury drop electrode.

Science.gov (United States)

dos Santos, Luciana B O; Infante, Carlos M C; Masini, Jorge C

2010-03-01

This work describes the development and optimization of a sequential injection method to automate the determination of paraquat by square-wave voltammetry employing a hanging mercury drop electrode. Automation by sequential injection enhanced the sampling throughput, improving the sensitivity and precision of the measurements as a consequence of the highly reproducible and efficient conditions of mass transport of the analyte toward the electrode surface. For instance, 212 analyses can be made per hour if the sample/standard solution is prepared off-line and the sequential injection system is used just to inject the solution towards the flow cell. In-line sample conditioning reduces the sampling frequency to 44 h(-1). Experiments were performed in 0.10 M NaCl, which was the carrier solution, using a frequency of 200 Hz, a pulse height of 25 mV, a potential step of 2 mV, and a flow rate of 100 µL s(-1). For a concentration range between 0.010 and 0.25 mg L(-1), the current (i(p), µA) read at the potential corresponding to the peak maximum fitted the following linear equation with the paraquat concentration (mg L(-1)): i(p) = (-20.5 ± 0.3)C (paraquat) - (0.02 ± 0.03). The limits of detection and quantification were 2.0 and 7.0 µg L(-1), respectively. The accuracy of the method was evaluated by recovery studies using spiked water samples that were also analyzed by molecular absorption spectrophotometry after reduction of paraquat with sodium dithionite in an alkaline medium. No evidence of statistically significant differences between the two methods was observed at the 95% confidence level.

Radiation induced lipid oxidation in fish

International Nuclear Information System (INIS)

Snauwaert, F.; Tobback, P.; Maes, E.; Thyssen, J.

1977-01-01

Oxidative rancidity in herring and redfish was studied as a function of the applied irradiation dose, the storage time and storage temperature and the packaging conditions. - Measurements of the TBA (thiobarbituric acid) value and the peroxide value were used to evaluate the degree of oxidation of lipids, and were related with sensory scores. - Especially for the fatty fish species (herring) irradiation accelerated lipid oxidation and induced oxidative rancidity. Irradiation of vacuum-packed herring fillets and subsequent storage at +2 C seems to be an interesting process. For the experiments conducted on a semi-fatty fish (redfish), oxidative rancidity was never the limiting factor for organoleptic acceptability. (orig.) [de

Efeitos dos herbicidas glyphosate e paraquat, aplicados ao solo, sobre a emergência de feijão e soja e de algumas espécies daninhas Effects of the herbicides glyphosate and paraquat, applied to the soil, on the emergence of dry beans and soybeans and some weed species

Directory of Open Access Journals (Sweden)

C.A. Dias

1982-06-01

Full Text Available Em trabalho conduzido a campo na Estação Experimental Agronômica da UFRGS, Guaíba, RS em 1979/80, usaram-se os herbicidas glyphosate, paraquat e sua combinação, objetivando determinar os efe itos de doses e de épocas de aplicação destes herbicidas em plântulas de feijão e de soja e sobre nutrientes do solo. Pelos resultados obtidos para emergência e peso de maté ria seca da parte aé re a de soja , não houve di ferenças para os tratamentos testados. Também não ocorreram diferenças significativas à população in ic ia l de feijão e sobre os elementos de solo analisados (Ca, Mg e K. Com relação ao peso de matéria seca da parte aérea do feijão, verificou-se que houve interação entre herbicida e doses usadas, tendo glyphosate isolado e glyphosate mais paraquat aplicados seqüencialmente nas doses máximas causado redução significativa naquele parâmetro. Com relação ao paraquat, não foram detectadas diferenças significativas entre as doses testadas.A field xeperiment was conducted during the 1979/80 growing season at the Agronomic Experimental Station of the Federal University of Rio Grande do Sul, in Guaíba, RS, Brazil, in order to evaluate the efects of rates and times of appl ication of the herbicides glyphosate, paraqu at, and the ir combin at ion, on dry beans (Phaseolus vulgaris L. and soybeans (Glvcine max (L. Merrill, and on some soil nutrierts. The results indicated no significant differences among the soybeans treatments tested fo r plant population and shoot dry weight. Also no sta ti sti cal diffe re nces occurred fo r dry beans plant population and for soil nutrients analysed (Ca, Mg, and K. For dry beans shoot dry weight, there was an interaction of herbicides and rates, where glyphosate sprayed alone and glyphosate plus paraquat applied at the maxima ra te s te sted caused significant decreases on that variable. For paraquat utilized alone, no significant effects were detected among the rates applied.

Melatonin Improves the Photosynthetic Apparatus in Pea Leaves Stressed by Paraquat via Chlorophyll Breakdown Regulation and Its Accelerated de novo Synthesis

Directory of Open Access Journals (Sweden)

Katarzyna Szafrańska

2017-05-01

Full Text Available The positive effect of melatonin on the function of the photosynthetic apparatus is known, but little is known about the specific mechanisms of melatonin's action in plants. The influence of melatonin on chlorophyll metabolism of 24-day-old Pisum sativum L. seedlings during paraquat (PQ-induced oxidative stress was investigated in this study. Seeds were hydro-primed with water (H, 50 and 200 μM melatonin/water solutions (H-MEL50, H-MEL200, while non-primed seeds were used as controls (C. Increases in chlorophyllase activity (key enzyme in chlorophyll degradation and 5-aminolevulinic acid contents (the first compound in the porphyrin synthesis pathway were observed in H-MEL50 and H-MEL200 leaf disks. This suggests that melatonin may accelerate damaged chlorophyll breakdown and its de novo synthesis during the first hours of PQ treatment. Elevated level of pheophytin in control leaf disks following 24 h of PQ incubation probably was associated with an enhanced rate of chlorophyll degradation through formation of pheophytin as a chlorophyll derivative. This validates the hypothesis that chlorophyllide, considered for many years, as a first intermediate of chlorophyll breakdown is not. This is indicated by the almost unchanged chlorophyll to chlorophyllide ratio after 24 h of PQ treatment. However, prolonged effects of PQ-induced stress (48 h revealed extensive discolouration of control and water-treated leaf disks, while melatonin treatment alleviated PQ-induced photobleaching. Also the ratio of chlorophyll to chlorophyllide and porphyrin contents were significantly higher in plants treated with melatonin, which may indicate that this indoleamine both retards chlorophyll breakdown and stimulates its de novo synthesis during extended stress. We concluded that melatonin added into the seeds enhances the ability of pea seedlings to accelerate chlorophyll breakdown and its de novo synthesis before stress appeared and for several hours after, while

Long-lived ames dwarf mice are resistant to chemical stressors.

Science.gov (United States)

Bokov, Alex F; Lindsey, Merry L; Khodr, Christina; Sabia, Marian R; Richardson, Arlan

2009-08-01

To probe the connection between longevity and stress resistance, we compared the sensitivity of Ames long-lived dwarf mice and control littermates with paraquat, diquat, and dobutamine. In young adult animals, 95% of male and 39% of female controls died after paraquat administration, but no dwarf animals died. When the experiment was repeated at an older age or a higher dosage of paraquat, dwarf mice still showed greater resistance. Dwarf mice also were more resistant to diquat; 80% of male and 60% of female controls died compared with 40% and 20% of dwarf mice, despite greater sensitivity of dwarf liver to diquat. Dwarf mice were also less sensitive to dobutamine-induced cardiac stress and had lower levels of liver and lung F(2)-isoprostanes. This is the first direct in vivo evidence that long-lived Ames dwarf mice have enhanced resistance to chemical insult, particularly oxidative stressors.

Oxidative stress-induced autophagy: Role in pulmonary toxicity

International Nuclear Information System (INIS)

Malaviya, Rama; Laskin, Jeffrey D.; Laskin, Debra L.

2014-01-01

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

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.

Reactivity of paraquat with sodium salicylate: Formation of stable complexes

International Nuclear Information System (INIS)

Dinis-Oliveira, Ricardo Jorge; Guedes de Pinho, Paula; Ferreira, Antonio Cesar Silva; Silva, Artur M.S.; Afonso, Carlos; Bastos, Maria de Lourdes; Remiao, Fernando; Duarte, Jose Alberto; Carvalho, Felix

2008-01-01

Sodium salicylate (NaSAL) has been shown to be a promising antidote for the treatment of paraquat (PQ) poisonings. The modulation of the pro-oxidant and pro-inflammatory pathways, as well as the anti-thrombogenic properties of NaSAL are probably essential features for the healing effects provided by this drug. Nevertheless, a possible direct chemical reactivity between PQ and NaSAL is also a putative pathway to be considered, this hypothesis being the ground of the present study. In accordance, it is shown, for the first time that PQ and NaSAL react immediately in aqueous medium and within 2-3 min in the solid state. Photographs and scanning electron photomicrographs indicated that a new chemical entity is formed when both compounds are mixed. This assumption was corroborated by the evaluation of the melting point, and through several analytical techniques, namely ultraviolet/visible spectroscopy, nuclear magnetic resonance spectroscopy, gas chromatography/mass spectrometry/mass spectrometry (GC/MS/MS), liquid chromatography/electrospray ionization/mass spectrometry/mass spectrometry (LC/ESI/MS/MS) and infrared spectroscopy, which revealed that stable charge-transfer complexes are formed when PQ is mixed with NaSAL. LC/ESI/MS/MS allowed obtaining the stoichiometry of the charge-transfer complexes. In order to increase resolution, single value decomposition, acting as a filter, showed that the charge-transfer complexes with m/z 483, 643 and 803 correspond to the pseudo-molecular ions, respectively 1:2, 1:3 and 1:4 (PQ:NaSAL). In conclusion, these results provided a new and important mechanism of action of NaSAL against the toxicity mediated by PQ

Cadmium(Cd)-induced oxidative stress down-regulates the gene expression of DNA mismatch recognition proteins MutS homolog 2 (MSH2) and MSH6 in zebrafish (Danio rerio) embryos

Energy Technology Data Exchange (ETDEWEB)

Hsu, Todd, E-mail: toddhsu@mail.ntou.edu.tw [Institute of Bioscience and Biotechnology and Center of Excellence for Marine Bioenvironment and Biotechnology, National Taiwan Ocean University, Keelung 20224, Taiwan (China); Huang, Kuan-Ming; Tsai, Huei-Ting; Sung, Shih-Tsung; Ho, Tsung-Nan [Institute of Bioscience and Biotechnology and Center of Excellence for Marine Bioenvironment and Biotechnology, National Taiwan Ocean University, Keelung 20224, Taiwan (China)

2013-01-15

DNA mismatch repair (MMR) of simple base mismatches and small insertion-deletion loops in eukaryotes is initiated by the binding of the MutS homolog 2 (MSH2)-MSH6 heterodimer to mismatched DNA. Cadmium (Cd) is a genotoxic heavy metal that has been recognized as a human carcinogen. Oxidant stress and inhibition of DNA repair have been proposed as major factors underlying Cd genotoxicity. Our previous studies indicated the ability of Cd to disturb the gene expression of MSH6 in zebrafish (Danio rerio) embryos. This study was undertaken to explore if Cd-induced oxidative stress down-regulated MSH gene activities. Following the exposure of zebrafish embryos at 1 h post fertilization (hpf) to sublethal concentrations of Cd at 3-5 {mu}M for 4 or 9 h, a parallel down-regulation of MSH2, MSH6 and Cu/Zn superoxide dismutase (Cu/Zn-SOD) gene expression was detected by real-time RT-PCR and the expression levels were 40-50% of control after a 9-h exposure. Cd exposure also induced oxidative stress, yet no inhibition of catalase gene activity was observed. Whole mount in situ hybridization revealed a wide distribution of msh6 mRNA in the head regions of 10 hpf embryos and pretreatment of embryos with antioxidants butylhydroxytoluene (BHT), D-mannitol or N-acetylcysteine (NAC) at 1-10 {mu}M restored Cd-suppressed msh6 expression. QPCR confirmed the protective effects of antioxidants on Cd-suppressed msh2/msh6 mRNA production. Down-regulated MSH gene activities reaching about 50% of control were also induced in embryos exposed to paraquat, a reactive oxygen species (ROS)-generating herbicide, or hydrogen peroxide at 200 {mu}M. Hence, Cd at sublethal levels down-regulates msh2/msh6 expression primarily via ROS as signaling molecules. The transcriptional activation of human msh6 is known to be fully dependent on the specificity factor 1 (Sp1). Cd failed to inhibit the DNA binding activity of zebrafish Sp1 unless at lethal concentrations based on band shift assay, therefore

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.

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.

Leaching of the S-metolachlor herbicide associated with paraquat or glyphosate in a no-tillage system

Directory of Open Access Journals (Sweden)

Anderson Luis Nunes

2016-09-01

Full Text Available The combined use of desiccant and residual herbicides is a common management practice under no-tillage systems. However, the effect of desiccant herbicides and mulch on the leaching of residual herbicide is unknown. This study aimed at assessing the leaching of the S-metolachlor herbicide applied to ryegrass sequentially or in association with paraquat or glyphosate. A randomized blocks design was used, with four repetitions and treatments distributed over split-plots. The desiccant herbicides paraquat (600 g ha-1 or glyphosate (720 g ha-1 were used in the main plot, while S-metolachlor (2,800 g ha-1 was applied sequentially or in association with the desiccant herbicides in the subplots. There was also a control containing only desiccant herbicide, with no application of residual herbicide. The type of desiccant did not affect the leaching of the residual herbicide. In addition, the chosen method to apply the residual herbicide, sequentially or in association with the desiccant, did not impact the S-metolachlor behavior in the soil. The bioavailable concentration in the soil, 25 days after the application, was 90 g a.i. ha-1, at a depth of 18 cm.

Linkages between the life-history evolution of tropical and temperate birds and the resistance of cultured skin fibroblasts to oxidative and non-oxidative chemical injury.

Science.gov (United States)

Jimenez, Ana Gabriela; Harper, James M; Queenborough, Simon A; Williams, Joseph B

2013-04-15

A fundamental challenge facing physiological ecologists is to understand how variation in life history at the whole-organism level might be linked to cellular function. Thus, because tropical birds have higher annual survival and lower rates of metabolism, we hypothesized that cells from tropical species would have greater cellular resistance to chemical injury than cells from temperate species. We cultured dermal fibroblasts from 26 tropical and 26 temperate species of birds and examined cellular resistance to cadmium, H(2)O(2), paraquat, thapsigargin, tunicamycium, methane methylsulfonate (MMS) and UV light. Using ANCOVA, we found that the values for the dose that killed 50% of cells (LD(50)) from tropical birds were significantly higher for H(2)O(2) and MMS. When we tested for significance using a generalized least squares approach accounting for phylogenetic relationships among species to model LD(50), we found that cells from tropical birds had greater tolerance for Cd, H(2)O(2), paraquat, tunicamycin and MMS than cells from temperate birds. In contrast, tropical birds showed either lower or no difference in tolerance to thapsigargin and UV light in comparison with temperate birds. These findings are consistent with the idea that natural selection has uniquely fashioned cells of long-lived tropical bird species to be more resistant to forms of oxidative and non-oxidative stress than cells from shorter-lived temperate species.

Influence of diet with kale on lipid peroxides and malondialdehyde levels in blood serum of laboratory rats over intoxication with paraquat.

Science.gov (United States)

Sikora, Elżbieta; Bodziarczyk, Izabela

2013-01-01

Organism's lipid peroxidation is one of the most often examined and known physiological process evoked by free radicals. It concerns oxidation reaction of unsaturated fatty acid and/or other lipids leading to lipid oxidation products (LOP), which as a result of further changes generate among others the malondialdehyde molecules. The aim of the work was an estimation if raw or cooked kale addition to rat's diet influences antioxidant defense efficiency in their organisms in comparison to rats fed with standard AIN-93G diet. The experiment was conducted with 36 Wistar strain, male rats over 21 days. The rats were divided into 3 groups (each 12 stuck) which were fed with: standard diet AIN-93G (2 groups), AIN-93G diet with 10% addition of raw kale (2 groups), and AIN-93G with 10% addition of cooked lyophilised kale. The total content of polyphenols (FC method) and antioxidant activity (ABTS+•) were previously determined in raw and then in cooked kale. On the 20th day of experiment, half of rats (6 stuck) of each kind of the diet were injected intraperitoneally by the solution of paraquat (PQ) in physiological salt to evoke the oxidative stress. The next day animals were stunned and blood from their hearts was sampled. In the obtained serum, the levels of lipid oxidation products (LOP) and malondialdehyde (MDA) were assessed. It was observed that in blood serum of rats fed with modified diet with raw and cooked lyophilised kale addition the lipid oxides level was lower in comparison to control group fed with standard diet (p kale addition. Diet with kale, both raw and cooked, efficiently inhibited the lipid peroxidation process in rats' organisms, ongoing during natural metabolism and during evoked oxidative stress.

Potent Protective Effect Of α -Tocopherol And Fish Oil On In Vivo ...

African Journals Online (AJOL)

The potential protective role of α-tocopherol and fish oil against oxidative damage induced by paraquat were investigated. Forty male albino rats with average body weight of 100-120 gm were housed in 8 groups of 5 rats each. The first group served as control and injected with saline, group 2 was injected with a single dose ...

Reduced coupling of oxidative phosphorylation in vivo precedes electron transport chain defects due to mild oxidative stress in mice.

Directory of Open Access Journals (Sweden)

Michael P Siegel

Full Text Available Oxidative stress and mitochondrial function are at the core of many degenerative conditions. However, the interaction between oxidative stress and in vivo mitochondrial function is unclear. We used both pharmacological (2 week paraquat (PQ treatment of wild type mice and transgenic (mice lacking Cu, Zn-superoxide dismutase (SOD1(-/- models to test the effect of oxidative stress on in vivo mitochondrial function in skeletal muscle. Magnetic resonance and optical spectroscopy were used to measure mitochondrial ATP and oxygen fluxes and cell energetic state. In both models of oxidative stress, coupling of oxidative phosphorylation was significantly lower (lower P/O at rest in vivo in skeletal muscle and was dose-dependent in the PQ model. Despite this reduction in efficiency, in vivo mitochondrial phosphorylation capacity (ATPmax was maintained in both models, and ex vivo mitochondrial respiration in permeabilized muscle fibers was unchanged following PQ treatment. In association with the reduced P/O, PQ treatment led to a dose-dependent reduction in PCr/ATP ratio and increased phosphorylation of AMPK. These results indicate that oxidative stress uncouples oxidative phosphorylation in vivo and results in energetic stress in the absence of defects in the mitochondrial electron transport chain.

ROS-mediated inhibition of S-nitrosoglutathione reductase contributes to the activation of anti-oxidative mechanisms

Directory of Open Access Journals (Sweden)

Izabella Kovacs

2016-11-01

Full Text Available Nitric oxide (NO has emerged as a signaling molecule in plants being involved in diverse physiological processes like germination, root growth, stomata closing and response to biotic and abiotic stress. S-nitrosoglutathione (GSNO as a biological NO donor has a very important function in NO signaling since it can transfer its NO moiety to other proteins (trans-nitrosylation. Such trans-nitrosylation reactions are equilibrium reactions and depend on GSNO level. The breakdown of GSNO and thus the level of S-nitrosylated proteins are regulated by GSNO-reductase (GSNOR. In this way, this enzyme controls S-nitrosothiol levels and regulates NO signaling. Here we report that Arabidopsis thaliana GSNOR activity is reversibly inhibited by H2O2 in-vitro and by paraquat-induced oxidative stress in-vivo. Light scattering analyses of reduced and oxidized recombinant GSNOR demonstrated that GSNOR proteins form dimers under both reducing and oxidizing conditions. Moreover, mass spectrometric analyses revealed that H2O2-treatment increased the amount of oxidative modifications on Zn2+-coordinating Cys47 and Cys177. Inhibition of GSNOR results in enhanced levels of S-nitrosothiols followed by accumulation of glutathione. Moreover, transcript levels of redox-regulated genes and activities of glutathione-dependent enzymes are increased in gsnor-ko plants, which may contribute to the enhanced resistance against oxidative stress. In sum, our results demonstrate that ROS-dependent inhibition of GSNOR is playing an important role in activation of anti-oxidative mechanisms to damping oxidative damage and imply a direct crosstalk between ROS- and NO-signaling.

The Intervention of Sucralfate Suspension Gel on Paraquat Poisoned Patients%硫糖铝干预百草枯中毒的研究

Institute of Scientific and Technical Information of China (English)

朱峻波; 于勇涛; 李洪波; 郑粉双; 苏敬; 杨春爱

2016-01-01

目的：探讨硫糖铝治疗百草枯中毒患者的疗效。方法：将100例百草枯中毒的患者分成两组，对照组（50例）与硫糖铝治疗组（50）例，经治疗后对比病人的死亡率，生存率和肺损伤的情况。结果：硫糖铝治疗组病人肺损伤下降，出院时间缩短。结论：早期使用硫糖铝进行胃肠灌洗的病人肺损伤下降，提高了生存率。%Objective: To investigate the effect of sucralfate suspension gel in paraquat-poisoned patients. Methods: 100 paraquat-poisoned patients were divided into two groups: control group (50) and sucralfate suspension gel group (50). The death rate, survival rate and the acute lung injury of the patients after treatment were compared between two groups. Results: The acute lung injury in the sucralfate suspension gel group more reduced, and their recovery time was shorter. Conclusions: Early use of sucralfate suspension gel reduced the acute lung injury reduced, improved the survival rate in paraquat-poisoned patients.

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.

Laser induced single spot oxidation of titanium

International Nuclear Information System (INIS)

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

2016-01-01

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.

Laser-Induced, Local Oxidation of Copper Nanoparticle Films During Raman Measurements

Science.gov (United States)

Hight Walker, Angela R.; Cheng, Guangjun; Calizo, Irene

2011-03-01

The optical properties of gold and silver nanoparticles and their films have been thoroughly investigated as surface enhanced Raman scattering (SERS) substrates and chemical reaction promoters. Similar to gold and silver nanoparticles, copper nanoparticles exhibit distinct plasmon absorptions in the visible region. The work on copper nanoparticles and their films is limited due to their oxidization in air. However, their high reactivity actually provides an opportunity to exploit the laser-induced thermal effect and chemical reactions of these nanoparticles. Here, we present our investigation of the local oxidation of a copper nanoparticle film induced by a visible laser source during Raman spectroscopic measurements. The copper nanoparticle film is prepared by drop-casting chemically synthesized copper colloid onto silicon oxide/silicon substrate. The local oxidation induced by visible lasers in Raman spectroscopy is monitored with the distinct scattering peaks for copper oxides. Optical microscopy and scanning electron microscopy have been used to characterize the laser-induced morphological changes in the film. The results of this oxidation process with different excitation wavelengths and different laser powers will be presented.

Acid-base balance and cardiac index in SO2-bronchitic, papaine-emphysematous and paraquat-fibrotic rats after isoproterenol treatment.

Science.gov (United States)

Vértes, K; Debreczeni, L A

1990-01-01

SO2-bronchitis, papaine-emphysema and paraquat fibrosis were induced in Wistar rats. Blood pressure, cardiac index, total peripheral resistance, arterial blood gas values, parameters of acid-base balance were determined. Effects of 0.1 and 0.3 microgram.-1.min-1 isoproterenol iv. infusion were examined. Morphologic alterations of the lungs were verified by histopathological examinations. All the parameters investigated were found to be normal in the control rats. The treated groups differed from the normal ones: an increased blood pressure was observed in emphysema and fibrosis. A decreased cardiac index was characteristic of chronic bronchitis, high cardiac index of emphysema, high TPR of bronchitis and arterial hypoxaemy of fibrosis. The groups reacted differently to beta adrenergic stimulation: in bronchitic and fibrotic rats the cardiac index was augmented, whereas in emphysematous ones the increase proved to be smaller. The effects of isoproterenol infusion can be related to the altered beta-receptor function in the various experimental pulmonary diseases.

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.

Ablation of the mitochondrial complex IV assembly protein Surf1 leads to increased expression of the UPRMT and increased resistance to oxidative stress in primary cultures of fibroblasts

Directory of Open Access Journals (Sweden)

Gavin Pharaoh

2016-08-01

Full Text Available Mice deficient in the electron transport chain (ETC complex IV assembly protein SURF1 have reduced assembly and activity of cytochrome c oxidase that is associated with an upregulation of components of the mitochondrial unfolded protein response (UPRMT and increased mitochondrial number. We hypothesized that the upregulation of proteins associated with the UPRMT in response to reduced cytochrome c oxidase activity in Surf1−/− mice might contribute to increased stress resistance. To test this hypothesis we asked whether primary cultures of fibroblasts from Surf1−/− mice exhibit enhanced resistance to stressors compared to wild-type fibroblasts. Here we show that primary dermal fibroblasts isolated from Surf1−/− mice have increased expression of UPRMT components ClpP and Hsp60, and increased expression of Lon protease. Fibroblasts from Surf1−/− mice are significantly more resistant to cell death caused by oxidative stress induced by paraquat or tert-Butyl hydroperoxide compared to cells from wild-type mice. In contrast, Surf1−/− fibroblasts show no difference in sensitivity to hydrogen peroxide stress. The enhanced cell survival in response to paraquat or tert-Butyl hydroperoxide in Surf1−/− fibroblasts compared to wild-type fibroblasts is associated with induced expression of Lon, ClpP, and Hsp60, increased maximal respiration, and increased reserve capacity as measured using the Seahorse Extracellular Flux Analyzer. Overall these data support a protective role for the activation of the UPRMT in cell survival.

Electrochemical determination of paraquat in citric fruit based on electrodeposition of silver particles onto carbon paste electrode

OpenAIRE

Abdelfettah Farahi; Mounia Achak; Laila El Gaini; Moulay Abderrahim El Mhammedi; Mina Bakasse

2015-01-01

Carbon paste electrodes (CPEs) modified with silver particles present an interesting tool in the determination of paraquat (PQ) using square wave voltammetry. Metallic silver particle deposits have been obtained via electrochemical deposition in acidic media using cyclic voltammetry. Scanning electron microscopy and X-ray diffraction measurements show that the silver particles are deposited onto carbon surfaces in aggregate form. The response of PQ with modified electrode (Ag-CPE) related to ...

Sodium nitroprusside (SNP) alleviates the oxidative stress induced ...

African Journals Online (AJOL)

Oxidative damage is often induced by abiotic stress, nitric oxide (NO) is considered as a functional molecule in modulating antioxidant metabolism of plants. In the present study, effects of sodium nitroprusside (SNP), a NO donor, on the phenotype, antioxidant capacity and chloroplast ultrastructure of cucumber leaves were ...

Persistence of paraquat in the soil and observations with other herbicides relevant to the theme of bound residues

International Nuclear Information System (INIS)

Hance, R.J.; Byast, T.H.

1984-01-01

Results from three separate experiments that have some relevance to bound residues are reported. In the first, 14 C-labelled paraquat was lost when applied to soil in the field, about 26% of the radioactivity disappearing in 15 months, whereas in laboratory incubation studies there was no loss of radioactivity in one year. Two possible explanations are (i) that there was photolytic decomposition in the field, (ii) the preparation of the soil for the laboratory study upset the microbial ecology of the soil to the detriment of organisms that can degrade paraquat. In an experiment with 14 C-labelled isoproturon, there was an indication that there was slightly more 14 C in the unextractable humin fraction in soil in which wheat plants were grown than in bare soil. Work in the UK, Federal Republic of Germany and in Switzerland has shown that the phytotoxicity of residues of atrazine, carbetamide, chloridazone, propyzamide, simazine, lenacil, monolinuron, linuron, propachlor and methabenzthiazuron can be satisfactorily predicted on the basis of the amount that is extractable with water. This implies that bound residues of these compounds, if they exist, are unlikely to be phytotoxic. (author)

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

2018-01-01

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-pro...

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. Copyright © 2017 Elsevier B.V. All rights reserved.

The Mitochondrial Lon Protease Is Required for Age-Specific and Sex-Specific Adaptation to Oxidative Stress.

Science.gov (United States)

Pomatto, Laura C D; Carney, Caroline; Shen, Brenda; Wong, Sarah; Halaszynski, Kelly; Salomon, Matthew P; Davies, Kelvin J A; Tower, John

2017-01-09

Multiple human diseases involving chronic oxidative stress show a significant sex bias, including neurodegenerative diseases, cancer, immune dysfunction, diabetes, and cardiovascular disease. However, a possible molecular mechanism for the sex bias in physiological adaptation to oxidative stress remains unclear. Here, we report that Drosophila melanogaster females but not males adapt to hydrogen peroxide stress, whereas males but not females adapt to paraquat (superoxide) stress. Stress adaptation in each sex requires the conserved mitochondrial Lon protease and is associated with sex-specific expression of Lon protein isoforms and proteolytic activity. Adaptation to oxidative stress is lost with age in both sexes. Transgenic expression of transformer gene during development transforms chromosomal males into pseudo-females and confers the female-specific pattern of Lon isoform expression, Lon proteolytic activity induction, and H 2 O 2 stress adaptation; these effects were also observed using adult-specific transformation. Conversely, knockdown of transformer in chromosomal females eliminates the female-specific Lon isoform expression, Lon proteolytic activity induction, and H 2 O 2 stress adaptation and produces the male-specific paraquat (superoxide) stress adaptation. Sex-specific expression of alternative Lon isoforms was also observed in mouse tissues. The results develop Drosophila melanogaster as a model for sex-specific stress adaptation regulated by the Lon protease, with potential implications for understanding sexual dimorphism in human disease. Copyright © 2017 Elsevier Ltd. All rights reserved.

Oxidative Stress Induces Senescence in Cultured RPE Cells.

Science.gov (United States)

Aryan, Nona; Betts-Obregon, Brandi S; Perry, George; Tsin, Andrew T

2016-01-01

The aim of this research is to determine whether oxidative stress induces cellular senescence in human retinal pigment epithelial cells. Cultured ARPE19 cells were subjected to different concentrations of hydrogen peroxide to induce oxidative stress. Cells were seeded into 24-well plates with hydrogen peroxide added to cell medium and incubated at 37°C + 5% CO2 for a 90-minute period [at 0, 300, 400 and 800 micromolar (MCM) hydrogen peroxide]. The number of viable ARPE19 cells were recorded using the Trypan Blue Dye Exclusion Method and cell senescence was measured by positive staining for senescence-associated beta-galactosidase (SA-beta-Gal) protein. Without hydrogen peroxide treatment, the number of viable ARPE19 cells increased significantly from 50,000 cells/well to 197,000 within 72 hours. Treatment with hydrogen peroxide reduced this level of cell proliferation significantly (to 52,167 cells at 400 MCM; to 49,263 cells at 800 MCM). Meanwhile, cells with a high level of positive senescence-indicator SA-Beta-Gal-positive staining was induced by hydrogen peroxide treatment (from a baseline level of 12% to 80% at 400 MCM and at 800 MCM). Our data suggests that oxidative stress from hydrogen peroxide treatment inhibited ARPE19 cell proliferation and induced cellular senescence.

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.

Effects of Uric Acid on Exercise-induced Oxidative Stress

OpenAIRE

平井, 富弘

2001-01-01

We studied effects of uric acid on exercise― induced oxidative stress in humans based on a hypothesis that uric acid acts as an antioxidant to prevent from exercise―induced oxidative stress. Relation between uric acid level in plasma and increase of thiobarbituric acid reactive substance (TBARS)after the cycle ergometer exercise was examined. Thiobarbituricacid reactive substance in plasma increased after the ergometer exercise. High uric acid in plasma did not result in low increase of TBARS...

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.

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.

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

International Nuclear Information System (INIS)

Bakkal, B.H.; Gultekin, F.A.; Guven, B.; Turkcu, U.O.; Bektas, S.; Can, M.

2013-01-01

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

Metoprolol induces oxidative damage in common carp (Cyprinus carpio).

Science.gov (United States)

Martínez-Rodríguez, Héctor; Donkor, Kingsley; Brewer, Sharon; Galar-Martínez, Marcela; SanJuan-Reyes, Nely; Islas-Flores, Hariz; Sánchez-Aceves, Livier; Elizalde-Velázquez, Armando; Gómez-Oliván, Leobardo Manuel

2018-04-01

During the last decade, β-blockers such as metoprolol (MTP) have been frequently detected in surface water, aquatic systems and municipal water at concentrations of ng/L to μg/L. Only a small number of studies exist on the toxic effects induced by this group of pharmaceuticals on aquatic organisms. Therefore, the present study aimed to evaluate the oxidative damage induced by MTP in the common carp Cyprinus carpio, using oxidative stress biomarkers. To this end, indicators of cellular oxidation such as hydroperoxide content (HPC), lipid peroxidation (LPX) and protein carbonyl content (PCC) were determined, as well as the activity of the antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT). Also, concentrations of MTP and its metabolite O-desmethyl metoprolol were determined in water as well as carp gill, liver, kidney, brain and blood, along with the partial uptake pattern of these compounds. Results show that carp takes up MTP and its metabolite in the different organs evaluated, particularly liver and gill. The oxidative stress biomarkers, HPC, LPX, and PCC, as well as SOD and CAT activity all increased significantly at most exposure times in all organs evaluated. Results indicate that MTP and its metabolite induce oxidative stress on the teleost C. carpio and that the presence of these compounds may constitute a risk in water bodies for aquatic species. Copyright © 2018 Elsevier B.V. All rights reserved.

Efeito do dessecante paraquat na qualidade da fração lipídica da soja Effects of paraquat on the quality of lipidic fraction of soybean

Directory of Open Access Journals (Sweden)

José Carlos Gomes

2003-02-01

Full Text Available Para se determinar a qualidade da fração lipídica de grãos de soja submetidas à aplicação do dessecante bipiridílio (paraquat, foram estudados a composição química e os índices químicos de 3 (três amostras de óleo bruto e 1 (uma amostra de óleo refinado. Os óleos analisados no presente trabalho foram provenientes da região de Itumbiara - GO, extraídos de grãos de soja submetidos ou não à aplicação de paraquat. Utilizaram-se também amostras de óleo bruto extraídas por solvente, em laboratório, provenientes de grãos de soja sujeitos ou não à aplicação de dessecante. Nenhum resíduo do dessecante foi detectado, sensibilidade de 0,01 µg/g. O perfil de ácidos graxos, medido pelos teores dos ácidos palmítico, esteárico, oléico, linoléico e linolênico, encontrara-se dentro das faixas convencionais do óleo de soja de 9 a 4,5, 2,5 a 5,0, 18 a 34, 45 a 60 e 3,5 a 8,0%, respectivamente. No entanto, os índices de saponificação (de 161 a 171 ficaram abaixo dos valores estabelecidos pela legislação brasileira (189 a 198. Já os ácidos graxos livres, matéria insaponificável dos óleos brutos, e o índice de iodo do óleo refinado estão dentro desses padrões, máximos de 2,0%, 1,5% e 120 a 143, respectivamente. Os teores de ferro e de cadmio de 1,45 e 0,39 µg/g, respectivamente, de óleo refinado, atendem à legislação. Não se detectou chumbo, à sensibilidade de 0,01 µg/g. Esses metais foram analisados por espectrofotometria de absorção atômica.In order to determine the quality of lipidic fraction of soybean seeds from plants submitted to paraquat application, the composition and chemical indices of three crude extracts and one refined oil were studied. All samples were from Itumbiara-GO , Brazil. No residues of bipiridyls were detected, sensitivity less than 0.01µg/g. Fat acids profile, measured through palmitic, estearic, oleic, linoleic and linolenic acids were as espected for soybean oils

Neurobehavioral effects of concurrent exposure to cesium-137 and paraquat during neonatal development in mice

International Nuclear Information System (INIS)

Heredia, Luis; Bellés, Montserrat; Llovet, Maria Isabel; Domingo, Jose L.; Linares, Victoria

2015-01-01

As a result of nuclear power plants accidents such as Chernobyl or Fukushima, some people were exposed to external and internal ionizing radiation (IR). Human brain is highly sensitive to IR during fetal and postnatal period when the molecular processes are not completely finished. Various studies have shown that exposure to low doses of IR causes a higher incidence of cognitive impairment. On the other hand, in industrialized countries, people are daily exposed to a number of toxicant pollutants. Exposure to environmental chemicals, such as paraquat (PQ), may potentiate the toxic effects induced by radiation on brain development. In this study, we evaluated the cognitive effects of concomitant exposure to low doses of internal radiation ( 137 Cs) and PQ during neonatal brain development. At the postnatal day 10 (PND10), two groups of mice (C57BL/6J) were exposed to 137 Cs (4000 and 8000 Bq/kg) and/or PQ (7 mg/kg). To investigate the spontaneous behavior, learning, memory capacities and anxiety, behavioral tests were conducted in the offspring at two months of age. The results showed that cognitive functions were not significantly affected when 137 Cs or PQ were administered alone. However, alterations in the working memory and anxiety were detected in mice exposed to 137 Cs combined with PQ

Loss of Trx-2 enhances oxidative stress-dependent phenotypes in Drosophila.

Science.gov (United States)

Tsuda, Manabu; Ootaka, Ryousuke; Ohkura, Chiaki; Kishita, Yoshihito; Seong, Ki-Hyeon; Matsuo, Takashi; Aigaki, Toshiro

2010-08-04

Overexpression of thioredoxin (TRX) confers oxidative stress resistance and extends lifespan in mammals and insects. However, less is known about phenotypes associated with loss of TRX. We investigated loss-of-function phenotypes of Trx-2 in Drosophila, and found that the mutant flies are hyper-susceptible to paraquat, a free radical generator, but not to hydrogen peroxide. They contain a high amount of protein carbonyl, which dramatically increases with age. Trx-2 mutants express high levels of anti-oxidant genes, such as superoxide dismutase, catalase, and glutathione synthetase. This is the first demonstration of biochemical and physiological consequences caused by loss of Trx-2 in Drosophila. Copyright (c) 2010 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

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

Blue light-induced oxidative stress in live skin.

Science.gov (United States)

Nakashima, Yuya; Ohta, Shigeo; Wolf, Alexander M

2017-07-01

Skin damage from exposure to sunlight induces aging-like changes in appearance and is attributed to the ultraviolet (UV) component of light. Photosensitized production of reactive oxygen species (ROS) by UVA light is widely accepted to contribute to skin damage and carcinogenesis, but visible light is thought not to do so. Using mice expressing redox-sensitive GFP to detect ROS, blue light could produce oxidative stress in live skin. Blue light induced oxidative stress preferentially in mitochondria, but green, red, far red or infrared light did not. Blue light-induced oxidative stress was also detected in cultured human keratinocytes, but the per photon efficacy was only 25% of UVA in human keratinocyte mitochondria, compared to 68% of UVA in mouse skin. Skin autofluorescence was reduced by blue light, suggesting flavins are the photosensitizer. Exposing human skin to the blue light contained in sunlight depressed flavin autofluorescence, demonstrating that the visible component of sunlight has a physiologically significant effect on human skin. The ROS produced by blue light is probably superoxide, but not singlet oxygen. These results suggest that blue light contributes to skin aging similar to UVA. Copyright © 2017 Elsevier Inc. All rights reserved.

Mechanism for Prenatal LPS-Induced DA Neuron Loss

Science.gov (United States)

2006-09-01

Neurol 355:479–489. rooks AI, Chadwick CA, Gelbard HA, Cory-Slechta DA, Federoff HJ (1999) Paraquat elicited neurobehavioral syndrome caused by do...Stadler, J., Chandran, J., Klinefelter , G. R., Blackstone, C., and Cookson, M. R. (2003) J. Biol. Chem. 278, 36588–36595 4. Macedo, M. G., Anar, B...fluctuations Reserpine induced a parkinsonism-like syndrome in some PROGRESSION IN PD 241 Table 2. Comparison of Human PD Characteristics With Animal Models

Oxidative stress and Parkinson’s Disease

Directory of Open Access Journals (Sweden)

Javier eBlesa

2015-07-01

Full Text Available Parkinson disease is a chronic, progressive neurological disease that is associated with a loss of dopaminergic neurons in the substantia nigra of the brain. The molecular mechanisms underlying the loss of these neurons still remain elusive. Oxidative stress is thought to play an important role in dopaminergic neurotoxicity. Complex I deficiencies of the respiratory chain account for the majority of unfavorable neuronal degeneration in Parkinson’s Disease. Environmental factors, such as neurotoxins, insecticides like rotenone, pesticides like Paraquat, dopamine itself and genetic mutations in Parkinson’s Disease related proteins contribute to mitochondrial dysfunction which precedes reactive oxygen species formation. In this mini review, we give an update of the classical pathways involving these mechanisms of neurodegeneration, the biochemical and molecular events that mediate or regulate DA neuronal vulnerability, and the role of PD-related gene products in modulating cellular responses to oxidative stress in the course of the neurodegenerative process.

Heart tissue of harlequin (hq)/Big Blue mice has elevated reactive oxygen species without significant impact on the frequency and nature of point mutations in nuclear DNA

Energy Technology Data Exchange (ETDEWEB)

Crabbe, Rory A. [Department of Biology, University of Western Ontario, London, Ontario, N6A 5B7 (Canada); Hill, Kathleen A., E-mail: khill22@uwo.ca [Department of Biology, University of Western Ontario, London, Ontario, N6A 5B7 (Canada)

2010-09-10

Age is a major risk factor for heart disease, and cardiac aging is characterized by elevated mitochondrial reactive oxygen species (ROS) with compromised mitochondrial and nuclear DNA integrity. To assess links between increased ROS levels and mutations, we examined in situ levels of ROS and cII mutation frequency, pattern and spectrum in the heart of harlequin (hq)/Big Blue mice. The hq mouse is a model of premature aging with mitochondrial dysfunction and increased risk of oxidative stress-induced heart disease with the means for in vivo mutation detection. The hq mutation produces a significant downregulation in the X-linked apoptosis-inducing factor gene (Aif) impairing both the antioxidant and oxidative phosphorylation functions of AIF. Brain and skin of hq disease mice have elevated frequencies of point mutations in nuclear DNA and histopathology characterized by cell loss. Reports of associated elevations in ROS in brain and skin have mixed results. Herein, heart in situ ROS levels were elevated in hq disease compared to AIF-proficient mice (p < 0.0001) yet, mutation frequency and pattern were similar in hq disease, hq carrier and AIF-proficient mice. Heart cII mutations were also assessed 15 days following an acute exposure to an exogenous ROS inducer (10 mg paraquat/kg). Acute paraquat exposure with a short mutant manifestation period was insufficient to elevate mutation frequency or alter mutation pattern in the post-mitotic heart tissue of AIF-proficient mice. Paraquat induction of ROS requires mitochondrial complex I and thus is likely compromised in hq mice. Results of this preliminary survey and the context of recent literature suggest that determining causal links between AIF deficiency and the premature aging phenotypes of specific tissues is better addressed with assay of mitochondrial ROS and large-scale changes in mitochondrial DNA in specific cell types.

Heart tissue of harlequin (hq)/Big Blue mice has elevated reactive oxygen species without significant impact on the frequency and nature of point mutations in nuclear DNA

International Nuclear Information System (INIS)

Crabbe, Rory A.; Hill, Kathleen A.

2010-01-01

Age is a major risk factor for heart disease, and cardiac aging is characterized by elevated mitochondrial reactive oxygen species (ROS) with compromised mitochondrial and nuclear DNA integrity. To assess links between increased ROS levels and mutations, we examined in situ levels of ROS and cII mutation frequency, pattern and spectrum in the heart of harlequin (hq)/Big Blue mice. The hq mouse is a model of premature aging with mitochondrial dysfunction and increased risk of oxidative stress-induced heart disease with the means for in vivo mutation detection. The hq mutation produces a significant downregulation in the X-linked apoptosis-inducing factor gene (Aif) impairing both the antioxidant and oxidative phosphorylation functions of AIF. Brain and skin of hq disease mice have elevated frequencies of point mutations in nuclear DNA and histopathology characterized by cell loss. Reports of associated elevations in ROS in brain and skin have mixed results. Herein, heart in situ ROS levels were elevated in hq disease compared to AIF-proficient mice (p < 0.0001) yet, mutation frequency and pattern were similar in hq disease, hq carrier and AIF-proficient mice. Heart cII mutations were also assessed 15 days following an acute exposure to an exogenous ROS inducer (10 mg paraquat/kg). Acute paraquat exposure with a short mutant manifestation period was insufficient to elevate mutation frequency or alter mutation pattern in the post-mitotic heart tissue of AIF-proficient mice. Paraquat induction of ROS requires mitochondrial complex I and thus is likely compromised in hq mice. Results of this preliminary survey and the context of recent literature suggest that determining causal links between AIF deficiency and the premature aging phenotypes of specific tissues is better addressed with assay of mitochondrial ROS and large-scale changes in mitochondrial DNA in specific cell types.

Early Stage Blood Purification for Paraquat Poisoning: A Multicenter Retrospective Study.

Science.gov (United States)

Li, An; Li, Wenxiong; Hao, Fengtong; Wang, Haishi

2016-01-01

To evaluate the efficacy of conservative treatment vs. hemoperfusion (HP) vs. HP + continuous veno-venous hemofiltration (CVVH) for acute Paraquat (PQ) poisoning. This was a multicenter retrospective study of patients with PQ poisoning between January 2013 and June 2014. Clinical data and PQ serum levels were collected at baseline and after 24, 48, and 72 h of treatment. Seventy-five, 65, and 43 underwent conservative treatment only (conservative treatment group), conservative treatment + HP (HP group), and conservative treatment + HP + CVVH (HP + CVVH group), respectively. PQ serum levels decreased in all groups after 72 h of treatment (p treatment group. More importantly, PQ blood levels were significantly lower in the HP + CVVH group compared with the HP group at 24 h (p treatment group (p poisoning could decrease PQ blood levels, alleviate organ damage, and increase survival. © 2016 S. Karger AG, Basel.

Comparison of radiation-induced and thermal oxidative aging of polyethylene in the presence of inhibitors

International Nuclear Information System (INIS)

Dalinkevich, A.A.; Piskarev, I.M.

1996-01-01

Thermal oxidative and radiation-induced oxidative aging of inhibited polyethylene of commercial brands with known properties was studied at 60, 80 and 140 deg C. Radiation-induced oxidative aging was carried out under X-ray radiation with E max = 25 keV at dose rates providing specimen oxidation in kinetic conditions. The value of activation energy of thermal oxidative destruction of inhibited polyethylene under natural conditions of its employment at 60-140 deg C (E a = 60 kJ/mol) was obtained by comparison of data for radiation-induced and thermal oxidative destruction

Differential effects of experimental and cold-induced hyperthyroidism on factors inducing rat liver oxidative damage

OpenAIRE

Venditti, Paola; Pamplona Gras, Reinald; Ayala, Victoria; Rosa, R. de; Caldarone, G.; Di Meo, S.

2006-01-01

Thyroid hormone-induced increase in metabolic rates is often associated with increased oxidative stress. The aim of the present study was to investigate the contribution of iodothyronines to liver oxidative stress in the functional hyperthyroidism elicited by cold, using as models cold-exposed and 3,5,3'-triiodothyronine (T-3)- or thyroxine (T-4)-treated rats. The hyperthyroid state was always associated with increases in both oxidative capacity and oxidative damage of the tissue. The most ex...

Effect of atorvastatin on hyperglycemia-induced brain oxidative stress and neuropathy induced by diabetes

Directory of Open Access Journals (Sweden)

Nastaran Faghihi

2015-04-01

Conclusion: The findings of the present study reveal that atorvastatin is able to prevent hyperglycemia-induced diabetic neuropathy and inhibit brain oxidative stress during diabetes. It is probable that reduction of urea is one of the reasons for atorvastatin prevention of hyperglycemia-induced neuropathy.

Romo1 expression contributes to oxidative stress-induced death of lung epithelial cells

International Nuclear Information System (INIS)

Shin, Jung Ar; Chung, Jin Sil; Cho, Sang-Ho; Kim, Hyung Jung; Yoo, Young Do

2013-01-01

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 2 O 2 ) treatment increased Romo1 expression, and Romo1 knockdown suppressed the cellular ROS levels and cell death triggered by H 2 O 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

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.

The NADPH oxidase inhibitor apocynin (acetovanillone) induces oxidative stress

International Nuclear Information System (INIS)

Riganti, Chiara; Costamagna, Costanzo; Bosia, Amalia; Ghigo, Dario

2006-01-01

Apocynin (acetovanillone) is often used as a specific inhibitor of NADPH oxidase. In N11 glial cells, apocynin induced, in a dose-dependent way, a significant increase of both malonyldialdehyde level (index of lipid peroxidation) and lactate dehydrogenase release (index of a cytotoxic effect). Apocynin evoked also, in a significant way, an increase of H 2 O 2 concentration and a decrease of the intracellular glutathione/glutathione disulfide ratio, accompanied by augmented efflux of glutathione and glutathione disulfide. Apocynin induced the activation of both pentose phosphate pathway and tricarboxylic acid cycle, which was blocked when the cells were incubated with glutathione together with apocynin. The cell incubation with glutathione prevented also the apocynin-induced increase of malonyldialdehyde generation and lactate dehydrogenase leakage. Apocynin exerted an oxidant effect also in a cell-free system: indeed, in aqueous solution, it evoked a faster oxidation of the thiols glutathione and dithiothreitol, and elicited the generation of reactive oxygen species, mainly superoxide anions. Our results suggest that apocynin per se can induce an oxidative stress and exert a cytotoxic effect in N11 cells and other cell types, and that some effects of apocynin in in vitro and in vivo experimental models should be interpreted with caution

Efeito de doses reduzidas de glyphosate e paraquat simulando deriva na cultura do milho Effect of reduced rates of glyphosate and paraquat simulating drift in corn crop

Directory of Open Access Journals (Sweden)

P.C. Magalhães

2001-08-01

Full Text Available A aplicação de herbicidas, seja para a dissecação de culturas ou para o controle de plantas daninhas, vem crescendo, devido a expansão da fronteira agrícola brasileira. Esse fato aumenta os riscos de ocorrência de deriva acidental em culturas vizinhas suscetíveis. As perdas em produtividade são desconhecidas em muitas situações de ocorrência de deriva de herbicidas. O objetivo deste trabalho foi avaliar a possível toxicidade causada pela deriva de doses reduzidas de dois herbicidas (glyphosate e paraquat no período inicial de desenvolvimento da cultura do milho. Foram utilizadas cinco doses simulando deriva - 2, 4, 6, 8 e 12% da dose recomendada (1.440 g ha-1 de glyphosate e 400 g ha-1 de paraquat - sobre o cultivar de milho híbrido triplo BRS 3123. No florescimento, foram avaliados altura da planta, área foliar, peso da matéria seca, teor de clorofila e sintomas visuais de injúria. Na colheita, avaliaram-se estande final, peso de espigas, peso de 1.000 grãos e produção de grãos. A altura das plantas, a área foliar e o peso da matéria seca não foram afetados pelo efeito das derivas nos dois anos agrícolas (1996/97 e 1997/98, exceto pela área foliar, que em 1997/98 sofreu redução, sobretudo no tratamento com 12% da dose normal de glyphosate. De maneira geral, os resultados obtidos para as demais características foram semelhantes nos dois anos de condução do ensaio. O teor de clorofila nas folhas e o estande final não foram afetados pelas doses reduzidas. O grau de toxicidade, avaliado por meio de plantas injuriadas pela deriva, aos 7, 14 e 21 dias após a aplicação dos herbicidas, apresentou diferenças significativas. Os maiores danos foram observados com a maior subdose simulando deriva dos herbicidas. O peso de 1.000 grãos não foi afetado, ao passo que a produção de espigas e de grãos foi severamente prejudicada. Observou-se que a deriva simulada dos herbicidas em altas concentrações afetou o

Curcumin-Protected PC12 Cells Against Glutamate-Induced Oxidative Toxicity

Directory of Open Access Journals (Sweden)

Chi-Huang Chang

2014-01-01

Full Text Available Glutamate is a major excitatory neurotransmitter present in the central nervous system. The glutamate/cystine antiporter system xc– connects the antioxidant defense with neurotransmission and behaviour. Overactivation of ionotropic glutamate receptors induces neuronal death, a pathway called excitotoxicity. Glutamate-induced oxidative stress is a major contributor to neurodegenerative diseases including cerebral ischemia, Alzheimer’s and Huntington’s disease. Curcuma has a wide spectrum of biological activities regarding neuroprotection and neurocognition. By reducing the oxidative damage, curcumin attenuates a spinal cord ischemia-reperfusion injury, seizures and hippocampal neuronal loss. The rat pheochromocytoma (PC12 cell line exhibits many characteristics useful for the study of the neuroprotection and neurocognition. This investigation was carried out to determine whether the neuroprotective effects of curcumin can be observed via the glutamate-PC12 cell model. Results indicate that glutamate (20 mM upregulated glutathione peroxidase 1, glutathione disulphide, Ca2+ influx, nitric oxide production, cytochrome c release, Bax/Bcl-2 ratio, caspase-3 activity, lactate dehydrogenase release, reactive oxygen species, H2O2, and malondialdehyde; and downregulated glutathione, glutathione reductase, superoxide dismutase and catalase, resulting in enhanced cell apoptosis. Curcumin alleviates all these adverse effects. Conclusively, curcumin can effectively protect PC12 cells against the glutamate-induced oxidative toxicity. Its mode of action involves two pathways: the glutathione-dependent nitric oxide-reactive oxygen species pathway and the mitochondria-dependent nitric oxide-reactive oxygen species pathway.

Effect of vitamin C on N,N′-dimethyl-4,4′-bipyridinium dichloride ...

African Journals Online (AJOL)

Purpose: To evaluate the effectiveness of vitamin C on paraquat-induced hepatic and renal toxicity in Swiss albino mice. Methods: Three groups of Swiss albino mice (n = 10), i.e., control, paraquat (15 mg/kg) and paraquat (15 mg/kg) + vitamin C (20 mg/kg) were used in the study. The drugs were administered ...

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.

A high constitutive catalase activity confers resistance to methyl viologen-promoted oxidative stress in a mutant of the cyanobacterium Nostoc punctiforme ATCC 29133.

Science.gov (United States)

Moirangthem, Lakshmipyari Devi; Bhattacharya, Sudeshna; Stensjö, Karin; Lindblad, Peter; Bhattacharya, Jyotirmoy

2014-04-01

A spontaneous methyl viologen (MV)-resistant mutant of the nitrogen-fixing cyanobacterium Nostoc punctiforme ATCC 29133 was isolated and the major enzymatic antioxidants involved in combating MV-induced oxidative stress were evaluated. The mutant displayed a high constitutive catalase activity as a consequence of which, the intracellular level of reactive oxygen species in the mutant was lower than the wild type (N. punctiforme) in the presence of MV. The superoxide dismutase (SOD) activity that consisted of a SodA (manganese-SOD) and a SodB (iron-SOD) was not suppressed in the mutant following MV treatment. The mutant was, however, characterised by a lower peroxidase activity compared with its wild type, and its improved tolerance to externally added H₂O₂ could only be attributed to enhanced catalase activity. Furthermore, MV-induced toxic effects on the wild type such as (1) loss of photosynthetic performance assessed as maximal quantum yield of photosystem II, (2) nitrogenase inactivation, and (3) filament fragmentation and cell lysis were not observed in the mutant. These findings highlight the importance of catalase in preventing MV-promoted oxidative damage and cell death in the cyanobacterium N. punctiforme. Such oxidative stress resistant mutants of cyanobacteria are likely to be a better source of biofertilisers, as they can grow and fix nitrogen in an unhindered manner in agricultural fields that are often contaminated with the herbicide MV, also commonly known as paraquat.

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.

Role of inducible nitric oxide synthase-derived nitric oxide in lipopolysaccharide plus interferon-γ-induced pulmonary inflammation

International Nuclear Information System (INIS)

Zeidler, Patti C.; Millecchia, Lyndell M.; Castranova, Vincent

2004-01-01

Exposure of mice to lipopolysaccharide (LPS) plus interferon-γ (IFN-γ) increases nitric oxide (NO) production, which is proposed to play a role in the resulting pulmonary damage and inflammation. To determine the role of inducible nitric oxide synthase (iNOS)-induced NO in this lung reaction, the responses of inducible nitric oxide synthase knockout (iNOS KO) versus C57BL/6J wild-type (WT) mice to aspirated LPS + IFN-γ were compared. Male mice (8-10 weeks) were exposed to LPS (1.2 mg/kg) + IFN-γ (5000 U/mouse) or saline. At 24 or 72 h postexposure, lungs were lavaged with saline and the acellular fluid from the first bronchoalveolar lavage (BAL) was analyzed for total antioxidant capacity (TAC), lactate dehydrogenase (LDH) activity, albumin, tumor necrosis factor-α (TNF-α), and macrophage inflammatory protein-2 (MIP-2). The cellular fraction of the total BAL was used to determine alveolar macrophage (AM) and polymorphonuclear leukocyte (PMN) counts, and AM zymosan-stimulated chemiluminescence (AM-CL). Pulmonary responses 24 h postexposure to LPS + IFN-γ were characterized by significantly decreased TAC, increased BAL AMs and PMNs, LDH, albumin, TNF-α, and MIP-2, and enhanced AM-CL to the same extent in both WT and iNOS KO mice. Responses 72 h postexposure were similar; however, significant differences were found between WT and iNOS KO mice. iNOS KO mice demonstrated a greater decline in total antioxidant capacity, greater BAL PMNs, LDH, albumin, TNF-α, and MIP-2, and an enhanced AM-CL compared to the WT. These data suggest that the role of iNOS-derived NO in the pulmonary response to LPS + IFN-γ is anti-inflammatory, and this becomes evident over time

Passive smoking reduces and vitamin C increases exercise-induced oxidative stress: does this make passive smoking an anti-oxidant and vitamin C a pro-oxidant stimulus?

Science.gov (United States)

Theodorou, Anastasios A; Paschalis, Vassilis; Kyparos, Antonios; Panayiotou, George; Nikolaidis, Michalis G

2014-11-07

The current interpretative framework states that, for a certain experimental treatment (usually a chemical substance) to be classified as "anti-oxidant", it must possess the property of reducing (or even nullifying) exercise-induced oxidative stress. The aim of the study was to compare side by side, in the same experimental setup, redox biomarkers responses to an identical acute eccentric exercise session, before and after chronic passive smoking (considered a pro-oxidant stimulus) or vitamin C supplementation (considered an anti-oxidant stimulus). Twenty men were randomly assigned into either passive smoking or vitamin C group. All participants performed two acute eccentric exercise sessions, one before and one after either exposure to passive smoking or vitamin C supplementation for 12 days. Vitamin C, oxidant biomarkers (F2-isoprostanes and protein carbonyls) and the non-enzymatic antioxidant (glutathione) were measured, before and after passive smoking, vitamin C supplementation or exercise. It was found that chronic exposure to passive smoking increased the level of F2-isoprostanes and decreased the level of glutathione at rest, resulting in minimal increase or absence of oxidative stress after exercise. Conversely, chronic supplementation with vitamin C decreased the level of F2-isoprostanes and increased the level of glutathione at rest, resulting in marked exercise-induced oxidative stress. Contrary to the current scientific consensus, our results show that, when a pro-oxidant stimulus is chronically delivered, it is more likely that oxidative stress induced by subsequent exercise is decreased and not increased. Reversely, it is more likely to find greater exercise-induced oxidative stress after previous exposure to an anti-oxidant stimulus. We believe that the proposed framework will be a useful tool to reach more pragmatic explanations of redox biology phenomena. Copyright © 2014 Elsevier Inc. All rights reserved.

Melatonin protects against taurolithocholic-induced oxidative stress in rat liver.

Science.gov (United States)

Fuentes-Broto, Lorena; Miana-Mena, Francisco J; Piedrafita, Eduardo; Berzosa, César; Martínez-Ballarín, Enrique; García-Gil, Francisco A; Reiter, Russel J; García, Joaquín J

2010-08-01

Cholestasis, encountered in a variety of clinical disorders, is characterized by intracellular accumulation of toxic bile acids in the liver. Furthermore, oxidative stress plays an important role in the pathogenesis of bile acids. Taurolithocholic acid (TLC) was revealed in previous studies as the most pro-oxidative bile acid. Melatonin, a well-known antioxidant, is a safe and widely used therapeutic agent. Herein, we investigated the hepatoprotective role of melatonin on lipid and protein oxidation induced by TLC alone and in combination with FeCl(3) and ascorbic acid in rat liver homogenates and hepatic membranes. The lipid peroxidation products, malondialdehyde and 4-hydroxyalkenals (MDA + 4-HDA), and carbonyl levels were quantified as indices of oxidative damage to hepatic lipids and proteins, respectively. In the current study, the rise in MDA + 4-HDA levels induced by TLC was inhibited by melatonin in a concentration-dependent manner in both liver homogenates and in hepatic membranes. Melatonin also had protective effects against structural damage to proteins induced by TLC in membranes. These results suggest that the indoleamine melatonin may potentially act as a protective agent in the therapy of those diseases that involve bile acid toxicity. Published 2010 Wiley-Liss, Inc.

Isolation and characterization of a metallothionein-1 protein in Chloris virgata Swartz that enhances stress tolerances to oxidative, salinity and carbonate stress in Saccharomyces cerevisiae.

Science.gov (United States)

Nishiuchi, Shunsaku; Liu, Shenkui; Takano, Tetsuo

2007-08-01

Chloris virgata Swartz (C. virgata) is a gramineous wild plant that is found in alkaline soil areas in northeast China and is highly tolerant to carbonate stress. We constructed a cDNA library from C. virgata seedlings treated with NaHCO(3), and isolated a type 1 metallothionein (MT1) gene (ChlMT1: AB294238) from the library. The amino acid sequence of ChlMT1 contained 12 cysteine residues that constituted the Cys-X-Cys (X = amino acid except Cys) motifs in the N- and C-terminal regions. Northern hybridization showed that expression of ChlMT1 was induced by several abiotic stresses, from salts (NaCl and NaHCO(3)), a ROS inducer (paraquat), and metals (CuSO(4), ZnSO(4), and CoCl(2)). ChlMT1 expression in leaf was induced by 200 mM NaCl and 100 mM NaHCO(3). About 5 microM Paraquat, 500 microM Zn(2+), and 500 microM Co(2+) also induced expression of ChlMT1 in leaf after 6 h, and 100 microM Cu(2+) induced it after 24 h. Saccharomyces cerevisiae when transformed with the ChlMT1 gene had dramatically increased tolerances to salts (NaCl and NaHCO(3)) and ROS.

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

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

Cellular inactivation of nitric oxide induces p53-dependent ...

African Journals Online (AJOL)

Tropical Journal of Pharmaceutical Research August 2016; 15 (8): 1595-1603 ... Cellular inactivation of nitric oxide induces p53-dependent apoptosis in ... apoptosis induced by a selective iNOS inhibitor, N-[(3-aminomethyl) benzyl] acetamidine (1400W), .... and nitrate. ... Nitrite production was measured in culture media.

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.

A review: oxidative stress in fish induced by pesticides.

Science.gov (United States)

Slaninova, Andrea; Smutna, Miriam; Modra, Helena; Svobodova, Zdenka

2009-01-01

The knowledge in oxidative stress in fish has a great importance for environmental and aquatic toxicology. Because oxidative stress is evoked by many chemicals including some pesticides, pro-oxidant factors' action in fish organism can be used to assess specific area pollution or world sea pollution. Hepatotoxic effect of DDT may be related with lipid peroxidation. Releasing of reactive oxygen species (ROS) after HCB exposure can be realized via two ways: via the uncoupling of the electron transport chain from monooxygenase activity and via metabolism of HCB major metabolite pentachlorophenol. Chlorothalonil disrupts mitochondrial metabolism due to the impairment of NADPH oxidase function. Activation of spleen macrophages and a decrease of catalase (CAT) activity have been observed after endosulfan exposure. Excessive release of superoxide radicals after etoxazole exposure can cause a decrease of CAT activity and increase phagocytic activity of splenocytes. Anticholinergic activity of organophosphates leads to the accumulation of ROS and resulting lipid peroxidation. Carbaryl induces changes in the content of glutathione and antioxidant enzymes activities. The antioxidant enzymes changes have been observed after actuation of pesticides deltamethrin and cypermethrin. Bipyridyl herbicides are able to form redox cycles and thereby cause oxidative stress. Low concentrations of simazine do not cause oxidative stress in carps during sub-chronic tests while sublethal concentrations of atrazin can induce oxidative stress in bluegill sunfish. Butachlor causes increased activity of superoxide dismutase -catalase system in the kidney. Rotenon can inhibit the electron transport in mitochondria and thereby increase ROS production. Dichloroaniline, the metabolite of diuron, has oxidative effects. Oxidative damage from fenpyroximate actuation is related to the disruption of mitochondrial redox respiratory chain. Low concentration of glyphosate can cause mild oxidative stress.

Recombinational micro-evolution of functionally different metallothionein promoter alleles from Orchesella cincta

Directory of Open Access Journals (Sweden)

van Straalen Nico M

2007-06-01

Full Text Available Abstract Background Metallothionein (mt transcription is elevated in heavy metal tolerant field populations of Orchesella cincta (Collembola. This suggests that natural selection acts on transcriptional regulation of mt in springtails at sites where cadmium (Cd levels in soil reach toxic values This study investigates the nature and the evolutionary origin of polymorphisms in the metallothionein promoter (pmt and their functional significance for mt expression. Results We sequenced approximately 1600 bp upstream the mt coding region by genome walking. Nine pmt alleles were discovered in NW-European populations. They differ in the number of some indels, consensus transcription factor binding sites and core promoter elements. Extensive recombination events between some of the alleles can be inferred from the alignment. A deviation from neutral expectations was detected in a cadmium tolerant population, pointing towards balancing selection on some promoter stretches. Luciferase constructs were made from the most abundant alleles, and responses to Cd, paraquat (oxidative stress inducer and moulting hormone were studied in cell lines. By using paraquat we were able to dissect the effect of oxidative stress from the Cd specific effect, and extensive differences in mt induction levels between these two stressors were observed. Conclusion The pmt alleles evolved by a number of recombination events, and exhibited differential inducibilities by Cd, paraquat and molting hormone. In a tolerant population from a metal contaminated site, promoter allele frequencies differed significantly from a reference site and nucleotide polymorphisms in some promoter stretches deviated from neutral expectations, revealing a signature of balancing selection. Our results suggest that the structural differences in the Orchesella cincta metallothionein promoter alleles contribute to the metallothionein -over-expresser phenotype in cadmium tolerant populations.

Radiation-induced synthesis of gold, iron-oxide composite nanoparticles

International Nuclear Information System (INIS)

Seino, Satoshi; Yamamoto, Takao; Nakagawa, Takashi; Kinoshita, Takuya; Kojima, Takao; Taniguchi, Ryoichi; Okuda, Shuichi

2007-01-01

Composite nanoparticles consisting of magnetic iron oxide nanoparticles and gold nanoparticles were synthesized using gamma-rays or electron beam. Ionizing irradiation induces the generation of reducing species inside the aqueous solution, and gold ions are reduced to form metallic Au nanoparticles. The size of Au nanoparticles depended on the dose rate and the concentration of support iron oxide. The gold nanoparticles on iron oxide nanoparticles selectively adsorb biomolecules via Au-S bonding. By using magnetic property of the support iron oxide nanoparticles, the composite nanoparticles are expected as a new type of magnetic nanocarrier for biomedical applications. (author)

Characterization of vanadate-dependent NADH oxidation activity and isolation of yeast DNA which complements a class 1 vanadate resistance mutation

International Nuclear Information System (INIS)

Minasi, L.E.

1989-01-01

A vanadate-dependent NADH oxidation activity has been characterized in plasma membranes from the yeast S cerevisiae. NADH oxidation activity was maximally stimulated at pH 5.0 in phosphate buffer. NADH oxidation was not dependent on the concentration of plasma membranes. The vanadate-dependent NADH oxidation activity was abolished under anaerobic conditions and the concomitant uptake of oxygen occurred during NADH oxidation. The activity was inhibited by superoxide dismutase and stimulated by the presence of paraquat. These results indicate that the vanadate stimulation of NADH oxidation in yeast plasma membranes occurs as a result of the vanadate-dependent oxidation of NADH by superoxide, generated by a plasma membrane NADH oxidase. 51 V-NMR results indicated that a phosphate-vanadate anhydride was the stimulatory species in pH 5.0 and pH 7.0 phosphate buffer. Yeast DNA has been isolated which complements a class 1 vanadate resistance mutation

Thiamine deficiency induces endoplasmic reticulum stress and oxidative stress in human neurons derived from induced pluripotent stem cells

Energy Technology Data Exchange (ETDEWEB)

Wang, Xin; Xu, Mei; Frank, Jacqueline A. [Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536 (United States); Ke, Zun-ji [Department of Biochemistry, Shanghai University of Traditional Chinese Medicine, Shanghai, China 201203 (China); Luo, Jia, E-mail: jialuo888@uky.edu [Department of Pharmacology and Nutritional Sciences, University of Kentucky College of Medicine, Lexington, KY 40536 (United States); Department of Biochemistry, Shanghai University of Traditional Chinese Medicine, Shanghai, China 201203 (China)

2017-04-01

Thiamine (vitamin B1) deficiency (TD) plays a major role in the etiology of Wernicke's encephalopathy (WE) which is a severe neurological disorder. TD induces selective neuronal cell death, neuroinflammation, endoplasmic reticulum (ER) stress and oxidative stress in the brain which are commonly observed in many aging-related neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and progressive supranuclear palsy (PSP). However, the underlying cellular and molecular mechanisms remain unclear. The progress in this line of research is hindered due to the lack of appropriate in vitro models. The neurons derived for the human induced pluripotent stem cells (hiPSCs) provide a relevant and powerful tool for the research in pharmaceutical and environmental neurotoxicity. In this study, we for the first time used human induced pluripotent stem cells (hiPSCs)-derived neurons (iCell neurons) to investigate the mechanisms of TD-induced neurodegeneration. We showed that TD caused a concentration- and duration-dependent death of iCell neurons. TD induced ER stress which was evident by the increase in ER stress markers, such as GRP78, XBP-1, CHOP, ATF-6, phosphorylated eIF2α, and cleaved caspase-12. TD also triggered oxidative stress which was shown by the increase in the expression 2,4-dinitrophenyl (DNP) and 4-hydroxynonenal (HNE). ER stress inhibitors (STF-083010 and salubrinal) and antioxidant N-acetyl cysteine (NAC) were effective in alleviating TD-induced death of iCell neurons, supporting the involvement of ER stress and oxidative stress. It establishes that the iCell neurons are a novel tool to investigate cellular and molecular mechanisms for TD-induced neurodegeneration. - Highlights: • Thiamine deficiency (TD) causes death of human neurons in culture. • TD induces both endoplasmic reticulum (ER) stress and oxidative stress. • Alleviating ER stress and oxidative stress reduces TD-induced

Thiamine deficiency induces endoplasmic reticulum stress and oxidative stress in human neurons derived from induced pluripotent stem cells

International Nuclear Information System (INIS)

Wang, Xin; Xu, Mei; Frank, Jacqueline A.; Ke, Zun-ji; Luo, Jia

2017-01-01

Thiamine (vitamin B1) deficiency (TD) plays a major role in the etiology of Wernicke's encephalopathy (WE) which is a severe neurological disorder. TD induces selective neuronal cell death, neuroinflammation, endoplasmic reticulum (ER) stress and oxidative stress in the brain which are commonly observed in many aging-related neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and progressive supranuclear palsy (PSP). However, the underlying cellular and molecular mechanisms remain unclear. The progress in this line of research is hindered due to the lack of appropriate in vitro models. The neurons derived for the human induced pluripotent stem cells (hiPSCs) provide a relevant and powerful tool for the research in pharmaceutical and environmental neurotoxicity. In this study, we for the first time used human induced pluripotent stem cells (hiPSCs)-derived neurons (iCell neurons) to investigate the mechanisms of TD-induced neurodegeneration. We showed that TD caused a concentration- and duration-dependent death of iCell neurons. TD induced ER stress which was evident by the increase in ER stress markers, such as GRP78, XBP-1, CHOP, ATF-6, phosphorylated eIF2α, and cleaved caspase-12. TD also triggered oxidative stress which was shown by the increase in the expression 2,4-dinitrophenyl (DNP) and 4-hydroxynonenal (HNE). ER stress inhibitors (STF-083010 and salubrinal) and antioxidant N-acetyl cysteine (NAC) were effective in alleviating TD-induced death of iCell neurons, supporting the involvement of ER stress and oxidative stress. It establishes that the iCell neurons are a novel tool to investigate cellular and molecular mechanisms for TD-induced neurodegeneration. - Highlights: • Thiamine deficiency (TD) causes death of human neurons in culture. • TD induces both endoplasmic reticulum (ER) stress and oxidative stress. • Alleviating ER stress and oxidative stress reduces TD-induced

Radiation-induced cationic polymerization of limonene oxide, α-pinene oxide, and β-pinene oxide

International Nuclear Information System (INIS)

Aikins, J.A.; Williams, F.

1984-01-01

After suitable drying, the subject monomers in the form of neat liquids undergo radiation-induced polymerization with no apparent side reactions and high conversions to precipitatable polymers of low molecular weight. A cationic mechanism is evidenced by the strongly retarding effect of tri-n-propylamine on the polymerization rate. At 25 0 C, limonene oxide gives the highest polymerization rates, an average conversion of 36% per Mrad being obtained in comparison with values of 5.7 and 7.3% per Mrad for the α-pinene and β-pinene oxides, respectively. Similarly, the average anti DP/sub n/ decreases from 11.8 for the limonene oxide polymer to 5.6 and 4.0 for the α-pinene oxide and β-pinene oxide polymers, respectively. A high frequency of chain transfer to monomer is indicated in each case by the fact that the kinetic chain lengths are estimated to be on the order of a hundred times larger than the anti DP/sub n/ values. Structural characterization of the limonene oxide polymer by 1 H and 13 C NMR spectroscopy provides conclusive evidence that the polymerization proceeds by the opening of the epoxide ring to yield a 1,2-trans polyether. Similar NMR studies on the polymers formed from the α-pinene and β-pinene oxides show that in the polymerization of these monomers, the opening of the epoxide ring is generally accompanied by the concomitant ring opening of the cyclobutane ring structure to yield a gem-dimethyl group in the main chain. The detection of isopropenyl end groups in the pinene oxide polymers is also consistent with this mode of propagation being followed by chain (proton) transfer to monomer

Nitric oxide-induced calcium release: activation of type 1 ryanodine receptor by endogenous nitric oxide.

Science.gov (United States)

Kakizawa, Sho; Yamazawa, Toshiko; Iino, Masamitsu

2013-01-01

Ryanodine receptors (RyRs), located in the sarcoplasmic/endoplasmic reticulum (SR/ER) membrane, are required for intracellular Ca2+ release that is involved in a wide range of cellular functions. In addition to Ca2+-induced Ca2+ release in cardiac cells and voltage-induced Ca2+ release in skeletal muscle cells, we recently identified another mode of intracellular Ca2+ mobilization mediated by RyR, i.e., nitric oxide-induced Ca2+ release (NICR), in cerebellar Purkinje cells. NICR is evoked by neuronal activity, is dependent on S-nitrosylation of type 1 RyR (RyR1) and is involved in the induction of long-term potentiation (LTP) of cerebellar synapses. In this addendum, we examined whether peroxynitrite, which is produced by the reaction of nitric oxide with superoxide, may also have an effect on the Ca2+ release via RyR1 and the cerebellar LTP. We found that scavengers of peroxynitrite have no significant effect either on the Ca2+ release via RyR1 or on the cerebellar LTP. We also found that an application of a high concentration of peroxynitrite does not reproduce neuronal activity-dependent Ca2+ release in Purkinje cells. These results support that NICR is induced by endogenous nitric oxide produced by neuronal activity through S-nitrosylation of RyR1.

Neurobehavioral effects of concurrent exposure to cesium-137 and paraquat during neonatal development in mice.

Science.gov (United States)

Heredia, Luis; Bellés, Montserrat; Llovet, Maria Isabel; Domingo, Jose L; Linares, Victoria

2015-03-02

As a result of nuclear power plants accidents such as Chernobyl or Fukushima, some people were exposed to external and internal ionizing radiation (IR). Human brain is highly sensitive to IR during fetal and postnatal period when the molecular processes are not completely finished. Various studies have shown that exposure to low doses of IR causes a higher incidence of cognitive impairment. On the other hand, in industrialized countries, people are daily exposed to a number of toxicant pollutants. Exposure to environmental chemicals, such as paraquat (PQ), may potentiate the toxic effects induced by radiation on brain development. In this study, we evaluated the cognitive effects of concomitant exposure to low doses of internal radiation ((137)Cs) and PQ during neonatal brain development. At the postnatal day 10 (PND10), two groups of mice (C57BL/6J) were exposed to (137)Cs (4000 and 8000 Bq/kg) and/or PQ (7 mg/kg). To investigate the spontaneous behavior, learning, memory capacities and anxiety, behavioral tests were conducted in the offspring at two months of age. The results showed that cognitive functions were not significantly affected when (137)Cs or PQ were administered alone. However, alterations in the working memory and anxiety were detected in mice exposed to (137)Cs combined with PQ. Copyright © 2015. Published by Elsevier Ireland Ltd.

Petroselinum Crispum is Effective in Reducing Stress-Induced Gastric Oxidative Damage

OpenAIRE

Ayşin Akıncı; Mukaddes Eşrefoğlu; Elif Taşlıdere; Burhan Ateş

2017-01-01

Background: Oxidative stress has been shown to play a principal role in the pathogenesis of stress-induced gastric injury. Parsley (Petroselinum crispum) contains many antioxidants such as flavanoids, carotenoids and ascorbic acid. Aims: In this study, the histopathological and biochemical results of nutrition with a parsley-rich diet in terms of eliminating stress-induced oxidative gastric injury were evaluated. Study Design: Animal experimentation. Methods: Forty male Wistar albino...

Petroselinum Crispum is Effective in Reducing Stress-Induced Gastric Oxidative Damage

OpenAIRE

Ak?nc?, Ay?in; E?refo?lu, Mukaddes; Ta?l?dere, Elif; Ate?, Burhan

2017-01-01

Background: Oxidative stress has been shown to play a principal role in the pathogenesis of stress-induced gastric injury. Parsley (Petroselinum crispum) contains many antioxidants such as flavanoids, carotenoids and ascorbic acid. Aims: In this study, the histopathological and biochemical results of nutrition with a parsley-rich diet in terms of eliminating stress-induced oxidative gastric injury were evaluated. Study Design: Animal experimentation Methods: Forty male Wistar albino rats were...

Diacylglycerol kinase regulation of protein kinase D during oxidative stress-induced intestinal cell injury

International Nuclear Information System (INIS)

Song Jun; Li Jing; Mourot, Joshua M.; Mark Evers, B.; Chung, Dai H.

2008-01-01

We recently demonstrated that protein kinase D (PKD) exerts a protective function during oxidative stress-induced intestinal epithelial cell injury; however, the exact role of DAG kinase (DGK)ζ, an isoform expressed in intestine, during this process is unknown. We sought to determine the role of DGK during oxidative stress-induced intestinal cell injury and whether DGK acts as an upstream regulator of PKD. Inhibition of DGK with R59022 compound or DGKζ siRNA transfection decreased H 2 O 2 -induced RIE-1 cell apoptosis as measured by DNA fragmentation and increased PKD phosphorylation. Overexpression of kinase-dead DGKζ also significantly increased PKD phosphorylation. Additionally, endogenous nuclear DGKζ rapidly translocated to the cytoplasm following H 2 O 2 treatment. Our findings demonstrate that DGK is involved in the regulation of oxidative stress-induced intestinal cell injury. PKD activation is induced by DGKζ, suggesting DGK is an upstream regulator of oxidative stress-induced activation of the PKD signaling pathway in intestinal epithelial cells

Smog induces oxidative stress and microbiota disruption.

Science.gov (United States)

Wong, Tit-Yee

2017-04-01

Smog is created through the interactions between pollutants in the air, fog, and sunlight. Air pollutants, such as carbon monoxide, heavy metals, nitrogen oxides, ozone, sulfur dioxide, volatile organic vapors, and particulate matters, can induce oxidative stress in human directly or indirectly through the formation of reactive oxygen species. The outermost boundary of human skin and mucous layers are covered by a complex network of human-associated microbes. The relation between these microbial communities and their human host are mostly mutualistic. These microbes not only provide nutrients, vitamins, and protection against other pathogens, they also influence human's physical, immunological, nutritional, and mental developments. Elements in smog can induce oxidative stress to these microbes, leading to community collapse. Disruption of these mutualistic microbiota may introduce unexpected health risks, especially among the newborns and young children. Besides reducing the burning of fossil fuels as the ultimate solution of smog formation, advanced methods by using various physical, chemical, and biological means to reduce sulfur and nitrogen contains in fossil fuels could lower smog formation. Additionally, information on microbiota disruption, based on functional genomics, culturomics, and general ecological principles, should be included in the risk assessment of prolonged smog exposure to the health of human populations. Copyright © 2017. Published by Elsevier B.V.

Quantum confinement-induced tunable exciton states in graphene oxide.

Science.gov (United States)

Lee, Dongwook; Seo, Jiwon; Zhu, Xi; Lee, Jiyoul; Shin, Hyeon-Jin; Cole, Jacqueline M; Shin, Taeho; Lee, Jaichan; Lee, Hangil; Su, Haibin

2013-01-01

Graphene oxide has recently been considered to be a potential replacement for cadmium-based quantum dots due to its expected high fluorescence. Although previously reported, the origin of the luminescence in graphene oxide is still controversial. Here, we report the presence of core/valence excitons in graphene-based materials, a basic ingredient for optical devices, induced by quantum confinement. Electron confinement in the unreacted graphitic regions of graphene oxide was probed by high resolution X-ray absorption near edge structure spectroscopy and first-principles calculations. Using experiments and simulations, we were able to tune the core/valence exciton energy by manipulating the size of graphitic regions through the degree of oxidation. The binding energy of an exciton in highly oxidized graphene oxide is similar to that in organic electroluminescent materials. These results open the possibility of graphene oxide-based optoelectronic device technology.

Thiamine and benfotiamine prevent stress-induced suppression of hippocampal neurogenesis in mice exposed to predation without affecting brain thiamine diphosphate levels.

Science.gov (United States)

Vignisse, Julie; Sambon, Margaux; Gorlova, Anna; Pavlov, Dmitrii; Caron, Nicolas; Malgrange, Brigitte; Shevtsova, Elena; Svistunov, Andrey; Anthony, Daniel C; Markova, Natalyia; Bazhenova, Natalyia; Coumans, Bernard; Lakaye, Bernard; Wins, Pierre; Strekalova, Tatyana; Bettendorff, Lucien

2017-07-01

Thiamine is essential for normal brain function and its deficiency causes metabolic impairment, specific lesions, oxidative damage and reduced adult hippocampal neurogenesis (AHN). Thiamine precursors with increased bioavailability, especially benfotiamine, exert neuroprotective effects not only for thiamine deficiency (TD), but also in mouse models of neurodegeneration. As it is known that AHN is impaired by stress in rodents, we exposed C57BL6/J mice to predator stress for 5 consecutive nights and studied the proliferation (number of Ki67-positive cells) and survival (number of BrdU-positive cells) of newborn immature neurons in the subgranular zone of the dentate gyrus. In stressed mice, the number of Ki67- and BrdU-positive cells was reduced compared to non-stressed animals. This reduction was prevented when the mice were treated (200mg/kg/day in drinking water for 20days) with thiamine or benfotiamine, that were recently found to prevent stress-induced behavioral changes and glycogen synthase kinase-3β (GSK-3β) upregulation in the CNS. Moreover, we show that thiamine and benfotiamine counteract stress-induced bodyweight loss and suppress stress-induced anxiety-like behavior. Both treatments induced a modest increase in the brain content of free thiamine while the level of thiamine diphosphate (ThDP) remained unchanged, suggesting that the beneficial effects observed are not linked to the role of this coenzyme in energy metabolism. Predator stress increased hippocampal protein carbonylation, an indicator of oxidative stress. This effect was antagonized by both thiamine and benfotiamine. Moreover, using cultured mouse neuroblastoma cells, we show that in particular benfotiamine protects against paraquat-induced oxidative stress. We therefore hypothesize that thiamine compounds may act by boosting anti-oxidant cellular defenses, by a mechanism that still remains to be unveiled. Our study demonstrates, for the first time, that thiamine and benfotiamine prevent

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.

Transient light-induced intracellular oxidation revealed by redox biosensor

Energy Technology Data Exchange (ETDEWEB)

Kolossov, Vladimir L., E-mail: viadimer@illinois.edu [Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 W. Gregory Drive, Urbana, IL 61801 (United States); Beaudoin, Jessica N. [Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 W. Gregory Drive, Urbana, IL 61801 (United States); Department of Animal Sciences, University of Illinois at Urbana-Champaign, 1207 W. Gregory Drive, Urbana, IL 61801 (United States); Hanafin, William P. [Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 W. Gregory Drive, Urbana, IL 61801 (United States); DiLiberto, Stephen J. [Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 W. Gregory Drive, Urbana, IL 61801 (United States); Department of Animal Sciences, University of Illinois at Urbana-Champaign, 1207 W. Gregory Drive, Urbana, IL 61801 (United States); Kenis, Paul J.A. [Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 W. Gregory Drive, Urbana, IL 61801 (United States); Department of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, 600 S. Mathews Avenue, Urbana, IL 61801 (United States); Rex Gaskins, H. [Institute for Genomic Biology, University of Illinois at Urbana-Champaign, 1206 W. Gregory Drive, Urbana, IL 61801 (United States); Department of Animal Sciences, University of Illinois at Urbana-Champaign, 1207 W. Gregory Drive, Urbana, IL 61801 (United States); Department of Pathobiology, University of Illinois at Urbana-Champaign, 2001 S. Lincoln Avenue, Urbana, IL 61801 (United States); Division of Nutritional Sciences, University of Illinois at Urbana-Champaign, 905 S. Goodwin Avenue, Urbana, IL 61801 (United States)

2013-10-04

Highlights: •Time-resolved live cell imaging revealed light-induced oxidation. •Only the roGFP probe fused with glutaredoxin reveals photooxidation. •The transient oxidation is rapidly reduced by the cytosolic antioxidant system. •Intracellular photooxidation is media-dependent. •Oxidation is triggered exclusively by exposure to short wavelength excitation. -- Abstract: We have implemented a ratiometric, genetically encoded redox-sensitive green fluorescent protein fused to human glutaredoxin (Grx1-roGFP2) to monitor real time intracellular glutathione redox potentials of mammalian cells. This probe enabled detection of media-dependent oxidation of the cytosol triggered by short wavelength excitation. The transient nature of light-induced oxidation was revealed by time-lapse live cell imaging when time intervals of less than 30 s were implemented. In contrast, transient ROS generation was not observed with the parental roGFP2 probe without Grx1, which exhibits slower thiol-disulfide exchange. These data demonstrate that the enhanced sensitivity of the Grx1-roGFP2 fusion protein enables the detection of short-lived ROS in living cells. The superior sensitivity of Grx1-roGFP2, however, also enhances responsiveness to environmental cues introducing a greater likelihood of false positive results during image acquisition.

Transient light-induced intracellular oxidation revealed by redox biosensor

International Nuclear Information System (INIS)

Kolossov, Vladimir L.; Beaudoin, Jessica N.; Hanafin, William P.; DiLiberto, Stephen J.; Kenis, Paul J.A.; Rex Gaskins, H.

2013-01-01

Highlights: •Time-resolved live cell imaging revealed light-induced oxidation. •Only the roGFP probe fused with glutaredoxin reveals photooxidation. •The transient oxidation is rapidly reduced by the cytosolic antioxidant system. •Intracellular photooxidation is media-dependent. •Oxidation is triggered exclusively by exposure to short wavelength excitation. -- Abstract: We have implemented a ratiometric, genetically encoded redox-sensitive green fluorescent protein fused to human glutaredoxin (Grx1-roGFP2) to monitor real time intracellular glutathione redox potentials of mammalian cells. This probe enabled detection of media-dependent oxidation of the cytosol triggered by short wavelength excitation. The transient nature of light-induced oxidation was revealed by time-lapse live cell imaging when time intervals of less than 30 s were implemented. In contrast, transient ROS generation was not observed with the parental roGFP2 probe without Grx1, which exhibits slower thiol-disulfide exchange. These data demonstrate that the enhanced sensitivity of the Grx1-roGFP2 fusion protein enables the detection of short-lived ROS in living cells. The superior sensitivity of Grx1-roGFP2, however, also enhances responsiveness to environmental cues introducing a greater likelihood of false positive results during image acquisition

Oxidative stress induced by cerium oxide nanoparticles in cultured BEAS-2B cells

International Nuclear Information System (INIS)

Park, Eun-Jung; Choi, Jinhee; Park, Young-Kwon; Park, Kwangsik

2008-01-01

Cerium oxide nanoparticles of different sizes (15, 25, 30, 45 nm) were prepared by the supercritical synthesis method, and cytotoxicity was evaluated using cultured human lung epithelial cells (BEAS-2B). Exposure of the cultured cells to nanoparticles (5, 10, 20, 40 μg/ml) led to cell death, ROS increase, GSH decrease, and the inductions of oxidative stress-related genes such as heme oxygenase-1, catalase, glutathione S-transferase, and thioredoxin reductase. The increased ROS by cerium oxide nanoparticles triggered the activation of cytosolic caspase-3 and chromatin condensation, which means that cerium oxide nanoparticles exert cytotoxicity by an apoptotic process. Uptake of the nanoparticles to the cultured cells was also tested. It was observed that cerium oxide nanoparticles penetrated into the cytoplasm and located in the peri-region of the nucleus as aggregated particles, which may induce the direct interaction between nanoparticles and cellular molecules to cause adverse cellular responses

Characterization of a novel radiation-inducible transcript, uscA, and analysis of its transcriptional regulation

Energy Technology Data Exchange (ETDEWEB)

Lim, Sang Yong; Kim, Dong Ho; Joe, Min Ho

2010-03-15

The transcriptional expression of the uscA promote (P{sub uscA}) only occurred under aerobic conditions and a dose of 2Gy maximally activated transcription of P{sub uscA}. However, various environmental stress including physical shocks (pH, temperature, osmotic shock), DNA damaging agents (UV and MMC) or oxidative stressagents (paraquat, menadione, and H{sub 2}O{sub 2}) didn't cause the transcriptional activationof P{sub uscA}. The transcription of uscA was initiated at 170 bp upstream of the cyoA start codon, and ended around the ampG stop codon. The size of uscA was determined through reverse transcription assay, approximately 250 bp. The deletion analysis of uscA promoter demonstrates that radiation inducibility of P{sub uscA} is mediated by sequences present between -20 and +111 relativeto +1 of P{sub uscA} and radiation causes P{sub uscA} activation thorough permitting the expression that is repressed under non-irradiated conditions

Characterization of a novel radiation-inducible transcript, uscA, and analysis of its transcriptional regulation

International Nuclear Information System (INIS)

Lim, Sang Yong; Kim, Dong Ho; Joe, Min Ho

2010-03-01

The transcriptional expression of the uscA promote (P uscA ) only occurred under aerobic conditions and a dose of 2Gy maximally activated transcription of P uscA . However, various environmental stress including physical shocks (pH, temperature, osmotic shock), DNA damaging agents (UV and MMC) or oxidative stressagents (paraquat, menadione, and H 2 O 2 ) didn't cause the transcriptional activationof P uscA . The transcription of uscA was initiated at 170 bp upstream of the cyoA start codon, and ended around the ampG stop codon. The size of uscA was determined through reverse transcription assay, approximately 250 bp. The deletion analysis of uscA promoter demonstrates that radiation inducibility of P uscA is mediated by sequences present between -20 and +111 relativeto +1 of P uscA and radiation causes P uscA activation thorough permitting the expression that is repressed under non-irradiated conditions

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.

Salidroside Improves Homocysteine-Induced Endothelial Dysfunction by Reducing Oxidative Stress

Directory of Open Access Journals (Sweden)

Sin Bond Leung

2013-01-01

Full Text Available Hyperhomocysteinemia is associated with an increased risk for cardiovascular diseases through increased oxidative stress. Salidroside is an active ingredient of the root of Rhodiola rosea with documented antioxidative, antihypoxia and neuroprotective properties. However, the vascular benefits of salidroside against endothelial dysfunction have yet to be explored. The present study, therefore, aimed to investigate the protective effect of salidroside on homocysteine-induced endothelial dysfunction. Functional studies on the rat aortas were performed to delineate the vascular effect of salidroside. DHE imaging was used to evaluate the reactive oxygen species (ROS level in aortic wall and endothelial cells. Western blotting was performed to assess the protein expression associated with oxidative stress and nitric oxide (NO bioavailability. Exposure to homocysteine attenuated endothelium-dependent relaxations in rat aortas while salidroside pretreatment rescued it. Salidroside inhibited homocystein-induced elevation in the NOX2 expression and ROS overproduction in both aortas and cultured endothelial cells and increased phosphorylation of eNOS which was diminished by homocysteine. The present study shows that salidroside is effective in preserving the NO bioavailability and thus protects against homocysteine-induced impairment of endothelium-dependent relaxations, largely through inhibiting the NOX2 expression and ROS production. Our results indicate a therapeutic potential of salidroside in the management of oxidative-stress-associated cardiovascular dysfunction.

Salidroside Improves Homocysteine-Induced Endothelial Dysfunction by Reducing Oxidative Stress

Science.gov (United States)

Leung, Sin Bond; Zhang, Huina; Lau, Chi Wai; Huang, Yu; Lin, Zhixiu

2013-01-01

Hyperhomocysteinemia is associated with an increased risk for cardiovascular diseases through increased oxidative stress. Salidroside is an active ingredient of the root of Rhodiola rosea with documented antioxidative, antihypoxia and neuroprotective properties. However, the vascular benefits of salidroside against endothelial dysfunction have yet to be explored. The present study, therefore, aimed to investigate the protective effect of salidroside on homocysteine-induced endothelial dysfunction. Functional studies on the rat aortas were performed to delineate the vascular effect of salidroside. DHE imaging was used to evaluate the reactive oxygen species (ROS) level in aortic wall and endothelial cells. Western blotting was performed to assess the protein expression associated with oxidative stress and nitric oxide (NO) bioavailability. Exposure to homocysteine attenuated endothelium-dependent relaxations in rat aortas while salidroside pretreatment rescued it. Salidroside inhibited homocystein-induced elevation in the NOX2 expression and ROS overproduction in both aortas and cultured endothelial cells and increased phosphorylation of eNOS which was diminished by homocysteine. The present study shows that salidroside is effective in preserving the NO bioavailability and thus protects against homocysteine-induced impairment of endothelium-dependent relaxations, largely through inhibiting the NOX2 expression and ROS production. Our results indicate a therapeutic potential of salidroside in the management of oxidative-stress-associated cardiovascular dysfunction. PMID:23589720

Oxidative stress provokes distinct transcriptional responses in the stress-tolerant atr7 and stress-sensitive loh2 Arabidopsis thaliana mutants as revealed by multi-parallel quantitative real-time PCR analysis of ROS marker and antioxidant genes.

Science.gov (United States)

Mehterov, Nikolay; Balazadeh, Salma; Hille, Jacques; Toneva, Valentina; Mueller-Roeber, Bernd; Gechev, Tsanko

2012-10-01

The Arabidopsis thaliana atr7 mutant is tolerant to oxidative stress induced by paraquat (PQ) or the catalase inhibitor aminotriazole (AT), while its original background loh2 and wild-type plants are sensitive. Both, AT and PQ, which stimulate the intracellular formation of H₂O₂ or superoxide anions, respectively, trigger cell death in loh2 but do not lead to visible damage in atr7. To study gene expression during oxidative stress and ROS-induced programmed cell death, two platforms for multi-parallel quantitative real-time PCR (qRT-PCR) analysis of 217 antioxidant and 180 ROS marker genes were employed. The qRT-PCR analyses revealed AT- and PQ-induced expression of many ROS-responsive genes mainly in loh2, confirming that an oxidative burst plays a role in the activation of the cell death in this mutant. Some of the genes were specifically regulated by either AT or PQ, serving as markers for particular types of ROS. Genes significantly induced by both AT and PQ in loh2 included transcription factors (ANAC042/JUB1, ANAC102, DREB19, HSFA2, RRTF1, ZAT10, ZAT12, ethylene-responsive factors), signaling compounds, ferritins, alternative oxidases, and antioxidant enzymes. Many of these genes were upregulated in atr7 compared to loh2 under non-stress conditions at the first time point, indicating that higher basal levels of ROS and higher antioxidant capacity in atr7 are responsible for the enhanced tolerance to oxidative stress and suggesting a possible tolerance against multiple stresses of this mutant. Copyright © 2012 Elsevier Masson SAS. All rights reserved.

Oxidative stress is involved in Dasatinib-induced apoptosis in rat primary hepatocytes

Energy Technology Data Exchange (ETDEWEB)

Xue, Tao; Luo, Peihua; Zhu, Hong; Zhao, Yuqin [Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058 (China); Wu, Honghai; Gai, Renhua; Wu, Youping [Center for Drug Safety Evaluation and Research of Zhejiang University, Hangzhou 310058 (China); Yang, Bo [Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058 (China); Yang, Xiaochun, E-mail: yangxiaochun@zju.edu.cn [Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058 (China); Center for Drug Safety Evaluation and Research of Zhejiang University, Hangzhou 310058 (China); He, Qiaojun, E-mail: qiaojunhe@zju.edu.cn [Institute of Pharmacology and Toxicology, College of Pharmaceutical Sciences, Zhejiang University, Hangzhou 310058 (China); Center for Drug Safety Evaluation and Research of Zhejiang University, Hangzhou 310058 (China)

2012-06-15

Dasatinib, a multitargeted inhibitor of BCR–ABL and SRC kinases, exhibits antitumor activity and extends the survival of patients with chronic myeloid leukemia (CML) and Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL). However, some patients suffer from hepatotoxicity, which occurs through an unknown mechanism. In the present study, we found that Dasatinib could induce hepatotoxicity both in vitro and in vivo. Dasatinib reduced the cell viability of rat primary hepatocytes, induced the release of alanine aminotransferase (ALT) and lactate dehydrogenase (LDH) in vitro, and triggered the ballooning degeneration of hepatocytes in Sprague–Dawley rats in vivo. Apoptotic markers (chromatin condensation, cleaved caspase-3 and cleaved PARP) were detected to indicate that the injury induced by Dasatinib in hepatocytes in vitro was mediated by apoptosis. This result was further validated in vivo using terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assays. Here we found that Dasatinib dramatically increased the level of reactive oxygen species (ROS) in hepatocytes, reduced the intracellular glutathione (GSH) content, attenuated the activity of superoxide dismutase (SOD), generated malondialdehyde (MDA), a product of lipid peroxidation, decreased the mitochondrial membrane potential, and activated nuclear factor erythroid 2-related factor 2 (Nrf2) and mitogen-activated protein kinases (MAPK) related to oxidative stress and survival. These results confirm that oxidative stress plays a pivotal role in Dasatinib-mediated hepatotoxicity. N-acetylcysteine (NAC), a typical antioxidant, can scavenge free radicals, attenuate oxidative stress, and protect hepatocytes against Dasatinib-induced injury. Thus, relieving oxidative stress is a viable strategy for reducing Dasatinib-induced hepatotoxicity. -- Highlights: ►Dasatinib shows potential hepatotoxicity both in vitro and in vivo. ►Apoptosis plays a vital role in Dasatinib-induced

Mechanisms of carbon nanotube-induced toxicity: Focus on oxidative stress

Energy Technology Data Exchange (ETDEWEB)

Shvedova, Anna A., E-mail: ats1@cdc.gov [Pathology and Physiology Research Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, University of Rome “Tor Vergata”, Rome (Italy); Department of Physiology and Pharmacology, West Virginia University, Morgantown, WV, University of Rome “Tor Vergata”, Rome (Italy); Pietroiusti, Antonio [Department of Biopathology, University of Rome “Tor Vergata”, Rome (Italy); Fadeel, Bengt [Division of Molecular Toxicology, Institute of Environmental Medicine, Karolinska Institutet, Stockholm (Sweden); Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA (United States); Kagan, Valerian E. [Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA (United States)

2012-06-01

Nanotechnologies are emerging as highly promising technologies in many sectors in the society. However, the increasing use of engineered nanomaterials also raises concerns about inadvertent exposure to these materials and the potential for adverse effects on human health and the environment. Despite several years of intensive investigations, a common paradigm for the understanding of nanoparticle-induced toxicity remains to be firmly established. Here, the so-called oxidative stress paradigm is scrutinized. Does oxidative stress represent a secondary event resulting inevitably from disruption of biochemical processes and the demise of the cell, or a specific, non-random event that plays a role in the induction of cellular damage e.g. apoptosis? The answer to this question will have important ramifications for the development of strategies for mitigation of adverse effects of nanoparticles. Recent examples of global lipidomics studies of nanoparticle-induced tissue damage are discussed along with proteomics and transcriptomics approaches to achieve a comprehensive understanding of the complex and interrelated molecular changes in cells and tissues exposed to nanoparticles. We also discuss instances of non-oxidative stress-mediated cellular damage resulting from direct physical interference of nanomaterials with cellular structures. -- Highlights: ► CNT induced non-random oxidative stress associated with apoptosis. ► Non-oxidative mechanisms for cellular toxicity of carbon nanotubes. ► Biodegradation of CNT by cells of innate immune system. ► “Omics”-based biomarkers of CNT exposures.

Mechanisms of carbon nanotube-induced toxicity: Focus on oxidative stress

International Nuclear Information System (INIS)

Shvedova, Anna A.; Pietroiusti, Antonio; Fadeel, Bengt; Kagan, Valerian E.

2012-01-01

Nanotechnologies are emerging as highly promising technologies in many sectors in the society. However, the increasing use of engineered nanomaterials also raises concerns about inadvertent exposure to these materials and the potential for adverse effects on human health and the environment. Despite several years of intensive investigations, a common paradigm for the understanding of nanoparticle-induced toxicity remains to be firmly established. Here, the so-called oxidative stress paradigm is scrutinized. Does oxidative stress represent a secondary event resulting inevitably from disruption of biochemical processes and the demise of the cell, or a specific, non-random event that plays a role in the induction of cellular damage e.g. apoptosis? The answer to this question will have important ramifications for the development of strategies for mitigation of adverse effects of nanoparticles. Recent examples of global lipidomics studies of nanoparticle-induced tissue damage are discussed along with proteomics and transcriptomics approaches to achieve a comprehensive understanding of the complex and interrelated molecular changes in cells and tissues exposed to nanoparticles. We also discuss instances of non-oxidative stress-mediated cellular damage resulting from direct physical interference of nanomaterials with cellular structures. -- Highlights: ► CNT induced non-random oxidative stress associated with apoptosis. ► Non-oxidative mechanisms for cellular toxicity of carbon nanotubes. ► Biodegradation of CNT by cells of innate immune system. ► “Omics”-based biomarkers of CNT exposures.

Oxidized low-density lipoproteins induced inflammatory process during atherogenesis with aging

International Nuclear Information System (INIS)

Larbi, Anis; Khalil, Abdelouahed; Douziech, Nadine; Guerard, Karl-Philippe; Fueloep, Tamas

2005-01-01

Atherosclerosis is a chronic disease developing through decades with two life-threatening complications: myocardial infarction and stroke. Oxidized low-density lipoproteins (oxLDL) produced by oxidative modifications of LDL in the subendothelial space have been demonstrated to be critically involved in atherogenesis through their intensive pro-inflammatory activity. Recently, it was shown that oxLDL have an apoptosis-inducing effect in T cells depending on time and degree of oxidation. The goal of the current study is to elucidate the molecular mechanisms underlying the apoptotic-inducing effects of oxLDL on T lymphocytes. T cells of young and elderly subjects were incubated for various periods of time with LDL oxidized to various degrees. The proliferation, the apoptosis, the MAPK ERK1/2 activation and the expression of the Bcl-2 protein family members were measured upon different LDL treatments. Thus, more the LDL are oxidized more they induce apoptosis and this effect is highly accentuated with aging. The oxLDL decrease the activation of the surviving molecule ERK1/2 and modulate the ratio of Bax/Bcl-2 towards a pro-apoptotic profile, which is also accentuated with aging. These results partly explain why atherosclerosis is increasing with aging concomitantly to its complications

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

Arsenic toxicity induced endothelial dysfunction and dementia: Pharmacological interdiction by histone deacetylase and inducible nitric oxide synthase inhibitors

International Nuclear Information System (INIS)

Sharma, Bhupesh; Sharma, P.M.

2013-01-01

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 in

Chronic lead exposure induces cochlear oxidative stress and potentiates noise-induced hearing loss.

Science.gov (United States)

Jamesdaniel, Samson; Rosati, Rita; Westrick, Judy; Ruden, Douglas M

2018-08-01

Acquired hearing loss is caused by complex interactions of multiple environmental risk factors, such as elevated levels of lead and noise, which are prevalent in urban communities. This study delineates the mechanism underlying lead-induced auditory dysfunction and its potential interaction with noise exposure. Young-adult C57BL/6 mice were exposed to: 1) control conditions; 2) 2 mM lead acetate in drinking water for 28 days; 3) 90 dB broadband noise 2 h/day for two weeks; and 4) both lead and noise. Blood lead levels were measured by inductively coupled plasma mass spectrometry analysis (ICP-MS) lead-induced cochlear oxidative stress signaling was assessed using targeted gene arrays, and the hearing thresholds were assessed by recording auditory brainstem responses. Chronic lead exposure downregulated cochlear Sod1, Gpx1, and Gstk1, which encode critical antioxidant enzymes, and upregulated ApoE, Hspa1a, Ercc2, Prnp, Ccl5, and Sqstm1, which are indicative of cellular apoptosis. Isolated exposure to lead or noise induced 8-12 dB and 11-25 dB shifts in hearing thresholds, respectively. Combined exposure induced 18-30 dB shifts, which was significantly higher than that observed with isolated exposures. This study suggests that chronic exposure to lead induces cochlear oxidative stress and potentiates noise-induced hearing impairment, possibly through parallel pathways. Copyright © 2018 The Authors. Published by Elsevier B.V. All rights reserved.

Curcumin Attenuates Methotrexate-Induced Hepatic Oxidative Damage in Rats

International Nuclear Information System (INIS)

HEMEIDA, R.A.M.; MOHAFEZ, O.M.

2008-01-01

In the present study, we have addressed the ability of curcumin to suppress MTX-induced liver damage. Hepatotoxicity was induced by injection of a single dose of MTX (20 mg/kg I.P.). MTX challenge induced liver damage that was well characterized histopathologically and biochemically. MTX increased relative liver/body weight ratio. Histologically, MTX produced fatty changes in hepatocytes and sinusoidal lining cells, mild necrosis and inflammation. Biochemically, the test battery entailed elevated activities of serum ALT and AST. Liver activities of superoxide dismutase (SOD), catalase (CAT) and level of reduced glutathione (GSH), were notably reduced, while lipid peroxidation, expressed as malondialdhyde (MDA) level was significantly increased. Administration of curcumin (100mg/kg, I.P.) once daily for 5 consecutive days after MTX challenge mitigated the injurious effects of MTX and ameliorated all the altered biochemical parameters. These results showed that administration of curcumin decreases MTX-induced liver damage probably via regulation of oxidant/anti-oxidant balance. In conclusion, the present study indicates that curcumin may be of therapeutic benefit against MTX-cytotoxicity.

Oxidative damage and neurodegeneration in manganese-induced neurotoxicity

International Nuclear Information System (INIS)

Milatovic, Dejan; Zaja-Milatovic, Snjezana; Gupta, Ramesh C.; Yu, Yingchun; Aschner, Michael

2009-01-01

Exposure to excessive manganese (Mn) levels results in neurotoxicity to the extrapyramidal system and the development of Parkinson's disease (PD)-like movement disorder, referred to as manganism. Although the mechanisms by which Mn induces neuronal damage are not well defined, its neurotoxicity appears to be regulated by a number of factors, including oxidative injury, mitochondrial dysfunction and neuroinflammation. To investigate the mechanisms underlying Mn neurotoxicity, we studied the effects of Mn on reactive oxygen species (ROS) formation, changes in high-energy phosphates (HEP), neuroinflammation mediators and associated neuronal dysfunctions both in vitro and in vivo. Primary cortical neuronal cultures showed concentration-dependent alterations in biomarkers of oxidative damage, F 2 -isoprostanes (F 2 -IsoPs) and mitochondrial dysfunction (ATP), as early as 2 h following Mn exposure. Treatment of neurons with 500 μM Mn also resulted in time-dependent increases in the levels of the inflammatory biomarker, prostaglandin E 2 (PGE 2 ). In vivo analyses corroborated these findings, establishing that either a single or three (100 mg/kg, s.c.) Mn injections (days 1, 4 and 7) induced significant increases in F 2 -IsoPs and PGE 2 in adult mouse brain 24 h following the last injection. Quantitative morphometric analyses of Golgi-impregnated striatal sections from mice exposed to single or three Mn injections revealed progressive spine degeneration and dendritic damage of medium spiny neurons (MSNs). These findings suggest that oxidative stress, mitochondrial dysfunction and neuroinflammation are underlying mechanisms in Mn-induced neurodegeneration.

Nitric oxide-induced interstrand cross-links in DNA.

Science.gov (United States)

Caulfield, Jennifer L; Wishnok, John S; Tannenbaum, Steven R

2003-05-01

The DNA damaging effects of nitrous acid have been extensively studied, and the formation of interstrand cross-links have been observed. The potential for this cross-linking to occur through a common nitrosating intermediate derived from nitric oxide is investigated here. Using a HPLC laser-induced fluorescence (LIF) system, the amount of interstrand cross-link formed on nitric oxide treatment of the 5'-fluorescein-labeled oligomer ATATCGATCGATAT was determined. This self-complimentary sequence contains two 5'-CG sequences, which is the preferred site for nitrous acid-induced cross-linking. Nitric oxide was delivered to an 0.5 mM oligomer solution at 15 nmol/mL/min to give a final nitrite concentration of 652 microM. The resulting concentration of the deamination product, xanthine, in this sample was found to be 211 +/- 39 nM, using GC/MS, and the amount of interstrand cross-link was determined to be 13 +/- 2.5 nM. Therefore, upon nitric oxide treatment, the cross-link is found at approximately 6% of the amount of the deamination product. Using this system, detection of the cross-link is also possible for significantly lower doses of nitric oxide, as demonstrated by treatment of the same oligomer with NO at a rate of 18 nmol/mL/min resulting in a final nitrite concentration of 126 microM. The concentration of interstrand cross-link was determined to be 3.6 +/- 0.1 nM in this sample. Therefore, using the same dose rate, when the total nitric oxide concentration delivered drops by a factor of approximately 5, the concentration of cross-link drops by a factor of about 4-indicating a qausi-linear response. It may now be possible to predict the number of cross-links in a small genome based on the number of CpG sequences and the yield of xanthine derived from nitrosative deamination.

MicroRNA-122 is involved in oxidative stress in isoniazid-induced liver injury in mice.

Science.gov (United States)

Song, L; Zhang, Z R; Zhang, J L; Zhu, X B; He, L; Shi, Z; Gao, L; Li, Y; Hu, B; Feng, F M

2015-10-27

Many studies have shown that the pathogenesis of liver injury includes oxidative stress. MicroRNA-122 may be a marker for the early diagnosis of drug-induced liver injury. However, the relationship between microRNA-122 and oxidative stress in anti-tuberculosis drug-induced liver injury remains unknown. We measured changes in tissue microRNA-122 levels and indices of oxidative stress during liver injury in mice after administration of isoniazid, a first-line anti-tuberculosis drug. We quantified microRNA-122 expression and indices of oxidative stress at 7 time points, including 1, 3, and 5 days and 1, 2, 3, and 4 weeks. The tissue microRNA-122 levels and oxidative stress significantly changed at 3 and 5 days, suggesting that isoniazid-induced liver injury reduces oxidative stress and microRNA-122 expression compared to in the control group (P microRNA-122, began to change at 5 days (P microRNA-122 profile may affect oxidative stress by regulating mitochondrial ribosome protein S11 gene during isoniazid-induced liver injury, which may contribute to the response mechanisms of microRNA-122 and oxidative stress.

Ni-Si oxide as an inducing crystallization source for making poly-Si

Energy Technology Data Exchange (ETDEWEB)

Meng, Zhiguo; Liu, Zhaojun; Li, Juan; Wu, Chunya; Xiong, Shaozhen [Institute of Photo-electronics, Nankai University, Tianjin (China); Zhao, Shuyun; Wong, Man; Kwok, Hoi Sing [Department of Electronic and Computer Engineering, Hong Kong University of Science and Technology, Kowloon, Hong Kong (China)

2010-04-15

Nickel silicon oxide mixture was sputtered on a-Si with Ni-Si alloy target with Ni:Si weight ratio of 1:9 and used as a new inducing source for metal induced lateral crystallization (MILC). The characteristics of the resulted poly-Si materials induced by Ni-Si oxide with different thickness were nearly the same. This means the metal induced crystallization with this new inducing source has wide processing tolerance to make MILC poly-Si. Besides, it reduced the residual Ni content in the resulted poly-Si film. The transfer characteristic curve of poly-Si TFT and a TFT-OLED display demo made with this kind of new inducing source were also presented in this paper. (copyright 2010 WILEY-VCH Verlag GmbH and Co. KGaA, Weinheim) (orig.)

Nano rare-earth oxides induced size-dependent vacuolization: an independent pathway from autophagy.

Science.gov (United States)

Zhang, Ying; Yu, Chenguang; Huang, Guanyi; Wang, Changli; Wen, Longping

2010-09-07

Four rare earth oxides have been shown to induce autophagy. Interestingly, we often noticed plentiful vacuolization, which was not always involved in this autophagic process. In this study, we investigated three other rare-earth elements, including Yttrium (Y), Ytterbium (Yb), and Lanthanum (La). Autophagic effect could be induced by all of them but only Y(2)O(3) and Yb(2)O(3) could cause massive vacuolization. Y(2)O(3) and Yb(2)O(3) treated by sonication or centrifugation to reduce particle size were used to test vacuolization level in HeLa cell lines. The results showed that rare earth oxides-induced vacuolization is size-dependent and differs from autophagic pathway. To further clarify the characteristics of this autophagic process, we used MEF Atg-5 (autophagy associated gene 5) knockout cell line, and the result showed that the autophagic process induced by rare earth oxides is Atg-5-dependent and the observed vacuolization was independent from autophagy. Similar results could also be observed in our tests on 3-methyladenine(3-MA), a well-known autophagy inhibitor. In conclusion, for the first time, we clarified the relationship between massive vacuolization and autophagic process induced by rare earth oxides and pointed out the size effect of rare earth oxides on the formation of vacuoles, which give clues to further investigation on the mechanisms underlying their biological effects.

First evidence of pyrrolizidine alkaloid N-oxide-induced hepatic sinusoidal obstruction syndrome in humans.

Science.gov (United States)

Yang, Mengbi; Ruan, Jianqing; Gao, Hong; Li, Na; Ma, Jiang; Xue, Junyi; Ye, Yang; Fu, Peter Pi-Cheng; Wang, Jiyao; Lin, Ge

2017-12-01

Pyrrolizidine alkaloids (PAs) are among the most potent phytotoxins widely distributed in plant species around the world. PA is one of the major causes responsible for the development of hepatic sinusoidal obstruction syndrome (HSOS) and exerts hepatotoxicity via metabolic activation to form the reactive metabolites, which bind with cellular proteins to generate pyrrole-protein adducts, leading to hepatotoxicity. PA N-oxides coexist with their corresponding PAs in plants with varied quantities, sometimes even higher than that of PAs, but the toxicity of PA N-oxides remains unclear. The current study unequivocally identified PA N-oxides as the sole or predominant form of PAs in 18 Gynura segetum herbal samples ingested by patients with liver damage. For the first time, PA N-oxides were recorded to induce HSOS in human. PA N-oxide-induced hepatotoxicity was further confirmed on mice orally dosed of herbal extract containing 170 μmol PA N-oxides/kg/day, with its hepatotoxicity similar to but potency much lower than the corresponding PAs. Furthermore, toxicokinetic study after a single oral dose of senecionine N-oxide (55 μmol/kg) on rats revealed the toxic mechanism that PA N-oxides induced hepatotoxicity via their biotransformation to the corresponding PAs followed by the metabolic activation to form pyrrole-protein adducts. The remarkable differences in toxicokinetic profiles of PAs and PA N-oxides were found and attributed to their significantly different hepatotoxic potency. The findings of PA N-oxide-induced hepatotoxicity in humans and rodents suggested that the contents of both PAs and PA N-oxides present in herbs and foods should be regulated and controlled in use.

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.

Overexpression of a eukaryotic glutathione reductase gene from Brassica campestris improved resistance to oxidative stress in Escherichia coli

International Nuclear Information System (INIS)

Yoon, Ho-Sung; Lee, In-Ae; Lee, Hyoshin; Lee, Byung-Hyun; Jo, Jinki

2005-01-01

Glutathione reductase (GR) plays an essential role in a cell's defense against reactive oxygen metabolites by sustaining the reduced status of an important antioxidant glutathione. We constructed a recombinant plasmid based on the expression vector pET-18a that overexpresses a eukaryotic GR from Brassica campestris (BcGR) in Escherichia coli. For comparative analyses, E. coli GR (EcGR) was also subcloned in the same manner. The transformed E. coli with the recombinant constructs accumulated a high level of GR transcripts upon IPTG induction. Also, Western blot analysis showed overproduction of the BcGR protein in a soluble fraction of the transformed E. coli extract. When treated with oxidative stress generating reagents such as paraquat, salicylic acid, and cadmium, the BcGR overproducing E. coli exhibited a higher level of growth and survival rate than the control E. coli strain, but it was not as high as the E. coli strain transformed with the inducible EcGR. The translated amino acid sequences of BcGR and EcGR share 37.3% identity but all the functionally known important residues are conserved. It appears that eukaryotic BcGR functions in a prokaryotic system by providing protection against oxidative damages in E. coli

Nitrous oxide-induced slow and delta oscillations.

Science.gov (United States)

Pavone, Kara J; Akeju, Oluwaseun; Sampson, Aaron L; Ling, Kelly; Purdon, Patrick L; Brown, Emery N

2016-01-01

Switching from maintenance of general anesthesia with an ether anesthetic to maintenance with high-dose (concentration >50% and total gas flow rate >4 liters per minute) nitrous oxide is a common practice used to facilitate emergence from general anesthesia. The transition from the ether anesthetic to nitrous oxide is associated with a switch in the putative mechanisms and sites of anesthetic action. We investigated whether there is an electroencephalogram (EEG) marker of this transition. We retrospectively studied the ether anesthetic to nitrous oxide transition in 19 patients with EEG monitoring receiving general anesthesia using the ether anesthetic sevoflurane combined with oxygen and air. Following the transition to nitrous oxide, the alpha (8-12 Hz) oscillations associated with sevoflurane dissipated within 3-12 min (median 6 min) and were replaced by highly coherent large-amplitude slow-delta (0.1-4 Hz) oscillations that persisted for 2-12 min (median 3 min). Administration of high-dose nitrous oxide is associated with transient, large amplitude slow-delta oscillations. We postulate that these slow-delta oscillations may result from nitrous oxide-induced blockade of major excitatory inputs (NMDA glutamate projections) from the brainstem (parabrachial nucleus and medial pontine reticular formation) to the thalamus and cortex. This EEG signature of high-dose nitrous oxide may offer new insights into brain states during general anesthesia. Copyright © 2015 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.

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.

Oxidation of extracellular cysteine/cystine redox state in bleomycin-induced lung fibrosis.

Science.gov (United States)

Iyer, Smita S; Ramirez, Allan M; Ritzenthaler, Jeffrey D; Torres-Gonzalez, Edilson; Roser-Page, Susanne; Mora, Ana L; Brigham, Kenneth L; Jones, Dean P; Roman, Jesse; Rojas, Mauricio

2009-01-01

Several lines of evidence indicate that depletion of glutathione (GSH), a critical thiol antioxidant, is associated with the pathogenesis of idiopathic pulmonary fibrosis (IPF). However, GSH synthesis depends on the amino acid cysteine (Cys), and relatively little is known about the regulation of Cys in fibrosis. Cys and its disulfide, cystine (CySS), constitute the most abundant low-molecular weight thiol/disulfide redox couple in the plasma, and the Cys/CySS redox state (E(h) Cys/CySS) is oxidized in association with age and smoking, known risk factors for IPF. Furthermore, oxidized E(h) Cys/CySS in the culture media of lung fibroblasts stimulates proliferation and expression of transitional matrix components. The present study was undertaken to determine whether bleomycin-induced lung fibrosis is associated with a decrease in Cys and/or an oxidation of the Cys/CySS redox state and to determine whether these changes were associated with changes in E(h) GSH/glutathione disulfide (GSSG). We observed distinct effects on plasma GSH and Cys redox systems during the progression of bleomycin-induced lung injury. Plasma E(h) GSH/GSSG was selectively oxidized during the proinflammatory phase, whereas oxidation of E(h) Cys/CySS occurred at the fibrotic phase. In the epithelial lining fluid, oxidation of E(h) Cys/CySS was due to decreased food intake. Thus the data show that decreased precursor availability and enhanced oxidation of Cys each contribute to the oxidation of extracellular Cys/CySS redox state in bleomycin-induced lung fibrosis.

Metallothionein blocks oxidative DNA damage induced by acute inorganic arsenic exposure

Energy Technology Data Exchange (ETDEWEB)

Qu, Wei, E-mail: qu@niehs.nih.gov; Waalkes, Michael P.

2015-02-01

We studied how protein metallothionein (MT) impacts arsenic-induced oxidative DNA damage (ODD) using cells that poorly express MT (MT-I/II double knockout embryonic cells; called MT-null cells) and wild-type (WT) MT competent cells. Arsenic (as NaAsO{sub 2}) was less cytolethal over 24 h in WT cells (LC{sub 50} = 11.0 ± 1.3 μM; mean ± SEM) than in MT-null cells (LC{sub 50} = 5.6 ± 1.2 μM). ODD was measured by the immuno-spin trapping method. Arsenic (1 or 5 μM; 24 h) induced much less ODD in WT cells (121% and 141% of control, respectively) than in MT-null cells (202% and 260%). In WT cells arsenic caused concentration-dependent increases in MT expression (transcript and protein), and in the metal-responsive transcription factor-1 (MTF-1), which is required to induce the MT gene. In contrast, basal MT levels were not detectable in MT-null cells and unaltered by arsenic exposure. Transfection of MT-I gene into the MT-null cells markedly reduced arsenic-induced ODD levels. The transport genes, Abcc1 and Abcc2 were increased by arsenic in WT cells but either showed no or very limited increases in MT-null cells. Arsenic caused increases in oxidant stress defense genes HO-1 and GSTα2 in both WT and MT-null cells, but to much higher levels in WT cells. WT cells appear more adept at activating metal transport systems and oxidant response genes, although the role of MT in these responses is unclear. Overall, MT protects against arsenic-induced ODD in MT competent cells by potential sequestration of scavenging oxidant radicals and/or arsenic. - Highlights: • Metallothionein blocks arsenic toxicity. • Metallothionein reduces arsenic-induced DNA damage. • Metallothionein may bind arsenic or radicals produced by arsenic.

Mixed chemical-induced oxidative stress in occupational exposure ...

African Journals Online (AJOL)

Mixed chemical-induced oxidative stress in occupational exposure in Nigerians. JI Anetor, SA Yaqub, GO Anetor, AC Nsonwu, FAA Adeniyi, S Fukushima. Abstract. Exposure to single chemicals and associated disorders in occupational environments has received significant attention. Understanding these events holds ...

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.

Inflammation, gene mutation and photoimmunosuppression in response to UVR-induced oxidative damage contributes to photocarcinogenesis

International Nuclear Information System (INIS)

Halliday, Gary M.

2005-01-01

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

Neuroprotective effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis

Science.gov (United States)

Sun, Xin-zhi; Liao, Ying; Li, Wei; Guo, Li-mei

2017-01-01

Ganoderma lucidum polysaccharides have protective effects against apoptosis in neurons exposed to ischemia/reperfusion injury, but the mechanisms are unclear. The goal of this study was to investigate the underlying mechanisms of the effects of ganoderma lucidum polysaccharides against oxidative stress-induced neuronal apoptosis. Hydrogen peroxide (H2O2) was used to induce apoptosis in cultured cerebellar granule cells. In these cells, ganoderma lucidum polysaccharides remarkably suppressed H2O2-induced apoptosis, decreased expression of caspase-3, Bax and Bim and increased that of Bcl-2. These findings suggested that ganoderma lucidum polysaccharides regulate expression of apoptosis-associated proteins, inhibit oxidative stress-induced neuronal apoptosis and, therefore, have significant neuroprotective effects. PMID:28761429

Secondhand smoke exposure induces acutely airway acidification and oxidative stress.

Science.gov (United States)

Kostikas, Konstantinos; Minas, Markos; Nikolaou, Eftychia; Papaioannou, Andriana I; Liakos, Panagiotis; Gougoura, Sofia; Gourgoulianis, Konstantinos I; Dinas, Petros C; Metsios, Giorgos S; Jamurtas, Athanasios Z; Flouris, Andreas D; Koutedakis, Yiannis

2013-02-01

Previous studies have shown that secondhand smoke induces lung function impairment and increases proinflammatory cytokines. The aim of the present study was to evaluate the acute effects of secondhand smoke on airway acidification and airway oxidative stress in never-smokers. In a randomized controlled cross-over trial, 18 young healthy never-smokers were assessed at baseline and 0, 30, 60, 120, 180 and 240 min after one-hour secondhand smoke exposure at bar/restaurant levels. Exhaled NO and CO measurements, exhaled breath condensate collection (for pH, H(2)O(2) and NO(2)(-)/NO(3)(-) measurements) and spirometry were performed at all time-points. Secondhand smoke exposure induced increases in serum cotinine and exhaled CO that persisted until 240 min. Exhaled breath condensate pH decreased immediately after exposure (p secondhand smoke induced airway acidification and increased airway oxidative stress, accompanied by significant impairment of lung function. Despite the reversal in EBC pH and lung function, airway oxidative stress remained increased 4 h after the exposure. Clinical trial registration number (EudraCT): 2009-013545-28. Copyright © 2012 Elsevier Ltd. All rights reserved.

EFECTO DEL GLIFOSATO Y PARAQUAT SOBRE EL PROCESO DE NITRIFICACION EN UN SUELO DEL CORREGIMIENTO DE RÍO FRÍO (MAGDALENA, COLOMBIA

Directory of Open Access Journals (Sweden)

Dary Luz Mendoza M.

2010-08-01

Full Text Available Se realizaron ensayos in vitro para determinar el efecto tóxico de los herbicidas glifosato y paraquat sobre el proceso de nitrificación con suelo franco-arenoso (pH: 5.8, Humedad: 13.05%, en el corregimiento de Río Frío, Magdalena. Los experimentos se realizaron por cuantificación espectrofométrica (método del ácido fenoldisulfonico de la concentración de nitratos producidos durante un periodo de incubación de 30 días usando el producto comercial y el principio activo grado estándard, en concentraciones de 10, 100 y 1000 ppm de cada uno de los herbicidas. Se observó una reducción de la nitrificación y un incremento en el período de retardo al aumentar las concentraciones, sin embargo, solamente con altas dosis del glifosato comercial (100 y 1000 ppm de Round Up y paraquat comercial (1000 ppm de Gramoxone hubo inhibición de la nitrificación. Tanto el paraquat comercial como el estándard, a 10 y 100 ppm, causaron leves disturbios sobre la nitrificación, la cual retornó a una normalidad relativa después de 30 días de incubación. Se observó una diferencia significativa (p<0,00\\ entre el glifosato comercial (concentración máxima de nitrato 55,0pg/g y el glifosato estándar (510,12pg/g NO3' a una concentración de 1000 ppm, lo cual sugiere que los adyuvantes en el producto comercial contribuyen a aumentar el efecto tóxico del herbicida. Estos datos son de interés para desarrollar técnicas de utilización de plaguicidas que permitan la recuperación de las poblaciones microbianas importantes para la fertilidad de los suelos.

Enhanced 15-HPETE production during oxidant stress induces apoptosis of endothelial cells.

Science.gov (United States)

Sordillo, Lorraine M; Weaver, James A; Cao, Yu-Zhang; Corl, Chris; Sylte, Matt J; Mullarky, Isis K

2005-05-01

Oxidant stress plays an important role in the etiology of vascular diseases by increasing rates of endothelial cell apoptosis, but few data exist on the mechanisms involved. Using a unique model of oxidative stress based on selenium deficiency (-Se), the effects of altered eicosanoid production on bovine aortic endothelial cells (BAEC) apoptosis was evaluated. Oxidant stress significantly increased the immediate oxygenation product of arachidonic acid metabolized by the 15-lipoxygenase pathway, 15-hydroxyperoxyeicosatetraenoic acid (15-HPETE). Treatment of -Se BAEC with TNFalpha/cyclohexamide (CHX) exhibited elevated levels of apoptosis, which was significantly reduced by the addition of a specific 15-lipoxygenase inhibitor PD146176. Furthermore, the addition of 15-HPETE to PD146176-treated BAEC, partially restored TNF/CHX-induced apoptosis. Increased exposure to 15-HPETE induced apoptosis, as determined by internucleosomal DNA fragmentation, chromatin condensation, caspase-3 activation, and caspase-9 activation, which suggests mitochondrial dysfunction. The expression of Bcl-2 protein also was decreased in -Se BAEC. Addition of a caspase-9 inhibitor (LEHD-fmk) completely blocked 15-HPETE-induced chromatin condensation in -Se BAEC, suggesting that 15-HPETE-induced apoptosis is caspase-9 dependent. Increased apoptosis of BAEC as a result of oxidant stress and subsequent production of 15-HPETE may play a critical role in a variety of inflammatory based diseases.

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.

Oxidative stress induced inflammation initiates functional decline of tear production.

Directory of Open Access Journals (Sweden)

Yuichi Uchino

Full Text Available Oxidative damage and inflammation are proposed to be involved in an age-related functional decline of exocrine glands. However, the molecular mechanism of how oxidative stress affects the secretory function of exocrine glands is unclear. We developed a novel mev-1 conditional transgenic mouse model (Tet-mev-1 using a modified tetracycline system (Tet-On/Off system. This mouse model demonstrated decreased tear production with morphological changes including leukocytic infiltration and fibrosis. We found that the mev-1 gene encodes Cyt-1, which is the cytochrome b(560 large subunit of succinate-ubiquinone oxidoreductase in complex II of mitochondria (homologous to succinate dehydrogenase C subunit (SDHC in humans. The mev-1 gene induced excessive oxidative stress associated with ocular surface epithelial damage and a decrease in protein and aqueous secretory function. This new model provides evidence that mitochondrial oxidative damage in the lacrimal gland induces lacrimal dysfunction resulting in dry eye disease. Tear volume in Tet-mev-1 mice was lower than in wild type mice and histopathological analyses showed the hallmarks of lacrimal gland inflammation by intense mononuclear leukocytic infiltration and fibrosis in the lacrimal gland of Tet-mev-1 mice. These findings strongly suggest that oxidative stress can be a causative factor for the development of dry eye disease.

Heavy-ion induced current through an oxide layer

International Nuclear Information System (INIS)

Takahashi, Yoshihiro; Ohki, Takahiro; Nagasawa, Takaharu; Nakajima, Yasuhito; Kawanabe, Ryu; Ohnishi, Kazunori; Hirao, Toshio; Onoda, Shinobu; Mishima, Kenta; Kawano, Katsuyasu; Itoh, Hisayoshi

2007-01-01

In this paper, the heavy-ion induced current in MOS structure is investigated. We have measured the transient gate current in a MOS capacitor and a MOSFET induced by single heavy-ions, and found that a transient current can be observed when the semiconductor surface is under depletion condition. In the case of MOSFET, a transient gate current with both positive and negative peaks is observed if the ion hits the gate area, and that the total integrated charge is almost zero within 100-200 ns after irradiation. From these results, we conclude that the radiation-induced gate current is dominated by a displacement current. We also discuss the generation mechanism of the radiation-induced current through the oxide layer by device simulation

Arsenic-induced oxidative myocardial injury: protective role of arjunolic acid

Energy Technology Data Exchange (ETDEWEB)

Manna, Prasenjit; Sinha, Mahua; Sil, Parames C. [Bose Institute, Department of Chemistry, Kolkata, West Bengal (India)

2008-03-15

Arsenic, one of the most harmful metalloids, is ubiquitous in the environment. The present study has been carried out to investigate the protective role of a triterpenoid saponin, arjunolic acid (AA) against arsenic-induced cardiac oxidative damage. In the study, NaAsO{sub 2} was chosen as the source of arsenic. The free radical scavenging activity and the effect of AA on the intracellular antioxidant power were determined from its 2,2-diphenyl-1-picryl hydrazyl radical scavenging ability and ferric reducing/antioxidant power assay, respectively. Oral administration of NaAsO{sub 2} at a dose of 10 mg/kg body weight for 2 days caused significant accumulation of arsenic in cardiac tissues of the experimental mice in association with the reduction in cardiac antioxidant enzymes activities, namely superoxide dismutase, catalase, glutathione-S-transferase, glutathione reductase and glutathione peroxidase. Arsenic intoxication also decreased the cardiac glutathione (GSH) and total thiol contents and increased the levels of oxidized glutathione (GSSG), lipid peroxidation end products and protein carbonyl content. Treatment with AA at a dose of 20 mg/kg body weight for 4 days prior to NaAsO{sub 2} intoxication protected the cardiac tissue from arsenic-induced oxidative impairment. In addition to oxidative stress, arsenic administration increased total cholesterol level as well as the reduced high-density lipoprotein cholesterol level in the sera of the experimental mice. AA pretreatment, however, could prevent this hyperlipidemia. Histological studies on the ultrastructural changes in cardiac tissue supported the protective activity of AA also. Combining all, results suggest that AA could protect cardiac tissues against arsenic-induced oxidative stress probably due to its antioxidant property. (orig.)

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

Oxidative Stress in Fish induced by Environmental Pollutants

Directory of Open Access Journals (Sweden)

Anton Kováčik

2017-05-01

Full Text Available Environmental pollutants represent a risk factor for human and animals in all areas of occurrence. Environmental pollution caused by anthropogenic activities is a major problem in many countries. Numbers of studies deals with cumulation of xenobiotics in tissues but not all respond to the real impact on living organisms. Freshwater fishes are exposed to several anthropogenic contaminants. The most commonly studied are three metals: mercury (Hg, lead (Pb, cadmium (Cd. These contaminants could have several impacts to oxidative stress. In the normal healthy cell, ROS and pro-oxidant products are detoxified by antioxidant defences. Redox-active or Redox-inactive metals may cause an increase in production of reactive oxygen species (ROS. Mercury has a high affinity for thiol groups, and can non-specifically affect several enzymes, e. g. GSH (glutathione, which can induce GSH depletion and oxidative stress in tissue, also can induce lipid peroxidation, and mitochondrial dysfunction. The toxicity of Cd to aquatic species depends on speciation, with the free ion, Cd2+ concentration being proportional to bioavailability. Cadmium toxicity worsened of Ca, Na, and Mg ions homeostasis. Lead can be toxic to nervous and skeletal systems; at cellular level can cause apoptosis, also can affect mitochondria, neurotransmitters, and can substitute for Ca.

Neuromodulatory Effects of Hesperidin in Mitigating Oxidative Stress in Streptozotocin Induced Diabetes

Directory of Open Access Journals (Sweden)

Mohammad Ashafaq

2014-01-01

Full Text Available Oxidative stress has been implicated in pathogenesis of streptozotocin- (STZ- induced diabetes mellitus and its complication in central nervous system (CNS. Recent studies have provided insights on antioxidants and their emergence as potential therapeutic and nutraceutical. The present study examined the hypothesis that hesperidin (HP ameliorates oxidative stress and may be a limiting factor in the extent of CNS complication following diabetes. To test this hypothesis rats were divided into four groups: control, diabetic, diabetic-HP treated, and vehicle for HP treatment group. Diabetes mellitus was induced by a single injection of STZ (65 mg/kg body weight. Three days after STZ injection, HP was given (50 mg/kg b.wt. orally once daily for four weeks. The results of the present investigation suggest that the significant elevated levels of oxidative stress markers were observed in STZ-treated animals, whereas significant depletion in the activity of nonenzymatic antioxidants and enzymatic antioxidants was witnessed in diabetic rat brain. Neurotoxicity biomarker activity was also altered significantly. HP treatment significantly attenuated the altered levels of oxidative stress and neurotoxicity biomarkers. Our results demonstrate that HP exhibits potent antioxidant and neuroprotective effects on the brain tissue against the diabetic oxidative damage in STZ-induced rodent model.

Protection of swimming-induced oxidative stress in some vital ...

African Journals Online (AJOL)

Protection of swimming-induced oxidative stress in some vital organs by the treatment of composite extract of Withania somnifera, Ocimum sanctum and Zingiber officinalis in male rat. D Misra, B Maiti, D Ghosh ...

γ-irradiation-induced oxidative stress and aging of cultured endothelial cells

International Nuclear Information System (INIS)

Van Uye, A.; Agay, D.; Drouet, M.; Chancerelle, Y.; Mathieu, J.; Kergonou, J.F.; Mestries, J.C.

1995-01-01

The aim of this work was to study aging of cultured vascular cells. In order to induce an oxidative stress, which is known to participate in aging process, we apply γ-induced peroxidation and is revealed by indirect immunofluorescence. (author)

Radiation induced leakage current and stress induced leakage current in ultra-thin gate oxides

International Nuclear Information System (INIS)

Ceschia, M.; Paccagnella, A.; Cester, A.; Scarpa, A.

1998-01-01

Low-field leakage current has been measured in thin oxides after exposure to ionizing radiation. This Radiation Induced Leakage Current (RILC) can be described as an inelastic tunneling process mediated by neutral traps in the oxide, with an energy loss of about 1 eV. The neutral trap distribution is influenced by the oxide field applied during irradiation, thus indicating that the precursors of the neutral defects are charged, likely being defects associated to trapped holes. The maximum leakage current is found under zero-field condition during irradiation, and it rapidly decreases as the field is enhanced, due to a displacement of the defect distribution across the oxide towards the cathodic interface. The RILC kinetics are linear with the cumulative dose, in contrast with the power law found on electrically stressed devices

Field-induced resistance switching at metal/perovskite manganese oxide interface

International Nuclear Information System (INIS)

Ohkubo, I.; Tsubouchi, K.; Harada, T.; Kumigashira, H.; Itaka, K.; Matsumoto, Y.; Ohnishi, T.; Lippmaa, M.; Koinuma, H.; Oshima, M.

2008-01-01

Planar type metal/insulator/metal structures composed of an epitaxial perovskite manganese oxide layer and various metal electrodes were prepared for electric-field-induced resistance switching. Only the electrode pairs including Al show good resistance switching and the switching ratio reaches its maximum of 1000. This resistance switching occurs around the interface between Al electrodes and epitaxial perovskite manganese oxide thin films

Cuprous oxide nanoparticles selectively induce apoptosis of tumor cells

Science.gov (United States)

Wang, Ye; Zi, Xiao-Yuan; Su, Juan; Zhang, Hong-Xia; Zhang, Xin-Rong; Zhu, Hai-Ying; Li, Jian-Xiu; Yin, Meng; Yang, Feng; Hu, Yi-Ping

2012-01-01

In the rapid development of nanoscience and nanotechnology, many researchers have discovered that metal oxide nanoparticles have very useful pharmacological effects. Cuprous oxide nanoparticles (CONPs) can selectively induce apoptosis and suppress the proliferation of tumor cells, showing great potential as a clinical cancer therapy. Treatment with CONPs caused a G1/G0 cell cycle arrest in tumor cells. Furthermore, CONPs enclosed in vesicles entered, or were taken up by mitochondria, which damaged their membranes, thereby inducing apoptosis. CONPs can also produce reactive oxygen species (ROS) and initiate lipid peroxidation of the liposomal membrane, thereby regulating many signaling pathways and influencing the vital movements of cells. Our results demonstrate that CONPs have selective cytotoxicity towards tumor cells, and indicate that CONPs might be a potential nanomedicine for cancer therapy. PMID:22679374

Radioprotective efficacy of bisarylidene cyclopentanone on electron beam radiation induced oxidative stress in Drosophila melanogaster

International Nuclear Information System (INIS)

Darshan Raj, C.G.; Sarojini, B.K.; Musthafa Khaleel, V.; Ramesh, S.R.; Ramakrishna, M.K.; Narayana, B.; Sanjeev, Ganesh

2010-01-01

Present study was carried out for evaluating the radioprotective effect of bischalcone (2E, 5E) - 2,5-bis (3-methoxy-4-hydroxy-benzylidene) cyclopentanone (curcumin analog (CA)), on electron beam radiation induced oxidative stress in Drosophila melanogaster adults. The oxidative stress markers and antioxidants included superoxide dismutase (SOD) and catalase (CAT). The oxidative stress was induced at 1.5 Gy. (author)

Physicochemical Characterization and Functional Analysis of the Polysaccharide from the Edible Microalga Nostoc sphaeroides

Directory of Open Access Journals (Sweden)

Haifeng Li

2018-02-01

Full Text Available Nostoc colonies have been used as food and medicine for centuries, and their main supporting matrix is polysaccharides, which help Nostoc cells resist various environmental stresses including oxidative stress. Here we isolated a polysaccharide, nostoglycan, from cultured Nostoc sphaeroides colonies and determined its physicochemical properties, which revealed a characteristic infrared absorption spectrum typical of polysaccharides and an amorphous morphology with rough surfaces. We also show that nostoglycan has strong moisture absorption and retention capacities and a high relative viscosity. Using Caenorhabditis elegans models, we then demonstrate that nostoglycan is capable of improving overall survival rate of the animals under increased oxidative stress caused by paraquat. Nostoglycan also reduces reactive oxygen species level, inhibits protein carbonyl formation and lipid peroxidation, and increases activities of superoxide dismutase and catalase in paraquat-exposed nematodes. As oxidative stress may drive tumor progression, we further demonstrate that nostoglycan can suppress the proliferation of several types of tumor cells and induce apoptosis of human lung adenocarcinoma A549 cells via caspase-3 activation. Together, our results yield important information on the physicochemical characteristics and demonstrate the antioxidant and anti-proliferative functions of nostoglycan, and thus provide an insight into its potential in food and health industries.

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.

Strain induced anomalous red shift in mesoscopic iron oxide

Indian Academy of Sciences (India)

Nano magnetic oxides; red shift; magnetic storage. ... size and strain induced modifications of various physical properties viz. optical, magnetic and structural. ... ∼2, are synthesized by employing starch and ethylene glycol and starch and ...

Oxalic acid induced hydrothermal synthesis of single crystalline tungsten oxide nanorods

International Nuclear Information System (INIS)

Patil, V.B.; Adhyapak, P.V.; Suryavanshi, S.S.; Mulla, I.S.

2014-01-01

Highlights: • We report synthesis of 1D tungsten oxide using a hydrothermal route at 170 °C. • Oxalic acid plays an important role in the formation of 1D nanostructure. • Monoclinic transforms to hexagonal phase with increment in reaction duration. -- Abstract: One-dimensional single-crystalline tungsten oxide nanorods have been synthesized by the hydrothermal technique. The controlled morphology of tungsten oxide was obtained by using sodium tungstate and oxalic acid as an organic inducer. The reaction was carried out at 170 °C for 24, 48 and 72 h. The obtained tungsten oxides were investigated by using XRD, SEM and HRTEM techniques. In order to understand the role of organic inducer on the shape, size and phase formation of WO 3 was prepared with and without organic inducer. On heating of sodium tungstate without organic inducer for 72 h at 170 °C in the hydrothermal unit we obtain nanoparticles of monoclinic WO 3 , however, on addition of oxalic acid a single phase hexagonal WO 3 with distinct nanorods was formed. On addition of oxalic acid a systematic emergence of nanorod-like morphology was obtained with incrementing reaction times from 24 h to 48 h. The 72 h reaction generates self-assembled 20–30 nm diameter and 4–5 μm long h-WO 3 bundles of nanorods. The XRD studies show hexagonal structure of tungsten oxide, while SAED reveals its single crystalline nature. The photoluminescence (PL) emission spectrum shows a characteristic blue emission peak at 3 eV (410 nm). Raman spectra provide the evidence of hexagonal structure with stretching vibrations (830 cm −1 ) for 72 h of heating at 170 °C

Oxalic acid induced hydrothermal synthesis of single crystalline tungsten oxide nanorods

Energy Technology Data Exchange (ETDEWEB)

Patil, V.B. [School of Physical Sciences, Solapur University, Solapur 413255 (India); Adhyapak, P.V. [Centre for Materials for Electronic Technology (C-MET), Pune 411008 (India); Suryavanshi, S.S., E-mail: sssuryavanshi@rediffmail.com [School of Physical Sciences, Solapur University, Solapur 413255 (India); Mulla, I.S., E-mail: ismulla2001@gmail.com [Emeritus Scientist (CSIR), Centre for Materials for Electronic Technology (C-MET), Pune 411008 (India)

2014-03-25

Highlights: • We report synthesis of 1D tungsten oxide using a hydrothermal route at 170 °C. • Oxalic acid plays an important role in the formation of 1D nanostructure. • Monoclinic transforms to hexagonal phase with increment in reaction duration. -- Abstract: One-dimensional single-crystalline tungsten oxide nanorods have been synthesized by the hydrothermal technique. The controlled morphology of tungsten oxide was obtained by using sodium tungstate and oxalic acid as an organic inducer. The reaction was carried out at 170 °C for 24, 48 and 72 h. The obtained tungsten oxides were investigated by using XRD, SEM and HRTEM techniques. In order to understand the role of organic inducer on the shape, size and phase formation of WO{sub 3} was prepared with and without organic inducer. On heating of sodium tungstate without organic inducer for 72 h at 170 °C in the hydrothermal unit we obtain nanoparticles of monoclinic WO{sub 3}, however, on addition of oxalic acid a single phase hexagonal WO{sub 3} with distinct nanorods was formed. On addition of oxalic acid a systematic emergence of nanorod-like morphology was obtained with incrementing reaction times from 24 h to 48 h. The 72 h reaction generates self-assembled 20–30 nm diameter and 4–5 μm long h-WO{sub 3} bundles of nanorods. The XRD studies show hexagonal structure of tungsten oxide, while SAED reveals its single crystalline nature. The photoluminescence (PL) emission spectrum shows a characteristic blue emission peak at 3 eV (410 nm). Raman spectra provide the evidence of hexagonal structure with stretching vibrations (830 cm{sup −1}) for 72 h of heating at 170 °C.

Creatine affords protection against glutamate-induced nitrosative and oxidative stress.

Science.gov (United States)

Cunha, Mauricio P; Lieberknecht, Vicente; Ramos-Hryb, Ana Belén; Olescowicz, Gislaine; Ludka, Fabiana K; Tasca, Carla I; Gabilan, Nelson H; Rodrigues, Ana Lúcia S

2016-05-01

Creatine has been reported to exert beneficial effects in several neurodegenerative diseases in which glutamatergic excitotoxicity and oxidative stress play an etiological role. The purpose of this study was to investigate the protective effects of creatine, as compared to the N-Methyl-d-Aspartate (NMDA) receptor antagonist dizocilpine (MK-801), against glutamate or hydrogen peroxide (H2O2)-induced injury in human neuroblastoma SH-SY5Y cells. Exposure of cells to glutamate (60-80 mM) or H2O2 (200-300 μM) for 24 h decreased cellular viability and increased dichlorofluorescein (DCF) fluorescence (indicative of increased reactive oxygen species, ROS) and nitric oxide (NO) production (assessed by mono-nitrogen oxides, NOx, levels). Creatine (1-10 mM) or MK-801 (0.1-10 μM) reduced glutamate- and H2O2-induced toxicity. The protective effect of creatine against glutamate-induced toxicity involves its antioxidant effect, since creatine, similar to MK-801, prevented the increase on DCF fluorescence induced by glutamate or H2O2. Furthermore, creatine or MK-801 blocked glutamate- and H2O2-induced increases in NOx levels. In another set of experiments, the repeated, but not acute, administration of creatine (300 mg/kg, po) in mice prevented the decreases on cellular viability and mitochondrial membrane potential (assessed by tetramethylrhodamine ethyl ester, TMRE, probe) of hippocampal slices incubated with glutamate (10 mM). Creatine concentration-dependent decreased the amount of nitrite formed in the reaction of oxygen with NO produced from sodium nitroprusside solution, suggesting that its protective effect against glutamate or H2O2-induced toxicity might be due to its scavenger activity. Overall, the results suggest that creatine may be useful as adjuvant therapy for neurodegenerative disease treatments. Copyright © 2016 Elsevier Ltd. All rights reserved.

SIRT1 sensitizes hepatocellular carcinoma cells expressing hepatitis B virus X protein to oxidative stress-induced apoptosis

International Nuclear Information System (INIS)

Srisuttee, Ratakorn; Koh, Sang Seok; Malilas, Waraporn; Moon, Jeong; Cho, Il-Rae; Jhun, Byung Hak; Horio, Yoshiyuki; Chung, Young-Hwa

2012-01-01

Highlights: ► Up-regulation of SIRT1 protein and activity sensitizes Hep3B-HBX cells to oxidative stress-induced apoptosis. ► Nuclear localization of SIRT1 is not required for oxidation-induced apoptosis. ► Ectopic expression and enhanced activity of SIRT1 attenuate JNK phosphorylation. ► Inhibition of SIRT1 activity restores resistance to oxidation-induced apoptosis through JNK activation. -- Abstract: We previously showed that SIRT1 deacetylase inhibits proliferation of hepatocellular carcinoma cells expressing hepatitis B virus (HBV) X protein (HBX), by destabilization of β-catenin. Here, we report another role for SIRT1 in HBX-mediated resistance to oxidative stress. Ectopic expression and enhanced activity of SIRT1 sensitize Hep3B cells stably expressing HBX to oxidative stress-induced apoptosis. SIRT1 mutant analysis showed that nuclear localization of SIRT1 is not required for sensitization of oxidation-mediated apoptosis. Furthermore, ectopic expression of SIRT1 and treatment with resveratrol (a SIRT1 activator) attenuated JNK phosphorylation, which is a prerequisite for resistance to oxidative stress-induced apoptosis. Conversely, suppression of SIRT1 activity with nicotinamide inhibited the effect of resveratrol on JNK phosphorylation, leading to restoration of resistance to oxidation-induced apoptosis. Taken together, these results suggest that up-regulation of SIRT1 under oxidative stress may be a therapeutic strategy for treatment of hepatocellular carcinoma cells related to HBV through inhibition of JNK activation.

SIRT1 sensitizes hepatocellular carcinoma cells expressing hepatitis B virus X protein to oxidative stress-induced apoptosis

Energy Technology Data Exchange (ETDEWEB)

Srisuttee, Ratakorn [WCU, Department of Cogno-Mechatronics Engineering, Pusan National University, Busan 609-735 (Korea, Republic of); Koh, Sang Seok [Immunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, University of Science and Technology, Daejeon 305-333 (Korea, Republic of); Department of Functional Genomics, University of Science and Technology, Daejeon 305-333 (Korea, Republic of); Malilas, Waraporn; Moon, Jeong; Cho, Il-Rae [WCU, Department of Cogno-Mechatronics Engineering, Pusan National University, Busan 609-735 (Korea, Republic of); Jhun, Byung Hak [Department of Applied Nanoscience, Pusan National University, Busan 609-735 (Korea, Republic of); Horio, Yoshiyuki [Department of Pharmacology, Sapporo Medical University, Sapporo 060-8556 (Japan); Chung, Young-Hwa, E-mail: younghc@pusan.ac.kr [WCU, Department of Cogno-Mechatronics Engineering, Pusan National University, Busan 609-735 (Korea, Republic of)

2012-12-07

Highlights: Black-Right-Pointing-Pointer Up-regulation of SIRT1 protein and activity sensitizes Hep3B-HBX cells to oxidative stress-induced apoptosis. Black-Right-Pointing-Pointer Nuclear localization of SIRT1 is not required for oxidation-induced apoptosis. Black-Right-Pointing-Pointer Ectopic expression and enhanced activity of SIRT1 attenuate JNK phosphorylation. Black-Right-Pointing-Pointer Inhibition of SIRT1 activity restores resistance to oxidation-induced apoptosis through JNK activation. -- Abstract: We previously showed that SIRT1 deacetylase inhibits proliferation of hepatocellular carcinoma cells expressing hepatitis B virus (HBV) X protein (HBX), by destabilization of {beta}-catenin. Here, we report another role for SIRT1 in HBX-mediated resistance to oxidative stress. Ectopic expression and enhanced activity of SIRT1 sensitize Hep3B cells stably expressing HBX to oxidative stress-induced apoptosis. SIRT1 mutant analysis showed that nuclear localization of SIRT1 is not required for sensitization of oxidation-mediated apoptosis. Furthermore, ectopic expression of SIRT1 and treatment with resveratrol (a SIRT1 activator) attenuated JNK phosphorylation, which is a prerequisite for resistance to oxidative stress-induced apoptosis. Conversely, suppression of SIRT1 activity with nicotinamide inhibited the effect of resveratrol on JNK phosphorylation, leading to restoration of resistance to oxidation-induced apoptosis. Taken together, these results suggest that up-regulation of SIRT1 under oxidative stress may be a therapeutic strategy for treatment of hepatocellular carcinoma cells related to HBV through inhibition of JNK activation.

Magnetism in graphene oxide induced by epoxy groups

Energy Technology Data Exchange (ETDEWEB)

Lee, Dongwook, E-mail: dongwookleedl324@gmail.com [Cavendish Laboratory, University of Cambridge, Cambridge CB3 0HE (United Kingdom); Division of Physics and Applied Physics, Nanyang Technological University, Singapore 637371 (Singapore); Seo, Jiwon, E-mail: jiwonseo@yonsei.ac.kr [Department of Physics and IPAP, Yonsei University, Seoul 120-749 (Korea, Republic of); School of Advanced Materials Science and Engineering, Sungkyunkwan University, Suwon 440-746 (Korea, Republic of); Zhu, Xi; Su, Haibin [Division of Materials Science, School of Materials Science and Engineering, Nanyang Technological University, Singapore 639798 (Singapore); Cole, Jacqueline M. [Cavendish Laboratory, University of Cambridge, Cambridge CB3 0HE (United Kingdom); Argonne National Laboratory, 9700S Cass Avenue, Argonne, Illinois 60439 (United States)

2015-04-27

We have engineered magnetism in graphene oxide. Our approach transforms graphene into a magnetic insulator while maintaining graphene's structure. Fourier transform infrared spectroscopy spectra reveal that graphene oxide has various chemical groups (including epoxy, ketone, hydroxyl, and C-O groups) on its surface. Destroying the epoxy group with heat treatment or chemical treatment diminishes magnetism in the material. Local density approximation calculation results well reproduce the magnetic moments obtained from experiments, and these results indicate that the unpaired spin induced by the presence of epoxy groups is the origin of the magnetism. The calculation results also explain the magnetic properties, which are generated by the interaction between separated magnetic regions and domains. Our results demonstrate tunable magnetism in graphene oxide based on controlling the epoxy group with heat or chemical treatment.

Effects of Kombucha on oxidative stress induced nephrotoxicity in rats.

Science.gov (United States)

Gharib, Ola Ali

2009-11-27

Trichloroethylene (TCE) may induce oxidative stress which generates free radicals and alters antioxidants or oxygen-free radical scavenging enzymes. 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. 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. 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.

Classical and alternative macrophage activation in the lung following ozone-induced oxidative stress

Energy Technology Data Exchange (ETDEWEB)

Sunil, Vasanthi R., E-mail: sunilva@pharmacy.rutgers.edu [Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854 (United States); Patel-Vayas, Kinal; Shen, Jianliang [Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854 (United States); Laskin, Jeffrey D. [Department of Environmental and Occupational Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ (United States); Laskin, Debra L. [Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy, Piscataway, NJ 08854 (United States)

2012-09-01

Ozone is a pulmonary irritant known to cause oxidative stress, inflammation and tissue injury. Evidence suggests that macrophages play a role in the pathogenic response; however, their contribution depends on the mediators they encounter in the lung which dictate their function. In these studies we analyzed the effects of ozone-induced oxidative stress on the phenotype of alveolar macrophages (AM). Exposure of rats to ozone (2 ppm, 3 h) resulted in increased expression of 8-hydroxy-2′-deoxyguanosine (8-OHdG), as well as heme oxygenase-1 (HO-1) in AM. Whereas 8-OHdG was maximum at 24 h, expression of HO-1 was biphasic increasing after 3 h and 48–72 h. Cleaved caspase-9 and beclin-1, markers of apoptosis and autophagy, were also induced in AM 24 h post-ozone. This was associated with increased bronchoalveolar lavage protein and cells, as well as matrix metalloproteinase (MMP)-2 and MMP-9, demonstrating alveolar epithelial injury. Ozone intoxication resulted in biphasic activation of the transcription factor, NFκB. This correlated with expression of monocyte chemotactic protein‐1, inducible nitric oxide synthase and cyclooxygenase‐2, markers of proinflammatory macrophages. Increases in arginase-1, Ym1 and galectin-3 positive anti-inflammatory/wound repair macrophages were also observed in the lung after ozone inhalation, beginning at 24 h (arginase-1, Ym1), and persisting for 72 h (galectin-3). This was associated with increased expression of pro-surfactant protein-C, a marker of Type II cell proliferation and activation, important steps in wound repair. These data suggest that both proinflammatory/cytotoxic and anti-inflammatory/wound repair macrophages are activated early in the response to ozone-induced oxidative stress and tissue injury. -- Highlights: ► Lung macrophages are highly sensitive to ozone induced oxidative stress. ► Ozone induces autophagy and apoptosis in lung macrophages. ► Proinflammatory and wound repair macrophages are activated

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.

Advances in metal-induced oxidative stress and human disease

International Nuclear Information System (INIS)

Jomova, Klaudia; Valko, Marian

2011-01-01

Detailed studies in the past two decades have shown that redox active metals like iron (Fe), copper (Cu), chromium (Cr), cobalt (Co) and other metals undergo redox cycling reactions and possess the ability to produce reactive radicals such as superoxide anion radical and nitric oxide in biological systems. Disruption of metal ion homeostasis may lead to oxidative stress, a state where increased formation of reactive oxygen species (ROS) overwhelms body antioxidant protection and subsequently induces DNA damage, lipid peroxidation, protein modification and other effects, all symptomatic for numerous diseases, involving cancer, cardiovascular disease, diabetes, atherosclerosis, neurological disorders (Alzheimer's disease, Parkinson's disease), chronic inflammation and others. The underlying mechanism of action for all these metals involves formation of the superoxide radical, hydroxyl radical (mainly via Fenton reaction) and other ROS, finally producing mutagenic and carcinogenic malondialdehyde (MDA), 4-hydroxynonenal (HNE) and other exocyclic DNA adducts. On the other hand, the redox inactive metals, such as cadmium (Cd), arsenic (As) and lead (Pb) show their toxic effects via bonding to sulphydryl groups of proteins and depletion of glutathione. Interestingly, for arsenic an alternative mechanism of action based on the formation of hydrogen peroxide under physiological conditions has been proposed. A special position among metals is occupied by the redox inert metal zinc (Zn). Zn is an essential component of numerous proteins involved in the defense against oxidative stress. It has been shown, that depletion of Zn may enhance DNA damage via impairments of DNA repair mechanisms. In addition, Zn has an impact on the immune system and possesses neuroprotective properties. The mechanism of metal-induced formation of free radicals is tightly influenced by the action of cellular antioxidants. Many low-molecular weight antioxidants (ascorbic acid (vitamin C), alpha

Protective effects of gallic acid against spinal cord injury-induced oxidative stress.

Science.gov (United States)

Yang, Yong Hong; Wang, Zao; Zheng, Jie; Wang, Ran

2015-08-01

The present study aimed to investigate the role of gallic acid in oxidative stress induced during spinal cord injury (SCI). In order to measure oxidative stress, the levels of lipid peroxide, protein carbonyl, reactive oxygen species and nitrates/nitrites were determined. In addition, the antioxidant status during SCI injury and the protective role of gallic acid were investigated by determining glutathione levels as well as the activities of catalase, superoxide dismutase, glutathione peroxidase and glutathione-S-transferase. Adenosine triphophatase (ATPase) enzyme activities were determined to evaluate the role of gallic acid in SCI-induced deregulation of the activity of enzymes involved in ion homeostasis. The levels of inflammatory markers such as nuclear factor (NF)-κB and cycloxygenase (COX)-2 were determined by western blot analysis. Treatment with gallic acid was observed to significantly mitigate SCI-induced oxidative stress and the inflammatory response by reducing the oxidative stress, decreasing the expression of NF-κB and COX-2 as well as increasing the antioxidant status of cells. In addition, gallic acid modulated the activity of ATPase enzymes. Thus the present study indicated that gallic acid may have a role as a potent antioxidant and anti-inflammatory agent against SCI.

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...

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...

EFFECT OF PESTICIDES ON RAT (Rattus norvegicus ERYTHROCYTES ANTIOXIDANT ENZYMES IN VITRO

Directory of Open Access Journals (Sweden)

Jasna Friščić

2014-10-01

Full Text Available Abstract: In the last century, maximum in herbicide production was achieved. Growing use of herbicides initiated the need for continuous evaluation of damaging effects of herbicides on human health and environment. Paraquat is the trade name for N,N′-dimethyl-4,4′-bipyridinium dichloride and one of the most widely used herbicides in the world. Although mechanism of paraquat toxicity remains undefined, a great portion of toxicity is attributed to the process of redox cycling. In this research, rat erythrocytes were exposed to various paraquat concentrations (0, 0.25, 0.5, 0.75, 1.25 mM. Changes in antioxidant enzymes activity, catalase and superoxide dismutase were determined, and also the activity of erythrocyte acetylcholinesterase. Obtained results show damaging effects of paraquat on erythrocytes due to oxidative stress.

Oxidative Stress Induces Endothelial Cell Senescence via Downregulation of Sirt6

Directory of Open Access Journals (Sweden)

Rong Liu

2014-01-01

Full Text Available Accumulating evidence has shown that diabetes accelerates aging and endothelial cell senescence is involved in the pathogenesis of diabetic vascular complications, including diabetic retinopathy. Oxidative stress is recognized as a key factor in the induction of endothelial senescence and diabetic retinopathy. However, specific mechanisms involved in oxidative stress-induced endothelial senescence have not been elucidated. We hypothesized that Sirt6, which is a nuclear, chromatin-bound protein critically involved in many pathophysiologic processes such as aging and inflammation, may have a role in oxidative stress-induced vascular cell senescence. Measurement of Sirt6 expression in human endothelial cells revealed that H2O2 treatment significantly reduced Sirt6 protein. The loss of Sirt6 was associated with an induction of a senescence phenotype in endothelial cells, including decreased cell growth, proliferation and angiogenic ability, and increased expression of senescence-associated β-galactosidase activity. Additionally, H2O2 treatment reduced eNOS expression, enhanced p21 expression, and dephosphorylated (activated retinoblastoma (Rb protein. All of these alternations were attenuated by overexpression of Sirt6, while partial knockdown of Sirt6 expression by siRNA mimicked the effect of H2O2. In conclusion, these results suggest that Sirt6 is a critical regulator of endothelial senescence and oxidative stress-induced downregulation of Sirt6 is likely involved in the pathogenesis of diabetic retinopathy.

Oxidation-induced deformation of zircaloy-4 tubing in steam in the temperature range 600-1000 degree C

International Nuclear Information System (INIS)

Aly, A.E.; Hussein, A.G.; EL-Raghy, S.M.; EL-Sayed, A.A.; EL-Banna, O.A.

1992-01-01

The oxidation-induced deformation of zircaloy-4 (zry-4) tubing in steam has been studied in the temperature range 600 to 1000 degree C. The induced deformation has been measured in both radial and axial directions of the tube. The effect of hydrogen addition to steam was also investigated. The oxidation-induced deformation has been characterized by uniform and non-uniform (distortion) strain period. During the uniform strain period the radial strain kinetics were found in general, to be parallel to the oxidation kinetics. The axial strain (δA) induced by oxidation was found to be always lower than the radial strain (εR). The addition of 5% by volume hydrogen to steam leads to an increase in the oxidation rate and to a decrease in the degree of anisotropy between radial and axial strains

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. Copyright © 2015 Elsevier B.V. All rights reserved.

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.

Globally important nitrous oxide emissions from croplands induced by freeze-thaw cycles

NARCIS (Netherlands)

Wagner-Riddle, Claudia; Congreves, Katelyn A.; Abalos Rodriguez, Diego; Berg, Aaron A.; Brown, Shannon E.; Ambadan, Jaison Thomas; Gao, Xiaopeng; Tenuta, Mario

2017-01-01

Seasonal freezing induces large thaw emissions of nitrous oxide, a trace gas that contributes to stratospheric ozone destruction and atmospheric warming. Cropland soils are by far the largest anthropogenic source of nitrous oxide. However, the global contribution of seasonal freezing to nitrous

Mercury chloride-induced oxidative stress in human erythrocytes ...

African Journals Online (AJOL)

ONOS

2010-01-25

Jan 25, 2010 ... Mercury can exist in the environment as metal, as monovalent and divalent salts and as organomercurials, one of the most important of which is mercuric chloride (HgCl2). It has been shown to induce oxidative stress in erythrocytes through the generation of free radicals and alteration of the.

Cobalt-deficiency-induced hyperhomocysteinaemia and oxidative status of cattle.

Science.gov (United States)

Stangl, G I; Schwarz, F J; Jahn, B; Kirchgessner, M

2000-01-01

In ruminants, Co is required for the synthesis of vitamin B12, which in turn is needed for the resynthesis of methionine by methylation of homocysteine and thus, cobalamin deficiency may induce hyperhomocysteinaemia which is brought into context with perturbations of the antioxidative-prooxidative balance. The present study was conducted to explore whether Co deficiency in cattle is also associated with homocysteine-induced disturbances of oxidative status. Co deficiency was induced in cattle by feeding two groups of animals on either a basal maize-silage-based diet that was moderately low in Co (83 micrograms Co/kg DM), or the same diet supplemented with Co to a total of 200 micrograms Co/kg DM, for 43 weeks. Co deficiency was apparent from a reduced vitamin B12 status in serum and liver and an accumulation of homocysteine in plasma which was in excess of 4.8 times higher in Co-deprived cattle than in controls. The much increased level of circulating homocysteine did not indicate severe disturbances in antioxidant-prooxidant balance as measured by individual markers of lipid peroxidation, protein oxidation, and the antioxidative defence system. There were no quantitative difference in plasma thiol groups, nor were there significant changes in concentrations of alpha-tocopherol, microsomal thiobarbituric acid-reactive substances and carbonyl groups in liver. However, there was a trend toward increased plasma carbonyl levels indicating a slight degradation of plasma proteins in the hyperhomocysteinaemic cattle. Analysis of the hepatic catalase (EC 1.11.1.6) activity revealed an 11% reduction in Co-deficient cattle relative to the controls. These results indicate that long-term moderate Co deficiency may induce a severe accumulation of plasma homocysteine in cattle, but considerable abnormalities in oxidative status failed to appear.

Maltol, a Food Flavoring Agent, Attenuates Acute Alcohol-Induced Oxidative Damage in Mice

Directory of Open Access Journals (Sweden)

Ye Han

2015-01-01

Full Text Available The purpose of this study was to evaluate the hepatoprotective effect of maltol, a food-flavoring agent, on alcohol-induced acute oxidative damage in mice. Maltol used in this study was isolated from red ginseng (Panax ginseng C.A Meyer and analyzed by high performance liquid chromatography (HPLC and mass spectrometry. For hepatoprotective activity in vivo, pretreatment with maltol (12.5, 25 and 50 mg/kg; 15 days drastically prevented the elevated activities of aspartate transaminase (AST, alanine transaminase (ALT, alkaline phosphatase (ALP and triglyceride (TG in serum and the levels of malondialdehyde (MDA, tumor necrosis factor-α (TNF-α, interleukin-1β (IL-1β in liver tissue (p < 0.05. Meanwhile, the levels of hepatic antioxidant, such as catalase (CAT, superoxide dismutase (SOD, glutathione peroxidase (GSH-Px were elevated by maltol pretreatment, compared to the alcohol group (p < 0.05. Histopathological examination revealed that maltol pretreatment significantly inhibited alcohol-induced hepatocyte apoptosis and fatty degeneration. Interestingly, pretreatment of maltol effectively relieved alcohol-induced oxidative damage in a dose-dependent manner. Maltol appeared to possess promising anti-oxidative and anti-inflammatory capacities. It was suggested that the hepatoprotective effect exhibited by maltol on alcohol-induced liver oxidative injury may be due to its potent antioxidant properties.

Induction of hepatic carbonyl reductase/20β-hydroxysteroid dehydrogenase mRNA in rainbow trout downstream from sewage treatment works-Possible roles of aryl hydrocarbon receptor agonists and oxidative stress

International Nuclear Information System (INIS)

Albertsson, E.; Larsson, D.G.J.; Foerlin, L.

2010-01-01

Carbonyl reductase/20β-hydroxysteroid dehydrogenase (CR/20β-HSD) serves both as a key enzyme in the gonadal synthesis of maturing-inducing hormone in salmonids, and as an enzyme protecting against certain reactive oxygen species. We have previously shown that mRNA of the hepatic CR/20β-HSD B isoform is increased in rainbow trout caged downstream from a Swedish sewage treatment plant. Here, we report an increase of both the A as well as B form in fish kept downstream from a second sewage treatment plant. The two mRNAs were also induced in fish hepatoma cells in vitro after exposure to effluent extract. This indicates that the effects observed in vivo could be a direct effect on the liver, i.e. the mRNA induction does not require a signal from any other organ. When fish were exposed in vivo to several effluents treated with more advanced methods (ozone, moving bed biofilm reactor or membrane bioreactor) the expression of hepatic mRNA CR/20β-HSD A and B was significantly reduced. Their abundance did not parallel the reduction of estrogen-responsive transcripts, in agreement with our previous observations that ethinylestradiol is not a potent inducer. Treatment with norethisterone, methyltestosterone or hydrocortisone in vivo did not induce the hepatic CR/20β-HSD A and B mRNA expression. In contrast, both isoforms were markedly induced by the aryl hydrocarbon receptor agonist β-naphthoflavone as well as by the pro-oxidant herbicide paraquat. We hypothesize that the induction of CR/20β-HSD A and B by sewage effluents could be due to anthropogenic contaminants stimulating the aryl hydrocarbon receptor and/or causing oxidative stress.

Protective effect of taurine against potassium bromate-induced hemoglobin oxidation, oxidative stress, and impairment of antioxidant defense system in blood.

Science.gov (United States)

Ahmad, Mir Kaisar; Mahmood, Riaz

2016-03-01

Potassium bromate (KBrO3 ) is widely used as a food-additive and is a major water disinfection by-product. KBrO3 causes severe toxicity in humans and experimental animals. Bromate is considered a probable human carcinogen and a complete carcinogen in animals. We have investigated the potential role of taurine in protecting against KBrO3 -induced oxidative stress in rat blood. Animals were given taurine for 5 days prior to KBrO3 and then sacrificed. Blood was collected and used to prepare hemolysates and plasma, which were then used for the analysis of several biochemical parameters. Administration of single oral dose of KBrO3 alone induced hepato- and nephro-toxicity as evident by elevated marker levels in plasma. Lipid peroxidation and protein oxidation were increased both in plasma and erythrocytes, suggesting the induction of oxidative stress. KBrO3 increased methemoglobin, nitric oxide, and hydrogen peroxide levels. It also altered the activities of the major antioxidant enzymes and lowered the antioxidant power of blood. Administration of taurine, prior to treatment with KBrO3 , resulted in significant attenuation in all these parameters but the administration of taurine alone had no effect. These results show that taurine is effective in mitigating the oxidative insult induced in rat blood by KBrO3 . © 2014 Wiley Periodicals, Inc.

Palladium induced oxidative stress and cell death in normal ...

African Journals Online (AJOL)

Our findings clearly indicate that Pd induces reactive oxygen species (ROS) formation and oxidative stress, mitochondrial and lysosomal injury and finally cell death. These effects are reversed by antioxidants and ROS scavengers, mitochondrial permeability transmission [1] pore sealing agent, ATP progenitor, and ...

Role of reactive nitrogen species generated via inducible nitric oxide synthase in vesicant-induced lung injury, inflammation and altered lung functioning

Energy Technology Data Exchange (ETDEWEB)

Sunil, Vasanthi R., E-mail: sunilvr@eohsi.rutgers.edu [Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy Piscataway, NJ (United States); Shen, Jianliang; Patel-Vayas, Kinal; Gow, Andrew J. [Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy Piscataway, NJ (United States); Laskin, Jeffrey D. [Department of Environmental and Occupational Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway, NJ (United States); Laskin, Debra L. [Department of Pharmacology and Toxicology, Rutgers University, Ernest Mario School of Pharmacy Piscataway, NJ (United States)

2012-05-15

Pulmonary toxicity induced by sulfur mustard and related vesicants is associated with oxidative stress. In the present studies we analyzed the role of reactive nitrogen species (RNS) generated via inducible nitric oxide synthase (iNOS) in lung injury and inflammation induced by vesicants using 2-chloroethyl ethyl sulfide (CEES) as a model. C57Bl/6 (WT) and iNOS −/− mice were sacrificed 3 days or 14 days following intratracheal administration of CEES (6 mg/kg) or control. CEES intoxication resulted in transient (3 days) increases in bronchoalveolar lavage (BAL) cell and protein content in WT, but not iNOS −/− mice. This correlated with expression of Ym1, a marker of oxidative stress in alveolar macrophages and epithelial cells. In contrast, in iNOS −/− mice, Ym1 was only observed 14 days post-exposure in enlarged alveolar macrophages, suggesting that they are alternatively activated. This is supported by findings that lung tumor necrosis factor and lipocalin Lcn2 expression, mediators involved in tissue repair were also upregulated at this time in iNOS −/− mice. Conversely, CEES-induced increases in the proinflammatory genes, monocyte chemotactic protein-1 and cyclooxygenase-2, were abrogated in iNOS −/− mice. In WT mice, CEES treatment also resulted in increases in total lung resistance and decreases in compliance in response to methacholine, effects blunted by loss of iNOS. These data demonstrate that RNS, generated via iNOS play a role in the pathogenic responses to CEES, augmenting oxidative stress and inflammation and suppressing tissue repair. Elucidating inflammatory mechanisms mediating vesicant-induced lung injury is key to the development of therapeutics to treat mustard poisoning. -- Highlights: ► Lung injury, inflammation and oxidative stress are induced by the model vesicant CEES ► RNS generated via iNOS are important in the CEES-induced pulmonary toxicity ► iNOS −/− mice are protected from CEES-induced lung toxicity and

Uranium induces oxidative stress in lung epithelial cells

International Nuclear Information System (INIS)

Periyakaruppan, Adaikkappan; Kumar, Felix; Sarkar, Shubhashish; Sharma, Chidananda S.; Ramesh, Govindarajan T.

2007-01-01

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.)

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.

Oxidative stress inhibits adhesion and transendothelial migration, and induces apoptosis and senescence of induced pluripotent stem cells.

Science.gov (United States)

Wu, Yi; Zhang, Xueqing; Kang, Xueling; Li, Ning; Wang, Rong; Hu, Tiantian; Xiang, Meng; Wang, Xinhong; Yuan, Wenjun; Chen, Alex; Meng, Dan; Chen, Sifeng

2013-09-01

Oxidative stress caused by cellular accumulation of reactive oxygen species (ROS) is a major contributor to disease and cell death. However, how induced pluripotent stem cells (iPSC) respond to different levels of oxidative stress is largely unknown. Here, we investigated the effect of H2 O2 -induced oxidative stress on iPSC function in vitro. Mouse iPSC were treated with H2 O2 (25-100 μmol/L). IPSC adhesion, migration, viability, apoptosis and senescence were analysed. Expression of adhesion-related genes, stress defence genes, and osteoblast- and adipocyte-associated genes were determined by reverse transcription polymerase chain reaction. The present study found that H2 O2 (25-100 μmol/L) decreased iPSC adhesion to matrix proteins and endothelial cells, and downregulated gene expression levels of adhesion-related molecules, such as integrin alpha 7, cadherin 1 and 5, melanoma cell adhesion molecule, vascular cell adhesion molecule 1, and monocyte chemoattractant protein-1. H2 O2 (100 μmol/L) decreased iPSC viability and inhibited the capacity of iPSC migration and transendothelial migration. iPSC were sensitive to H2 O2 -induced G2/M arrest, senescence and apoptosis when exposed to H2 O2 at concentrations above 25 μmol/L. H2 O2 increased the expression of stress defence genes, including catalase, cytochrome B alpha, lactoperoxidase and thioredoxin domain containing 2. H2 O2 upregulated the expression of osteoblast- and adipocyte-associated genes in iPSC during their differentiation; however, short-term H2 O2 -induced oxidative stress did not affect the protein expression of the pluripotency markers, octamer-binding transcription factor 4 and sex-determining region Y-box 2. The present results suggest that iPSC are sensitive to H2 O2 toxicity, and inhibition of oxidative stress might be a strategy for improving their functions. © 2013 Wiley Publishing Asia Pty Ltd.

Thiamine deficiency induces endoplasmic reticulum stress and oxidative stress in human neurons derived from induced pluripotent stem cells.

Science.gov (United States)

Wang, Xin; Xu, Mei; Frank, Jacqueline A; Ke, Zun-Ji; Luo, Jia

2017-04-01

Thiamine (vitamin B1) deficiency (TD) plays a major role in the etiology of Wernicke's encephalopathy (WE) which is a severe neurological disorder. TD induces selective neuronal cell death, neuroinflammation, endoplasmic reticulum (ER) stress and oxidative stress in the brain which are commonly observed in many aging-related neurodegenerative diseases, such as Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD) and progressive supranuclear palsy (PSP). However, the underlying cellular and molecular mechanisms remain unclear. The progress in this line of research is hindered due to the lack of appropriate in vitro models. The neurons derived for the human induced pluripotent stem cells (hiPSCs) provide a relevant and powerful tool for the research in pharmaceutical and environmental neurotoxicity. In this study, we for the first time used human induced pluripotent stem cells (hiPSCs)-derived neurons (iCell neurons) to investigate the mechanisms of TD-induced neurodegeneration. We showed that TD caused a concentration- and duration-dependent death of iCell neurons. TD induced ER stress which was evident by the increase in ER stress markers, such as GRP78, XBP-1, CHOP, ATF-6, phosphorylated eIF2α, and cleaved caspase-12. TD also triggered oxidative stress which was shown by the increase in the expression 2,4-dinitrophenyl (DNP) and 4-hydroxynonenal (HNE). ER stress inhibitors (STF-083010 and salubrinal) and antioxidant N-acetyl cysteine (NAC) were effective in alleviating TD-induced death of iCell neurons, supporting the involvement of ER stress and oxidative stress. It establishes that the iCell neurons are a novel tool to investigate cellular and molecular mechanisms for TD-induced neurodegeneration. Copyright © 2017 Elsevier Inc. All rights reserved.

Neuronal nitric oxide synthase mediates insulin- and oxidative stress-induced glucose uptake in skeletal muscle myotubes.

Science.gov (United States)

Kellogg, Dean L; McCammon, Karen M; Hinchee-Rodriguez, Kathryn S; Adamo, Martin L; Roman, Linda J

2017-09-01

Previously published studies strongly suggested that insulin- and exercise-induced skeletal muscle glucose uptake require nitric oxide (NO) production. However, the signal transduction mechanisms by which insulin and contraction regulated NO production and subsequent glucose transport are not known. In the present study, we utilized the myotube cell lines treated with insulin or hydrogen peroxide, the latter to mimic contraction-induced oxidative stress, to characterize these mechanisms. We found that insulin stimulation of neuronal nitric oxide synthase (nNOS) phosphorylation, NO production, and GLUT4 translocation were all significantly reduced by inhibition of either nNOS or Akt2. Hydrogen peroxide (H 2 O 2 ) induced phosphorylation of nNOS at the same residue as did insulin, and also stimulated NO production and GLUT4 translocation. nNOS inhibition prevented H 2 O 2 -induced GLUT4 translocation. AMP activated protein kinase (AMPK) inhibition prevented H 2 O 2 activation and phosphorylation of nNOS, leading to reduced NO production and significantly attenuated GLUT4 translocation. We conclude that nNOS phosphorylation and subsequently increased NO production are required for both insulin- and H 2 O 2 -stimulated glucose transport. Although the two stimuli result in phosphorylation of the same residue on nNOS, they do so through distinct protein kinases. Thus, insulin and H 2 O 2 -activated signaling pathways converge on nNOS, which is a common mediator of glucose uptake in both pathways. However, the fact that different kinases are utilized provides a basis for the use of exercise to activate glucose transport in the face of insulin resistance. Copyright © 2017. Published by Elsevier Inc.

The NADPH oxidase inhibitor apocynin induces nitric oxide synthesis via oxidative stress

International Nuclear Information System (INIS)

Riganti, Chiara; Costamagna, Costanzo; Doublier, Sophie; Miraglia, Erica; Polimeni, Manuela; Bosia, Amalia; Ghigo, Dario

2008-01-01

We have recently shown that apocynin elicits an oxidative stress in N11 mouse glial cells and other cell types. Here we report that apocynin increased the accumulation of nitrite, the stable derivative of nitric oxide (NO), in the extracellular medium of N11 cell cultures, and the NO synthase (NOS) activity in cell lysates. The increased synthesis of NO was associated with increased expression of inducible NOS (iNOS) mRNA, increased nuclear translocation of the redox-sensitive transcription factor NF-κB and decreased intracellular level of its inhibitor IkBα. These effects, accompanied by increased production of H 2 O 2 , were very similar to those observed after incubation with bacterial lipopolysaccharide (LPS) and were inhibited by catalase. These results suggest that apocynin, similarly to LPS, induces increased NO synthesis by eliciting a generation of reactive oxygen species (ROS), which in turn causes NF-κB activation and increased expression of iNOS. Therefore, the increased bioavailability of NO reported in the literature after in vivo or in vitro treatments with apocynin might depend, at least partly, on the drug-elicited induction of iNOS, and not only on the inhibition of NADPH oxidase and the subsequent decreased scavenging of NO by oxidase-derived ROS, as it is often supposed

Melatonin resists oxidative stress-induced apoptosis in nucleus pulposus cells.

Science.gov (United States)

He, Ruijun; Cui, Min; Lin, Hui; Zhao, Lei; Wang, Jiayu; Chen, Songfeng; Shao, Zengwu

2018-04-15

Intervertebral disc degeneration (IVDD) is thought to be the major cause of low back pain (LBP), which is still in lack of effective etiological treatment. Oxidative stress has been demonstrated to participate in the impairment of nucleus pulposus cells (NPCs). As the most important neuroendocrine hormone in biological clock regulation, melatonin (MLT) is also featured by good antioxidant effect. In this study, we investigated the effect and mechanisms of melatonin on oxidative stress-induced damage in rat NPCs. Cytotoxicity of H 2 O 2 and protecting effect of melatonin were analyzed with Cell Counting kit-8 (CCK-8). Cell apoptosis rate was detected by Annexin V-FITC/PI staining. DCFH-DA probe was used for the reactive oxygen species (ROS) detection. The mitochondrial membrane potential (MMP) changes were analyzed with JC-1 probe. Intracellular oxidation product and reductants were measured through enzymatic reactions. Extracellular matrix (ECM) and apoptosis associated proteins were analyzed with Western blot assays. Melatonin preserved cell viability of NPCs under oxidative stress. The apoptosis rate, ROS level and malonaldehyde (MDA) declined with melatonin. MLT/H 2 O 2 group showed higher activities of GSH and SOD. The fall of MMP receded and the expression of ECM protein increased with treatment of melatonin. The mitochondrial pathway of apoptosis was inhibited by melatonin. Melatonin alleviated the oxidative stress-induced apoptosis of NPCs. Melatonin could be a promising alternative in treatment of IVDD. Copyright © 2018 Elsevier Inc. All rights reserved.

DISTINCT FUNCTIONS OF JNK AND C-JUN IN OXIDANT-INDUCED HEPATOCYTE DEATH

Science.gov (United States)

Amir, Muhammad; Liu, Kun; Zhao, Enpeng; Czaja, Mark J.

2013-01-01

Overactivation of c-Jun N-terminal kinase (JNK)/c-Jun signaling is a central mechanism of hepatocyte injury and death including that from oxidative stress. However, the functions of JNK and c-Jun are still unclear, and this pathway also inhibits hepatocyte death. Previous studies of menadione-induced oxidant stress demonstrated that toxicity resulted from sustained JNK/c-Jun activation as death was blocked by the c-Jun dominant negative TAM67. To further delineate the function of JNK/c-Jun signaling in hepatocyte injury from oxidant stress, the effects of direct JNK inhibition on menadione-induced death were examined. In contrast to the inhibitory effect of TAM67, pharmacological JNK inhibition by SP600125 sensitized the rat hepatocyte cell line RALA255-10G to death from menadione. SP600125 similarly sensitized mouse primary hepatocytes to menadione toxicity. Death from SP600125/menadione was c-Jun dependent as it was blocked by TAM67, but independent of c-Jun phosphorylation. Death occurred by apoptosis and necrosis and activation of the mitochondrial death pathway. Short hairpin RNA knockdowns of total JNK or JNK2 sensitized to death from menadione, whereas a jnk1 knockdown was protective. Jnk2 null mouse primary hepatocytes were also sensitized to menadione death. JNK inhibition magnified decreases in cellular ATP content and β-oxidation induced by menadione. This effect mediated cell death as chemical inhibition of β-oxidation also sensitized cells to death from menadione, and supplementation with the β-oxidation substrate oleate blocked death. Components of the JNK/c-Jun signaling pathway have opposing functions in hepatocyte oxidant stress with JNK2 mediating resistance to cell death and c-Jun promoting death. PMID:22644775

Radiation-induced cationic polymerization of limonene oxide, α-pinene oxide, and β-pinene oxide

International Nuclear Information System (INIS)

Aikins, J.A.; Williams, F.

1985-01-01

After suitable drying, the subject monomers in the form of neat liquids undergo radiation-induced polymerization with no apparent side reactions and high conversions to precipitatable polymers of low molecular weights. A high frequency of chain (proton) transfer to monomer is indicated by the fact that the kinetic chain lengths are estimated to be several hundred times larger than the range of DP/sub n/ values (12-4). Structural characterization of the limonene oxide polymer by 1 H and 13 C NMR spectroscopy provides conclusive evidence that the polymerization proceeds by the opening of the epoxide ring to yield a 1,2-trans polyether. Similar NMR studies on the polymers formed from the α-pinene and β-pinene oxides show that the opening of the epoxide ring for these monomers is generally accompanied by the concomitant ring opening of the cyclobutane ring structure to yield a gem-di-methyl group in the main chain

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.

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.

Mercury-induced oxidative stress in Indian mustard (Brassica juncea L.).

Science.gov (United States)

Shiyab, Safwan; Chen, Jian; Han, Fengxiang X; Monts, David L; Matta, Fank B; Gu, Mengmeng; Su, Yi; Masad, Motasim A

2009-10-01

Mercury, a potent neurotoxin, is released to the environment in significant amounts by both natural processes and anthropogenic activities. No natural hyperaccumulator plant has been reported for mercury phytoremediation. Few studies have been conducted on the physiological responses of Indian mustard, a higher biomass plant with faster growth rates, to mercury pollution. This study investigated the phytotoxicity of mercury to Indian mustard (Brassica juncea L.) and mercury-induced oxidative stress in order to examine the potential application of Indian mustard to mercury phytoremediation. Two common cultivars (Florida Broadleaf and Longstanding) of Indian mustard were grown hydroponically in a mercury-spiked solution. Plant uptake, antioxidative enzymes, peroxides, and lipid peroxidation under mercury stress were investigated. Antioxidant enzymes (catalase, CAT; peroxidase, POD; and superoxide dismutase, SOD) were the most sensitive indices of mercury-induced oxidative response of Indian mustard plants. Indian mustard effectively generated an enzymatic antioxidant defense system (especially CAT) to scavenge H(2)O(2), resulting in lower H(2)O(2) in shoots with higher mercury concentrations. These two cultivars of Indian mustard demonstrated an efficient metabolic defense and adaptation system to mercury-induced oxidative stress. A majority of Hg was accumulated in the roots and low translocations of Hg from roots to shoots were found in two cultivars of Indian mustard. Thus Indian mustard might be a potential candidate plant for phytofiltration/phytostabilization of mercury contaminated waters and wastewater.

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.

Anesthetic-Induced Oxidative Stress and Potential Protection

Directory of Open Access Journals (Sweden)

Cheng Wang

2010-01-01

Full Text Available Prolonged exposure of developing mammals to general anesthetics affects the N-methyl-D-aspartate (NMDA–type glutamate or γ-aminobutyric acid (GABA receptor systems and enhances neuronal toxicity. Stimulation of immature neurons by NMDA antagonists or GABA agonists is thought to increase overall nervous system excitability and may contribute to abnormal neuronal cell death during development. Although the precise mechanisms by which NMDA antagonists or GABA agonists cause neuronal cell death are still not completely understood, up-regulation of the NMDA receptor subunit NR1 may be an initiative factor in neuronal cell death. It is increasingly apparent that mitochondria lie at the center of the cell death regulation process. Evidence for the role of oxidative stress in anesthetic-induced neurotoxicity has been generated in studies that apply oxidative stress blockers. Prevention of neuronal death by catalase and superoxide dismutase in vitro, or by M40403 (superoxide dismutase mimetic in vivo, supports the contention that the involvement of reactive oxygen species (ROS and the nature of neuronal cell death in rodents is mainly apoptotic. However, more evidence is necessary to in order verify the role of the NMDA receptor subunit NR1 and ROS in anesthetic-induced neurodegeneration.

Chlorpyrifos induces oxidative stress in oligodendrocyte progenitor cells

International Nuclear Information System (INIS)

Saulsbury, Marilyn D.; Heyliger, Simone O.; Wang, Kaiyu; Johnson, Deadre J.

2009-01-01

There are increasing concerns regarding the relative safety of chlorpyrifos (CPF) to various facets of the environment. Although published works suggest that CPF is relatively safe in adult animals, recent evidence indicates that juveniles, both animals and humans, may be more sensitive to CPF toxicity than adults. In young animals, CPF is neurotoxic and mechanistically interferes with cellular replication and cellular differentiation, which culminates in the alteration of synaptic neurotransmission in neurons. However, the effects of CPF on glial cells are not fully elucidated. Here we report that chlorpyrifos is toxic to oligodendrocyte progenitors. In addition, CPF produced dose-dependent increases in 2',7'-dichlorodihydrofluorescein diacetate (H 2 DCF-DA) and dihydroethidium (DHE) fluorescence intensities relative to the vehicle control. Moreover, CPF toxicity is associated with nuclear condensation and elevation of caspase 3/7 activity and Heme oxygenase-1 mRNA expression. Pan-caspase inhibitor QVDOPh and cholinergic receptor antagonists' atropine and mecamylamine failed to protect oligodendrocyte progenitors from CPF-induced injury. Finally, glutathione (GSH) depletion enhanced CPF-induced toxicity whereas nitric oxide synthetase inhibitor L-NAME partially protected progenitors and the non-specific antioxidant vitamin E (alpha-tocopherol) completely spared cells from injury. Collectively, this data suggests that CPF induced toxicity is independent of cholinergic stimulation and is most likely caused by the induction of oxidative stress.

Morphology and phase structures of CW laser-induced oxide layers on iron surface with evolving reflectivity and colors

Energy Technology Data Exchange (ETDEWEB)

Wu, Taotao, E-mail: wutaotao@nint.ac.cn; Wang, Lijun; Wei, Chenghua; Zhou, Menglian; He, Minbo; Wu, Lixiong

2016-11-30

Highlights: • Firstly, iron samples with different color features were obtained by continuous wave laser irradiation depending on progressive durations. The real-time reflectivity and temperature of samples were measured. The color and the reflectivity evolution were related. They were both caused by the forming oxide films. • Secondly, laser-induced oxidation process of iron was studied by microscope, X-ray diffraction and Raman spectrum. The first formed magnetite made the surface reflectivity decline rapidly and caused the “positive feedback” effect because of molecular absorption. The later formed hematite oscillated the reflectivity by interference effect. • Lastly, the laser-induced oxide films were thin, orientated and badly crystallized. The Wagner oxidation theory was incapable of describing the non-isothermal and early stage oxidation process. So we emphasized that a precise oxidation model depending on the experiment and the optical constants of the laser-induced oxides must be studied. - Abstract: Laser-induced oxidation will change the laser reflectivity and color features of metal surface. Both changes can be theoretically calculated based on the oxidation kinetics and the optical constants of oxides. For the purpose of calculation, the laser-induced oxidation process of pure polycrystalline iron was studied. Samples with various color features were obtained by continuous wave Nd:YAG fiber laser (1.06 μm) irradiation depending on progressive durations in the intensity of 1.90 W/cm{sup 2}. The real-time reflectivity and temperature were measured with integral sphere and thermocouples. The irradiated surface morphology and phase structures were characterized by microscope, X-ray diffraction and Raman spectrum. It was found that the first formed magnetite made the surface reflectivity decline rapidly and caused the “positive feedback” effect because of molecular absorption. The later formed hematite oscillated the reflectivity by

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.

Requirement of the inducible nitric oxide synthase pathway for IL-1-induced osteoclastic bone resorption

OpenAIRE

van't Hof, R. J.; Armour, K. J.; Smith, L. M.; Armour, K. E.; Wei, X. Q.; Liew, F. Y.; Ralston, S. H.

2000-01-01

Nitric oxide has been suggested to be involved in the regulation of bone turnover, especially in pathological conditions characterized by release of bone-resorbing cytokines. The cytokine IL-1 is thought to act as a mediator of periarticular bone loss and tissue damage in inflammatory diseases such as rheumatoid arthritis. IL-1 is a potent stimulator of both osteoclastic bone resorption and expression of inducible nitric oxide synthase (iNOS) in bone cells and other cell types. In this study,...

Multidisciplinary research program directed toward utilization of solar energy through bioconversion of renewable resources. Progress report

Energy Technology Data Exchange (ETDEWEB)

Finnerty, W. R.

1976-07-01

Progress is reported in four research areas of solar bioconversion. The first program deals with the genetic selection of superior trees, physiological basis of vigor, tissue culture, haploid cell lines, and somatic hybridization. The second deals with the physiology of paraquat-induced oleoresin biogenesis. Separate abstracts were prepared for the other two program areas: biochemical basis of paraquat-induced oleoresin production in pines and biochemistry of methanogenesis. (JSR)

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. Copyright © 2016. Published by Elsevier Masson SAS.

Hesperidin, a citrus bioflavonoid, alleviates trichloroethylene-induced oxidative stress in Drosophila melanogaster.

Science.gov (United States)

Abolaji, Amos Olalekan; Babalola, Oluwatoyin Victoria; Adegoke, Abimbola Kehinde; Farombi, Ebenezer Olatunde

2017-10-01

Trichloroethylene (TCE) is a chlorinated organic pollutant of groundwater with diverse toxic effects in animals and humans. Here, we investigated the ameliorative role of hesperidin, a citrus bioflavonoid on TCE-induced toxicity in Drosophila melanogaster. Four groups of D. melanogaster (50 flies/vial, with 5 vials/group) were exposed to ethanol (2.5%, control), HSP (400mg/10g diet), TCE (10μM/10g diet) and TCE (10μM/10g diet)+HSP (400mg/10g diet) respectively in the diet for 5days. Then, selected oxidative stress and antioxidant markers were evaluated. The results showed that TCE significantly increased the level of reactive oxygen species (ROS) and inhibited catalase, glutathione S-transferase and acetylcholinesterase (AChE) activities with concurrent depletion of total thiol level. However, co-administration of TCE and hesperidin mitigated TCE-induced depletion of antioxidants, and restored ROS level and AChE activity in the flies (p<0.05). Overall, hesperidin offered protective potency on TCE-induced oxidative stress in the flies via anti-oxidative mechanism. Copyright © 2017 Elsevier B.V. All rights reserved.

Hydrogen-peroxide-induced oxidative stress responses in Desulfovibrio vulgaris Hildenborough

Energy Technology Data Exchange (ETDEWEB)

Zhou, A.; He, Z.; Redding-Johanson, A.M.; Mukhopadhyay, A.; Hemme, C.L.; Joachimiak, M.P.; Bender, K.S.; Keasling, J.D.; Stahl, D.A.; Fields, M.W.; Hazen, T.C.; Arkin, A.P.; Wall, J.D.; Zhou, J.; Luo, F.; Deng, Y.; He, Q.

2010-07-01

To understand how sulphate-reducing bacteria respond to oxidative stresses, the responses of Desulfovibrio vulgaris Hildenborough to H{sub 2}O{sub 2}-induced stresses were investigated with transcriptomic, proteomic and genetic approaches. H{sub 2}O{sub 2} and induced chemical species (e.g. polysulfide, ROS) and redox potential shift increased the expressions of the genes involved in detoxification, thioredoxin-dependent reduction system, protein and DNA repair, and decreased those involved in sulfate reduction, lactate oxidation and protein synthesis. A gene coexpression network analysis revealed complicated network interactions among differentially expressed genes, and suggested possible importance of several hypothetical genes in H{sub 2}O{sub 2} stress. Also, most of the genes in PerR and Fur regulons were highly induced, and the abundance of a Fur regulon protein increased. Mutant analysis suggested that PerR and Fur are functionally overlapped in response to stresses induced by H{sub 2}O{sub 2} and reaction products, and the upregulation of thioredoxin-dependent reduction genes was independent of PerR or Fur. It appears that induction of those stress response genes could contribute to the increased resistance of deletion mutants to H{sub 2}O{sub 2}-induced stresses. In addition, a conceptual cellular model of D. vulgaris responses to H{sub 2}O{sub 2} stress was constructed to illustrate that this bacterium may employ a complicated molecular mechanism to defend against the H{sub 2}O{sub 2}-induced stresses.

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.

Schisandrin B protects against solar irradiation-induced oxidative injury in BJ human fibroblasts.

Science.gov (United States)

Chiu, Po Yee; Lam, Philip Y; Yan, Chung Wai; Ko, Kam Ming

2011-06-01

The effects of schisandrin B (Sch B) and its analogs on solar irradiation-induced oxidative injury were examined in BJ human fibroblasts. Sch B and schisandrin C (Sch C) increased cellular reduced glutathione (GSH) level and protected against solar irradiation-induced oxidative injury. The photoprotection was paralleled by decreases in the elastases-type protease activity and matrix-metalloproteinases-1 expression in solar-irradiated fibroblasts. The cytochrome P-450-mediated metabolism of Sch B or Sch C caused ROS production. The results suggest that by virtue of its pro-oxidant action and the subsequent glutathione antioxidant response, Sch B or Sch C may offer the prospect of preventing skin photo-aging. Copyright © 2011 Elsevier B.V. All rights reserved.

Requirement of the inducible nitric oxide synthase pathway for IL-1-induced osteoclastic bone resorption.

Science.gov (United States)

van't Hof, R J; Armour, K J; Smith, L M; Armour, K E; Wei, X Q; Liew, F Y; Ralston, S H

2000-07-05

Nitric oxide has been suggested to be involved in the regulation of bone turnover, especially in pathological conditions characterized by release of bone-resorbing cytokines. The cytokine IL-1 is thought to act as a mediator of periarticular bone loss and tissue damage in inflammatory diseases such as rheumatoid arthritis. IL-1 is a potent stimulator of both osteoclastic bone resorption and expression of inducible nitric oxide synthase (iNOS) in bone cells and other cell types. In this study, we investigated the role that the iNOS pathway plays in mediating the bone-resorbing effects of IL-1 by studying mice with targeted disruption of the iNOS gene. Studies in vitro and in vivo showed that iNOS-deficient mice exhibited profound defects of IL-1-induced osteoclastic bone resorption but responded normally to calciotropic hormones such as 1,25 dihydroxyvitamin D3 and parathyroid hormone. Immunohistochemical studies and electrophoretic mobility shift assays performed on bone marrow cocultures from iNOS-deficient mice showed abnormalities in IL-1-induced nuclear translocation of the p65 component of NFkappaB and in NFkappaB-DNA binding, which were reversed by treatment with the NO donor S-nitroso-acetyl penicillamine. These results show that the iNOS pathway is essential for IL-1-induced bone resorption and suggest that the effects of NO may be mediated by modulating IL-1-induced nuclear activation of NFkappaB in osteoclast precursors.

Requirement of the inducible nitric oxide synthase pathway for IL-1-induced osteoclastic bone resorption

Science.gov (United States)

van't Hof, R. J.; Armour, K. J.; Smith, L. M.; Armour, K. E.; Wei, X. Q.; Liew, F. Y.; Ralston, S. H.

2000-01-01

Nitric oxide has been suggested to be involved in the regulation of bone turnover, especially in pathological conditions characterized by release of bone-resorbing cytokines. The cytokine IL-1 is thought to act as a mediator of periarticular bone loss and tissue damage in inflammatory diseases such as rheumatoid arthritis. IL-1 is a potent stimulator of both osteoclastic bone resorption and expression of inducible nitric oxide synthase (iNOS) in bone cells and other cell types. In this study, we investigated the role that the iNOS pathway plays in mediating the bone-resorbing effects of IL-1 by studying mice with targeted disruption of the iNOS gene. Studies in vitro and in vivo showed that iNOS-deficient mice exhibited profound defects of IL-1-induced osteoclastic bone resorption but responded normally to calciotropic hormones such as 1,25 dihydroxyvitamin D3 and parathyroid hormone. Immunohistochemical studies and electrophoretic mobility shift assays performed on bone marrow cocultures from iNOS-deficient mice showed abnormalities in IL-1-induced nuclear translocation of the p65 component of NFκB and in NFκB-DNA binding, which were reversed by treatment with the NO donor S-nitroso-acetyl penicillamine. These results show that the iNOS pathway is essential for IL-1-induced bone resorption and suggest that the effects of NO may be mediated by modulating IL-1-induced nuclear activation of NFκB in osteoclast precursors. PMID:10869429

Oxidation induced crack healing of Cr2(Al,Si)C max phase ceramic

NARCIS (Netherlands)

Shen, L.; Li, S.B.; Van der Zwaag, S.; Sloof, W.G.

2013-01-01

The oxidation crack healing of Cr2AlC and Cr2(Al,Si)C was studied and compared with known healing of Ti2AlC. The oxidation induced crack healing of Ti2AlC is relatively fast and leads to full strength recovery, but the oxidation product contains besides ?-Al2O3 also undesired TiO2. However, when

Effects of curcumin on angiotensin-converting enzyme gene expression, oxidative stress and anti-oxidant status in thioacetamide-induced hepatotoxicity.

Science.gov (United States)

Fazal, Yumna; Fatima, Syeda Nuzhat; Shahid, Syed Muhammad; Mahboob, Tabassum

2015-12-01

This study aimed to evaluate the protective effects of curcumin on angiotensin-converting enzyme (ACE) gene expression, oxidative stress and anti-oxidant status in thioacetamide (TAA)-induced hepatotoxicity in rats. Total 32 albino Wistar rats (male, 200-250 g) were divided into six groups (n=8). Group 1: untreated controls; Group 2: received TAA (200 mg/kg body weight (b.w.); i.p.) for 12 weeks; Group 3: received curcumin (75 mg/kg b.w.) for 24 weeks; Group 4: received TAA (200 mg/kg b.w.; i.p.) for 12 weeks+curcumin (75 mg/kg b.w.) for 12 weeks. A significantly higher ACE gene expression was observed in TAA-induced groups as compared with control, indicating more synthesis of ACE proteins. Treatment with curcumin suppressed ACE expression in TAA liver and reversed the toxicity produced. TAA treatment results in higher lipid peroxidation and lower GSH, SOD and CAT than the normal, and this produces oxidative stress in the liver. Cirrhotic conditions were confirmed by serum enzymes (ALT, AST and ALP) as well as histopathological observations. Curcumin treatment reduced oxidative stress in animals by scavenging reactive oxygen species, protecting the anti-oxidant enzymes from being denatured and reducing the oxidative stress marker lipid peroxidation. Curcumin treatment restores hepatocytes, damaged by TAA, and protects liver tissue approaching cirrhosis. © The Author(s) 2014.

Ethylene signalling is mediating the early cadmium-induced oxidative challenge in Arabidopsis thaliana.

Science.gov (United States)

Schellingen, Kerim; Van Der Straeten, Dominique; Remans, Tony; Vangronsveld, Jaco; Keunen, Els; Cuypers, Ann

2015-10-01

Cadmium (Cd) induces the generation of reactive oxygen species (ROS) and stimulates ethylene biosynthesis. The phytohormone ethylene is a regulator of many developmental and physiological plant processes as well as stress responses. Previous research indicated various links between ethylene signalling and oxidative stress. Our results support a correlation between the Cd-induced oxidative challenge and ethylene signalling in Arabidopsis thaliana leaves. The effects of 24 or 72 h exposure to 5 μM Cd on plant growth and several oxidative stress-related parameters were compared between wild-type (WT) and ethylene insensitive mutants (etr1-1, ein2-1, ein3-1). Cadmium-induced responses observed in WT plants were mainly affected in etr1-1 and ein2-1 mutants, of which the growth was less inhibited by Cd exposure as compared to WT and ein3-1 mutants. Both etr1-1 and ein2-1 showed a delayed response in the glutathione (GSH) metabolism, including GSH levels and transcript levels of GSH synthesising and recycling enzymes. Furthermore, the expression of different oxidative stress marker genes was significantly lower in Cd-exposed ein2-1 mutants, evidencing that ethylene signalling is involved in early responses to Cd stress. A model for the cross-talk between ethylene signalling and oxidative stress is proposed. Copyright © 2015 Elsevier Ireland Ltd. All rights reserved.

Autophagy induction by SIRT6 is involved in oxidative stress-induced neuronal damage

Directory of Open Access Journals (Sweden)

Jiaxiang Shao

2016-03-01

Full Text Available Abstract SIRT6 is a NAD+-dependent histone deacetylase and has been implicated in the regulation of genomic stability, DNA repair, metabolic homeostasis and several diseases. The effect of SIRT6 in cerebral ischemia and oxygen/glucose deprivation (OGD has been reported, however the role of SIRT6 in oxidative stress damage remains unclear. Here we used SH-SY5Y neuronal cells and found that overexpression of SIRT6 led to decreased cell viability and increased necrotic cell death and reactive oxygen species (ROS production under oxidative stress. Mechanistic study revealed that SIRT6 induced autophagy via attenuation of AKT signaling and treatment with autophagy inhibitor 3-MA or knockdown of autophagy-related protein Atg5 rescued H2O2-induced neuronal injury. Conversely, SIRT6 inhibition suppressed autophagy and reduced oxidative stress-induced neuronal damage. These results suggest that SIRT6 might be a potential therapeutic target for neuroprotection.

Loss of Hepatic Mitochondrial Long-Chain Fatty Acid Oxidation Confers Resistance to Diet-Induced Obesity and Glucose Intolerance

Directory of Open Access Journals (Sweden)

Jieun Lee

2017-07-01

Full Text Available The liver has a large capacity for mitochondrial fatty acid β-oxidation, which is critical for systemic metabolic adaptations such as gluconeogenesis and ketogenesis. To understand the role of hepatic fatty acid oxidation in response to a chronic high-fat diet (HFD, we generated mice with a liver-specific deficiency of mitochondrial long-chain fatty acid β-oxidation (Cpt2L−/− mice. Paradoxically, Cpt2L−/− mice were resistant to HFD-induced obesity and glucose intolerance with an absence of liver damage, although they exhibited serum dyslipidemia, hepatic oxidative stress, and systemic carnitine deficiency. Feeding an HFD induced hepatokines in mice, with a loss of hepatic fatty acid oxidation that enhanced systemic energy expenditure and suppressed adiposity. Additionally, the suppression in hepatic gluconeogenesis was sufficient to improve HFD-induced glucose intolerance. These data show that inhibiting hepatic fatty acid oxidation results in a systemic hormetic response that protects mice from HFD-induced obesity and glucose intolerance.

Mechanism of pyrogallol red oxidation induced by free radicals and reactive oxidant species. A kinetic and spectroelectrochemistry study.

Science.gov (United States)

Atala, E; Velásquez, G; Vergara, C; Mardones, C; Reyes, J; Tapia, R A; Quina, F; Mendes, M A; Speisky, H; Lissi, E; Ureta-Zañartu, M S; Aspée, A; López-Alarcón, C

2013-05-02

Pyrogallol red (PGR) presents high reactivity toward reactive (radical and nonradical) species (RS). This property of PGR, together with its characteristic spectroscopic absorption in the visible region, has allowed developing methodologies aimed at evaluating the antioxidant capacity of foods, beverages, and human fluids. These methods are based on the evaluation of the consumption of PGR induced by RS and its inhibition by antioxidants. However, at present, there are no reports regarding the degradation mechanism of PGR, limiting the extrapolation to how antioxidants behave in different systems comprising different RS. In the present study, we evaluate the kinetics of PGR consumption promoted by different RS (peroxyl radicals, peroxynitrite, nitrogen dioxide, and hypochlorite) using spectroscopic techniques and detection of product by HPLC mass spectrometry. The same pattern of oxidation and spectroscopic properties of the products is observed, independently of the RS employed. Mass analysis indicates the formation of only one product identified as a quinone derivative, excluding the formation of peroxides or hydroperoxides and/or chlorinated compounds, in agreement with FOX's assays and oxygen consumption experiments. Cyclic voltammetry, carried out at different pH's, shows an irreversible oxidation of PGR, indicating the initial formation of a phenoxy radical and a second charge transfer reaction generating an ortho-quinone derivative. Spectroelectrochemical oxidation of PGR shows oxidation products with identical UV-visible absorption properties to those observed in RS-induced oxidation.

Use of Saliva Biomarkers to Monitor Efficacy of Vitamin C in Exercise-Induced Oxidative Stress

Directory of Open Access Journals (Sweden)

Levi W. Evans

2017-01-01

Full Text Available Saliva is easily obtainable for medical research and requires little effort or training for collection. Because saliva contains a variety of biological compounds, including vitamin C, malondialdehyde, amylase, and proteomes, it has been successfully used as a biospecimen for the reflection of health status. A popular topic of discussion in medical research is the potential association between oxidative stress and negative outcomes. Systemic biomarkers that represent oxidative stress can be found in saliva. It is unclear, however, if saliva is an accurate biospecimen as is blood and/or plasma. Exercise can induce oxidative stress, resulting in a trend of antioxidant supplementation to combat its assumed detriments. Vitamin C is a popular antioxidant supplement in the realm of sports and exercise. One potential avenue for evaluating exercise induced oxidative stress is through assessment of biomarkers like vitamin C and malondialdehyde in saliva. At present, limited research has been done in this area. The current state of research involving exercise-induced oxidative stress, salivary biomarkers, and vitamin C supplementation is reviewed in this article.

Protective Effects of Alkaloid Compounds from Nelumbinis Plumula on tert-Butyl Hydroperoxide-Induced Oxidative Stress

Directory of Open Access Journals (Sweden)

Ze-Bin Guo

2013-08-01

Full Text Available This study was conducted to investigate the effect of Nelumbinis Plumula total alkaloid (NPA and its main alkaloid components on oxidative stress induced by tert-butyl hydroperoxide (t-BHP in the human hepatocellular HepG2 cell line. According to HPLC analysis, several major alkaloid compounds such as liensinine, isoliensinine and neferine were present in NPA. The cytotoxic effects in 0.55 mM t-BHP-induced HepG2 cells were significantly inhibited by NPA and the major compound in NPA, neferine, showed the strongest activities. The protective effect of neferine against oxidative stress induced by t-BHP may be associated with decreased ROS formation, TBARS generation, LDH release and increased GSH levels, suggesting their involvement of the cytoprotective on oxidative stress. The effects were comparable with quercetin, which was used as positive control. Overall, total alkaloid and alkaloid compounds from Nelumbinis Plumula displayed a significant cytoprotective effect against oxidative stress. Further study is needed to elucidate the relationship between the chemical structures of the components in NPA and their protective effect on oxidative stress.

Training-induced adaptation of oxidative phosphorylation in skeletal muscles.

Science.gov (United States)

Korzeniewski, Bernard; Zoladz, Jerzy A

2003-08-15

Muscle training/conditioning improves the adaptation of oxidative phosphorylation in skeletal muscles to physical exercise. However, the mechanisms underlying this adaptation are still not understood fully. By quantitative analysis of the existing experimental results, we show that training-induced acceleration of oxygen-uptake kinetics at the onset of exercise and improvement of ATP/ADP stability due to physical training are mainly caused by an increase in the amount of mitochondrial proteins and by an intensification of the parallel activation of ATP usage and ATP supply (increase in direct stimulation of oxidative phosphorylation complexes accompanying stimulation of ATP consumption) during exercise.

Silibinin attenuates sulfur mustard analog-induced skin injury by targeting multiple pathways connecting oxidative stress and inflammation.

Directory of Open Access Journals (Sweden)

Neera Tewari-Singh

Full Text Available Chemical warfare agent sulfur mustard (HD inflicts delayed blistering and incapacitating skin injuries. To identify effective countermeasures against HD-induced skin injuries, efficacy studies were carried out employing HD analog 2-chloroethyl ethyl sulfide (CEES-induced injury biomarkers in skin cells and SKH-1 hairless mouse skin. The data demonstrate strong therapeutic efficacy of silibinin, a natural flavanone, in attenuating CEES-induced skin injury and oxidative stress. In skin cells, silibinin (10 µM treatment 30 min after 0.35/0.5 mM CEES exposure caused a significant (p90%, and activation of transcription factors NF-κB and AP-1 (complete reversal. Similarly, silibinin treatment was also effective in attenuating CEES-induced oxidative stress measured by 4-hydroxynonenal and 5,5-dimethyl-2-(8-octanoic acid-1-pyrolline N-oxide protein adduct formation, and 8-oxo-2-deoxyguanosine levels. Since our previous studies implicated oxidative stress, in part, in CEES-induced toxic responses, the reversal of CEES-induced oxidative stress and other toxic effects by silibinin in this study indicate its pleiotropic therapeutic efficacy. Together, these findings support further optimization of silibinin in HD skin toxicity model to develop a novel effective therapy for skin injuries by vesicants.

Protective property of mulberry digest against oxidative stress - A potential approach to ameliorate dietary acrylamide-induced cytotoxicity.

Science.gov (United States)

Zhang, Linxia; Xu, Yang; Li, Yuting; Bao, Tao; Gowd, Vemana; Chen, Wei

2017-09-01

The aim of this study was investigating the protective effect of mulberry digest (MBD) on acrylamide-induced oxidative stress. Composition analysis of MBD revealed that it contained six major phenolic compounds (quercetin-3-O-rutinoside, quercetin hexoside, quercetin rhamnosylhexoside hexoside, kaempferol rhamnosylhexoside, cyanidin-3-O-glucoside and cyanidin-3-O-rutinoside). After in vitro digestion, the contents of two anthocyanins were both decreased significantly, while the contents of four flavonoid glycosides were all increased. In addition, MBD was found to successfully suppress acrylamide-induced ROS overproduction, restore the mitochondrial membrane potential, and inhibit the mitochondrial membrane lipid peroxidation and glutathione depletion. More interestingly, the protective effect of MBD against acrylamide-induced oxidative damage was enhanced compared with mulberry fruits without digestion (MBE). Further study revealed that MBD enhanced the cell resistance capacity to acrylamide-induced oxidative stress, rather than its direct reaction with acrylamide. Overall, our results indicate that MBD provides a potent protection against acrylamide-induced oxidative stress. Copyright © 2017 Elsevier Ltd. All rights reserved.

Analysis of oxide formation induced by UV laser coloration of stainless steel

Energy Technology Data Exchange (ETDEWEB)

Li, Z.L., E-mail: zlli@SIMTech.a-star.edu.sg [Singapore Institute of Manufacturing Technology, 71 Nanyang Drive, 638075 (Singapore); Zheng, H.Y.; Teh, K.M.; Liu, Y.C.; Lim, G.C. [Singapore Institute of Manufacturing Technology, 71 Nanyang Drive, 638075 (Singapore); Seng, H.L.; Yakovlev, N.L. [Institute of Materials Research and Engineering, 3 Research Link, 117602 (Singapore)

2009-12-15

Laser-induced coloration on metal surfaces has important applications in product identification, enhancing styles and aesthetics. The color generation is the result of controlled surface oxidation during laser beam interaction with the metal surfaces. In this study, we aim to obtain in-depth understanding of the oxide formation process when an UV laser beam interacts with stainless steel in air. The oxide layer is analysed by means of optical microscopy, scanning electron microscopy (SEM) and time-of-flight secondary ion mass spectrometer (TOF-SIMS). TOF-SIMS results clearly show the formation of duplex oxide structures. The duplex structure includes an inner layer of Cr oxide solution and an outer layer of Fe oxide solution. The oxide layer thickness increased as the results of Fe diffusion to surface during multiple laser scanning passes.

Analysis of oxide formation induced by UV laser coloration of stainless steel

International Nuclear Information System (INIS)

Li, Z.L.; Zheng, H.Y.; Teh, K.M.; Liu, Y.C.; Lim, G.C.; Seng, H.L.; Yakovlev, N.L.

2009-01-01

Laser-induced coloration on metal surfaces has important applications in product identification, enhancing styles and aesthetics. The color generation is the result of controlled surface oxidation during laser beam interaction with the metal surfaces. In this study, we aim to obtain in-depth understanding of the oxide formation process when an UV laser beam interacts with stainless steel in air. The oxide layer is analysed by means of optical microscopy, scanning electron microscopy (SEM) and time-of-flight secondary ion mass spectrometer (TOF-SIMS). TOF-SIMS results clearly show the formation of duplex oxide structures. The duplex structure includes an inner layer of Cr oxide solution and an outer layer of Fe oxide solution. The oxide layer thickness increased as the results of Fe diffusion to surface during multiple laser scanning passes.

Hyperglycemia-induced diaphragm weakness is mediated by oxidative stress

Science.gov (United States)

2014-01-01

Introduction A major consequence of ICU-acquired weakness (ICUAW) is diaphragm weakness, which prolongs the duration of mechanical ventilation. Hyperglycemia (HG) is a risk factor for ICUAW. However, the mechanisms underlying HG-induced respiratory muscle weakness are not known. Excessive reactive oxygen species (ROS) injure multiple tissues during HG, but only one study suggests that excessive ROS generation may be linked to HG-induced diaphragm weakness. We hypothesized that HG-induced diaphragm dysfunction is mediated by excessive superoxide generation and that administration of a specific superoxide scavenger, polyethylene glycol superoxide dismutase (PEG-SOD), would ameliorate these effects. Methods HG was induced in rats using streptozotocin (60 mg/kg intravenously) and the following groups assessed at two weeks: controls, HG, HG + PEG-SOD (2,000U/kg/d intraperitoneally for seven days), and HG + denatured (dn)PEG-SOD (2000U/kg/d intraperitoneally for seven days). PEG-SOD and dnPEG-SOD were administered on day 8, we measured diaphragm specific force generation in muscle strips, force-pCa relationships in single permeabilized fibers, contractile protein content and indices of oxidative stress. Results HG reduced diaphragm specific force generation, altered single fiber force-pCa relationships, depleted troponin T, and increased oxidative stress. PEG-SOD prevented HG-induced reductions in diaphragm specific force generation (for example 80 Hz force was 26.4 ± 0.9, 15.4 ± 0.9, 24.0 ± 1.5 and 14.9 ± 0.9 N/cm2 for control, HG, HG + PEG-SOD, and HG + dnPEG-SOD groups, respectively, P hyperglycemia-induced diaphragm dysfunction. This new mechanistic information could explain how HG alters diaphragm function during critical illness. PMID:24886999

Inhibition of inducible nitric oxide synthesis by azathioprine in a macrophage cell line.

Science.gov (United States)

Moeslinger, Thomas; Friedl, Roswitha; Spieckermann, Paul Gerhard

2006-06-20

Azathioprine is used as an anti-inflammatory agent. Although there are numerous data demonstrating cytotoxic and immunosuppressive properties of azathioprine and its metabolite 6-mercaptopurine, the mechanism of the anti-inflammatory action of azathioprine has not yet been fully clarified. During our study, we investigated the effects of azathioprine on the inducible nitric oxide synthase (iNOS) in lipopolysaccharide stimulated murine macrophages (RAW 264.7) by measurement of iNOS protein (immunoblotting), iNOS mRNA (semiquantitative competitive RT-PCR), and NO production (nitrite levels). Azathioprine (0-210 muM) induces a concentration dependent inhibition of inducible nitric oxide synthesis (IC50: 33.5 muM). iNOS protein expression showed a concentration dependent reduction as revealed by immunoblotting when cells were incubated with increasing amounts of azathioprine. Azathioprine decreases iNOS mRNA levels as shown by semiquantitative competitive RT-PCR. In contrast, 6-mercaptopurine showed no inhibition of inducible nitric oxide synthesis. Azathioprine did not reduce iNOS mRNA stability after the addition of actinomycin D. Enzymatic activity assays with increasing concentrations of azathioprine (0-210 muM) showed no statistically significant inhibition of iNOS enzyme activity compared to cell lysates without azathioprine. Nuclear translocation of NF-kappaB p65 subunit and binding of NF-kappaB p50 subunit from nuclear extracts to a biotinylated-consensus sequence was unaffected by azathioprine treatment. iNOS inhibition by azathioprine was associated with a decreased expression of IRF-1 (interferon regulatory factor 1) and IFN-beta (beta-interferon) mRNA. Azathioprine induced iNOS inhibition seems to be associated with an action of the methylnitroimidazolyl substituent. This suggests a route to the rational design of nontoxic anti-inflammatory agents by replacing the 6-mercaptopurine component of azathioprine with other substituents. The inhibition of

Age-dependent oxidative stress-induced DNA damage in Down's lymphocytes

International Nuclear Information System (INIS)

Zana, Marianna; Szecsenyi, Anita; Czibula, Agnes; Bjelik, Annamaria; Juhasz, Anna; Rimanoczy, Agnes; Szabo, Krisztina; Vetro, Agnes; Szucs, Peter; Varkonyi, Agnes; Pakaski, Magdolna; Boda, Krisztina; Rasko, Istvan; Janka, Zoltan; Kalman, Janos

2006-01-01

The aim of the present study was to investigate the oxidative status of lymphocytes from children (n = 7) and adults (n = 18) with Down's syndrome (DS). The basal oxidative condition, the vulnerability to in vitro hydrogen peroxide exposure, and the repair capacity were measured by means of the damage-specific alkaline comet assay. Significantly and age-independently elevated numbers of single strand breaks and oxidized bases (pyrimidines and purines) were found in the nuclear DNA of the lymphocytes in the DS group in the basal condition. These results may support the role of an increased level of endogenous oxidative stress in DS and are similar to those previously demonstrated in Alzheimer's disease. In the in vitro oxidative stress-induced state, a markedly higher extent of DNA damage was observed in DS children as compared with age- and gender-matched healthy controls, suggesting that young trisomic lymphocytes are more sensitive to oxidative stress than normal ones. However, the repair ability itself was not found to be deteriorated in either DS children or DS adults

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.

Enhancement of nitrite on heme-induced oxidative reactions: A potential toxicological implication.

Science.gov (United States)

Lu, Naihao; Chen, Wei; Zhu, Jingjie; Peng, Yi-Yuan

2012-02-01

Evidence to support the role of heme as major inducers of oxidative damage is increasingly present. Nitrite (NO(2)(-)) is one of the major end products of NO metabolism. Although the biological significance of heme/NO(2)(-)-mediated protein tyrosine nitration is a subject of great interest, the important roles of NO(2)(-) on heme-dependent redox reaction have been greatly underestimated. In this study, we investigated the influence of NO(2)(-) on heme -dependent oxidative reactions. It was found that NO(2)(-) had the capacity to act as a reducing agent to remove high oxidation states of heme iron. In the reduction of ferryl heme to ferric heme, NO(2)(-) was oxidized to a nitrating agent NO(2), and subsequently, tyrosine residues in bovine serum albumin (BSA) were nitrated. However, the presence of NO(2)(-) surprisingly exerted pro-oxidant effect on heme-H(2)O(2)-induced formation of BSA carbonyls at lower concentrations and enhanced the loss of HepG2 cell viability dose-dependently, which was probably due to the ability of this inorganic compound to efficiently enhance the peroxidase activity and oxidative degradation of heme. These data provide novel evidence that the dietary intake and experimental use of NO(2)(-) in vivo and in vitro would possess the pro-oxidant activity through interfering in heme-dependent oxidative reactions. Besides the classic role in protein tyrosine nitration, the deleterious effects on heme redox reactions may provide new insights into the toxicological implications of NO(2)(-) with cellular heme proteins. Copyright © 2011 Elsevier Ltd. All rights reserved.

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

Protective effects of erythropoietin against cuprizone-induced oxidative stress and demyelination in the mouse corpus callosum

Directory of Open Access Journals (Sweden)

Iraj Ragerdi Kashani

2017-08-01

Full Text Available Objective(s: Increasing evidence in both experimental and clinical studies suggests that oxidative stress plays a major role in the pathogenesis of multiple sclerosis. The aim of the present work is to investigate the protective effects of erythropoietin against cuprizone-induced oxidative stress. Materials and Methods: Adult male C57BL/6J mice were fed a chow containing 0.2 % cuprizone for 6 weeks. After 3 weeks, mice were simultaneously treated with erythropoietin (5,000 IU/ kg body weight by daily intraperitoneal injections. Results: Our results showed that cuprizone induced oxidative stress accompanied with down-regulation of subunits of the respiratory chain complex and demyelination of corpus callosum. Erythropoietin antagonized these effects. Biochemical analysis showed that oxidative stress induced by cuprizone was regulated by erythropoietin. Similarly, erythropoietin induced the expression of subunits of the respiratory chain complex over normal control values reflecting a mechanism to compensate cuprizone-mediated down-regulation of these genes. Conclusion: The data implicate that erythropoietin abolishes destructive cuprizone effects in the corpus callosum by decreasing oxidative stress and restoring mitochondrial respiratory enzyme activity.

Impaired Mitochondrial Respiratory Functions and Oxidative Stress in Streptozotocin-Induced Diabetic Rats

Directory of Open Access Journals (Sweden)

Subbuswamy K. Prabu

2011-05-01

Full Text Available We have previously shown a tissue-specific increase in oxidative stress in the early stages of streptozotocin (STZ-induced diabetic rats. In this study, we investigated oxidative stress-related long-term complications and mitochondrial dysfunctions in the different tissues of STZ-induced diabetic rats (>15 mM blood glucose for 8 weeks. These animals showed a persistent increase in reactive oxygen and nitrogen species (ROS and RNS, respectively production. Oxidative protein carbonylation was also increased with the maximum effect observed in the pancreas of diabetic rats. The activities of mitochondrial respiratory enzymes ubiquinol: cytochrome c oxidoreductase (Complex III and cytochrome c oxidase (Complex IV were significantly decreased while that of NADH:ubiquinone oxidoreductase (Complex I and succinate:ubiquinone oxidoreductase (Complex II were moderately increased in diabetic rats, which was confirmed by the increased expression of the 70 kDa Complex II sub-unit. Mitochondrial matrix aconitase, a ROS sensitive enzyme, was markedly inhibited in the diabetic rat tissues. Increased expression of oxidative stress marker proteins Hsp-70 and HO-1 was also observed along with increased expression of nitric oxide synthase. These results suggest that mitochondrial respiratory complexes may play a critical role in ROS/RNS homeostasis and oxidative stress related changes in type 1 diabetes and may have implications in the etiology of diabetes and its complications.

Role of oxidative stress in methamphetamine-induced dopaminergic toxicity mediated by protein kinase Cδ.

Science.gov (United States)

Shin, Eun-Joo; Duong, Chu Xuan; Nguyen, Xuan-Khanh Thi; Li, Zhengyi; Bing, Guoying; Bach, Jae-Hyung; Park, Dae Hun; Nakayama, Keiichi; Ali, Syed F; Kanthasamy, Anumantha G; Cadet, Jean Lud; Nabeshima, Toshitaka; Kim, Hyoung-Chun

2012-06-15

This study examined the role of protein kinase C (PKC) isozymes in methamphetamine (MA)-induced dopaminergic toxicity. Multiple-dose administration of MA did not significantly alter PKCα, PKCβI, PKCβII, or PKCζ expression in the striatum, but did significantly increase PKCδ expression. Gö6976 (a co-inhibitor of PKCα and -β), hispidin (PKCβ inhibitor), and PKCζ pseudosubstrate inhibitor (PKCζ inhibitor) did not significantly alter MA-induced behavioral impairments. However, rottlerin (PKCδ inhibitor) significantly attenuated behavioral impairments in a dose-dependent manner. In addition, MA-induced behavioral impairments were not apparent in PKCδ knockout (-/-) mice. MA-induced oxidative stress (i.e., lipid peroxidation and protein oxidation) was significantly attenuated in rottlerin-treated mice and was not apparent in PKCδ (-/-) mice. Consistent with this, MA-induced apoptosis (i.e., terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive apoptotic cells) was significantly attenuated in rottlerin-treated mice. Furthermore, MA-induced increases in the dopamine (DA) turnover rate and decreases in tyrosine hydroxylase (TH) activity and the expression of TH, dopamine transporter (DAT), and vesicular monoamine transporter 2 (VMAT2) were not significantly observed in rottlerin-treated or PKCδ (-/-) mice. Our results suggest that PKCδ gene expression is a key mediator of oxidative stress and dopaminergic damage induced by MA. Thus, inhibition of PKCδ may be a useful target for protection against MA-induced neurotoxicity. Copyright © 2012 Elsevier B.V. All rights reserved.

Heavy Metal-Induced Oxidative DNA Damage in Earthworms: A Review

Directory of Open Access Journals (Sweden)

Takeshi Hirano

2010-01-01

Full Text Available Earthworms can be used as a bio-indicator of metal contamination in soil, Earlier reports claimed the bioaccumulation of heavy metals in earthworm tissues, while the metal-induced mutagenicity reared in contaminated soils for long duration. But we examined the metal-induced mutagenicity in earthworms reared in metal containing culture beddings. In this experiment we observed the generation of 8-oxoguanine (8-oxo-Gua in earthworms exposed to cadmium and nickel in soil. 8-oxo-Gua is a major premutagenic form of oxidative DNA damage that induces GC-to-TA point mutations, leading to carcinogenesis.

Bifunctional effects of fucoidan on the expression of inducible nitric oxide synthase

International Nuclear Information System (INIS)

Yang, Jin Won; Yoon, Se Young; Oh, Soo Jin; Kim, Sang Kyum; Kang, Keon Wook

2006-01-01

Algal fucoidan is a marine sulfated polysaccharide with a wide variety of biological activities including anti-thrombotic and anti-inflammatory effects. This study evaluated the effect of fucoidan on the expression of inducible nitric oxide synthase (iNOS) in a macrophage cell line, RAW264.7. Low concentration range of fucoidan (10 μg/ml) increased the basal expression level of iNOS in quiescent macrophages. However, we found for the first time that fucoidan inhibited the release of nitric oxide (NO) in RAW264.7 cells stimulated with lipopolysaccharide (LPS). Western blot analysis revealed that fucoidan suppressed the LPS-induced expression of the inducible nitric oxide synthase (iNOS) gene. Moreover, the activation of both nuclear factor-κB (NF-κB) and activator protein 1 (AP-1) are key steps in the transcriptional activation of the iNOS gene. Here, it was revealed that fucoidan selectively suppressed AP-1 activation, and that the activation of AP-1 appears to be essential for the induction of iNOS in activated macrophages. This inhibitory effect on AP-1 activation by fucoidan might be associated with its NO blocking and anti-inflammatory effects

Nitric oxide protects anterior pituitary cells from cadmium-induced apoptosis.

Science.gov (United States)

Poliandri, Ariel H B; Velardez, Miguel O; Cabilla, Jimena P; Bodo, Cristian C A; Machiavelli, Leticia I; Quinteros, Alnilan F; Duvilanski, Beatriz H

2004-11-01

Cadmium (Cd2+) is a potent toxic metal for both plants and animals. Chronic exposure to low doses of Cd2+ results in damage to several organs. We have previously reported that Cd2+ induces apoptosis in anterior pituitary cells by a caspase- and oxidative stress-dependent mechanism. Nitric oxide (NO) synthesis is affected by Cd2+ in several systems. NO has been shown to be either cytoprotective or cytotoxic in many systems. The aim of this study was to evaluate the possible participation of NO in the cytotoxic effect of Cd2+ on rat anterior pituitary cells. Cell viability was evaluated by mitochondrial dehydrogenase activity assay and confirmed by microscopy, studying nuclear morphology. Here we show that DETA NONOate ((Z)-1-[2 (2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate), a long-term NO donor, at concentrations below 0.5 mM, reduces nuclear condensation and fragmentation and reverses the decrease in cellular activity induced by Cd2+. Cd2+, by itself, induced NO synthesis, and inhibition of this synthesis enhanced Cd2+ cytotoxicity. NO also prevented caspase-3 activation and lipidic peroxidation induced by Cd2+. The NO/cGMP pathway does not seem to be involved in the cytoprotective effect of NO. These results indicate that NO has a cytoprotective role in Cd2+ -induced apoptosis, suggesting that endogenous NO could have a physiological role in protecting anterior pituitary cells.

Chloride secretion induced by rotavirus is oxidative stress-dependent and inhibited by Saccharomyces boulardii in human enterocytes.

Science.gov (United States)

Buccigrossi, Vittoria; Laudiero, Gabriella; Russo, Carla; Miele, Erasmo; Sofia, Morena; Monini, Marina; Ruggeri, Franco Maria; Guarino, Alfredo

2014-01-01

Rotavirus (RV) infection causes watery diarrhea via multiple mechanisms, primarily chloride secretion in intestinal epithelial cell. The chloride secretion largely depends on non-structural protein 4 (NSP4) enterotoxic activity in human enterocytes through mechanisms that have not been defined. Redox imbalance is a common event in cells infected by viruses, but the role of oxidative stress in RV infection is unknown. RV SA11 induced chloride secretion in association with an increase in reactive oxygen species (ROS) in Caco-2 cells. The ratio between reduced (GSH) and oxidized (GSSG) glutathione was decreased by RV. The same effects were observed when purified NSP4 was added to Caco-2 cells. N-acetylcysteine (NAC), a potent antioxidant, strongly inhibited the increase in ROS and GSH imbalance. These results suggest a link between oxidative stress and RV-induced diarrhea. Because Saccharomyces boulardii (Sb) has been effectively used to treat RV diarrhea, we tested its effects on RV-infected cells. Sb supernatant prevented RV-induced oxidative stress and strongly inhibited chloride secretion in Caco-2 cells. These results were confirmed in an organ culture model using human intestinal biopsies, demonstrating that chloride secretion induced by RV-NSP4 is oxidative stress-dependent and is inhibited by Sb, which produces soluble metabolites that prevent oxidative stress. The results of this study provide novel insights into RV-induced diarrhea and the efficacy of probiotics.

Green Synthesized Zinc Oxide (ZnO) Nanoparticles Induce Oxidative Stress and DNA Damage in Lathyrus sativus L. Root Bioassay System.

Science.gov (United States)

Panda, Kamal K; Golari, Dambaru; Venugopal, A; Achary, V Mohan M; Phaomei, Ganngam; Parinandi, Narasimham L; Sahu, Hrushi K; Panda, Brahma B

2017-05-18

Zinc oxide nanoparticles (ZnONP-GS) were synthesised from the precursor zinc acetate (Zn(CH₃COO)₂) through the green route using the milky latex from milk weed ( Calotropis gigantea L. R. Br) by alkaline precipitation. Formation of the ZnONP-GS was monitored by UV-visible spectroscopy followed by characterization and confirmation by energy-dispersive X-ray spectroscopy (EDX), transmission electron microscopy (TEM), and X-ray diffraction (XRD). Both the ZnONP-GS and the commercially available ZnONP-S (Sigma-Aldrich) and cationic Zn 2+ from Zn(CH₃COO)₂ were tested in a dose range of 0-100 mg·L -1 for their potency (i) to induce oxidative stress as measured by the generation reactive oxygen species (ROS: O₂ •- , H₂O₂ and • OH), cell death, and lipid peroxidation; (ii) to modulate the activities of antioxidant enzymes: catalase (CAT), superoxide dismutase (SOD), guaiacol peroxidase (GPX), and ascorbate peroxidase (APX); and (iii) to cause DNA damage as determined by Comet assay in Lathyrus sativus L. root bioassay system. Antioxidants such as Tiron and dimethylthiourea significantly attenuated the ZnONP-induced oxidative and DNA damage, suggesting the involvement of ROS therein. Our study demonstrated that both ZnONP-GS and ZnONP-S induced oxidative stress and DNA damage to a similar extent but were significantly less potent than Zn 2+ alone.

Exercise training attenuates sympathetic activation and oxidative stress in diet-induced obesity.

Science.gov (United States)

Li, G; Liu, J-Y; Zhang, H-X; Li, Q; Zhang, S-W

2015-01-01

It is known that excessive sympathetic activity and oxidative stress are enhanced in obesity. This study aimed to clarify whether exercise training (ET) attenuates sympathetic activation and oxidative stress in obesity. The obesity was induced by high-fat diet (HFD) for 12 weeks. Male Sprague-Dawley rats were assigned to four groups: regular diet (RD) plus sedentary (RD-S), RD plus ET (RD-ET), HFD plus sedentary (HFD-S), and HFD plus ET (HFD-ET). The rats in RD-ET and HFD-ET groups were trained on a motorized treadmill for 60 min/day, five days/week for 8 weeks. The sympathetic activity was evaluated by the plasma norepinephrine (NE) level. The superoxide anion, malondialdehyde and F2-isoprostanes levels in serum and muscles were measured to evaluate oxidative stress. The ET prevented the increases in the body weight, arterial pressure and white adipose tissue mass in HFD rats. The NE level in plasma and oxidative stress related parameters got lower in HFD-ET group compared with HFD-S group. We have found decreased mRNA and protein levels of toll-like receptor (TLR)-2 and TLR-4 by ET in HFD rats. These findings suggest that ET may be effective for attenuating sympathetic activation and oxidative stress in diet-induced obesity.

Crocin attenuates hemorrhagic shock-induced oxidative stress and organ injuries in rats.

Science.gov (United States)

Yang, Long; Dong, Xiujuan

2017-06-01

We aimed to evaluate the effect of natural antioxidant crocin in alleviating hemorrhagic shock (HS)-induced organ damages. HS rats were treated with crocin during resuscitation. Mortality at 12h and 24h post resuscitation was documented. HS and resuscitation induced organ injuries, as characterized by elevated wet/dry ratio, quantitative assessment ratio, blood urea nitrogen, creatinine, aspartate aminotransferase and alanine aminotransferase, whereas rats received crocin treatment demonstrated improvements in all the above characteristics. This protective effect coincided with reduced malondialdehyde and increased glutathione in both serum and lung tissues, indicating attenuated oxidative stress in crocin-treated rats. Myeloperoxide levels in lung, kidney and liver were also reduced. Crocin can potentially be used to protect organs from HS-induced damages during resuscitation due to its anti-oxidative role. Copyright © 2017 Elsevier B.V. All rights reserved.

Cellular membrane accommodation of copper-induced oxidative conditions in the coral Seriatopora caliendrum

Energy Technology Data Exchange (ETDEWEB)

Tang, Chuan-Ho, E-mail: chtang@nmmba.gov.tw [Institute of Marine Biodiversity and Evolutionary Biology, National Dong Hwa University, Pingtung, Taiwan, ROC (China); National Museum of Marine Biology and Aquarium, Pingtung, Taiwan, ROC (China); Lin, Ching-Yu [Institute of Environmental Health, National Taiwan University, Taipei City, Taiwan, ROC (China); Lee, Shu-Hui [Center of General Education, National Kaohsiung Marine University, Kaohsiung, Taiwan, ROC (China); Wang, Wei-Hsien [National Museum of Marine Biology and Aquarium, Pingtung, Taiwan, ROC (China); Department of Marine Biotechnology and Resources and Asia-Pacific Ocean Research Center, National Sun Yat-sen University, Kaohsiung, Taiwan, ROC (China)

2014-03-01

Highlights: • Coral cells alter membrane lipid to accommodate copper-induce oxidative conditions • Coral membrane repair occur due to lipid alterations • Zooxanthellae release results from membrane repair by symbiosome fusion • Copper-induced lipid alterations perturb membrane-related functions in coral cells • Copper chronic effect on coral fitness are related to long-term membrane perturbation - Abstract: Oxidative stress has been associated with copper-induced toxicity in scleractinian corals. To gain insight into the accommodation of the cellular membrane to oxidative conditions, a pocilloporid coral, Seriatopora caliendrum, was exposed to copper at distinct, environmentally relevant dose for various lengths of time. Glycerophosphocholine profiling of the response of the coral to copper exposure was characterized using a validated method. The results indicate that coral lipid metabolism is programmed to induce membrane alterations in response to the cellular deterioration that occurs during the copper exposure period. Decreasing lyso-phosphatidylcholines and exchanging polyunsaturated phosphatidylcholines for polyunsaturated plasmanylcholines were the initial actions taken to prevent membrane permeabilization. To relax/resist the resulting membrane strain caused by cell/organelle swelling, the coral cells inversely exchanged polyunsaturated plasmanylcholines for polyunsaturated phosphatidylcholines and further increased the levels of monounsaturated glycerophosphocholines. At the same time, the levels of saturated phosphatidylcholines were also increased to increase membrane rigidity and protect against oxidative attack. Interestingly, such alterations in lipid metabolism were also required for membrane fusion to repair the deteriorated membranes by repopulating them with proximal lipid reservoirs, similar to symbiosome membranes. Additionally, increasing saturated and monounsaturated plasmanylcholines and inhibiting the suppression of saturated lyso

Cellular membrane accommodation of copper-induced oxidative conditions in the coral Seriatopora caliendrum

International Nuclear Information System (INIS)

Tang, Chuan-Ho; Lin, Ching-Yu; Lee, Shu-Hui; Wang, Wei-Hsien

2014-01-01

Highlights: • Coral cells alter membrane lipid to accommodate copper-induce oxidative conditions • Coral membrane repair occur due to lipid alterations • Zooxanthellae release results from membrane repair by symbiosome fusion • Copper-induced lipid alterations perturb membrane-related functions in coral cells • Copper chronic effect on coral fitness are related to long-term membrane perturbation - Abstract: Oxidative stress has been associated with copper-induced toxicity in scleractinian corals. To gain insight into the accommodation of the cellular membrane to oxidative conditions, a pocilloporid coral, Seriatopora caliendrum, was exposed to copper at distinct, environmentally relevant dose for various lengths of time. Glycerophosphocholine profiling of the response of the coral to copper exposure was characterized using a validated method. The results indicate that coral lipid metabolism is programmed to induce membrane alterations in response to the cellular deterioration that occurs during the copper exposure period. Decreasing lyso-phosphatidylcholines and exchanging polyunsaturated phosphatidylcholines for polyunsaturated plasmanylcholines were the initial actions taken to prevent membrane permeabilization. To relax/resist the resulting membrane strain caused by cell/organelle swelling, the coral cells inversely exchanged polyunsaturated plasmanylcholines for polyunsaturated phosphatidylcholines and further increased the levels of monounsaturated glycerophosphocholines. At the same time, the levels of saturated phosphatidylcholines were also increased to increase membrane rigidity and protect against oxidative attack. Interestingly, such alterations in lipid metabolism were also required for membrane fusion to repair the deteriorated membranes by repopulating them with proximal lipid reservoirs, similar to symbiosome membranes. Additionally, increasing saturated and monounsaturated plasmanylcholines and inhibiting the suppression of saturated lyso

Loss of Hepatic Mitochondrial Long-Chain Fatty Acid Oxidation Confers Resistance to Diet-Induced Obesity and Glucose Intolerance.

Science.gov (United States)

Lee, Jieun; Choi, Joseph; Selen Alpergin, Ebru S; Zhao, Liang; Hartung, Thomas; Scafidi, Susanna; Riddle, Ryan C; Wolfgang, Michael J

2017-07-18

The liver has a large capacity for mitochondrial fatty acid β-oxidation, which is critical for systemic metabolic adaptations such as gluconeogenesis and ketogenesis. To understand the role of hepatic fatty acid oxidation in response to a chronic high-fat diet (HFD), we generated mice with a liver-specific deficiency of mitochondrial long-chain fatty acid β-oxidation (Cpt2 L-/- mice). Paradoxically, Cpt2 L-/- mice were resistant to HFD-induced obesity and glucose intolerance with an absence of liver damage, although they exhibited serum dyslipidemia, hepatic oxidative stress, and systemic carnitine deficiency. Feeding an HFD induced hepatokines in mice, with a loss of hepatic fatty acid oxidation that enhanced systemic energy expenditure and suppressed adiposity. Additionally, the suppression in hepatic gluconeogenesis was sufficient to improve HFD-induced glucose intolerance. These data show that inhibiting hepatic fatty acid oxidation results in a systemic hormetic response that protects mice from HFD-induced obesity and glucose intolerance. Copyright © 2017 The Author(s). Published by Elsevier Inc. All rights reserved.

The Role of Oxidative Stress in Carcinogenesis Induced by Metals and Xenobiotics

International Nuclear Information System (INIS)

Henkler, Frank; Brinkmann, Joep; Luch, Andreas

2010-01-01

In addition to a wide range of adverse effects on human health, toxic metals such as cadmium, arsenic and nickel can also promote carcinogenesis. The toxicological properties of these metals are partly related to generation of reactive oxygen species (ROS) that can induce DNA damage and trigger redox-dependent transcription factors. The precise mechanisms that induce oxidative stress are not fully understood. Further, it is not yet known whether chronic exposures to low doses of arsenic, cadmium or other metals are sufficient to induce mutations in vivo, leading to DNA repair responses and/or tumorigenesis. Oxidative stress can also be induced by environmental xenobiotics, when certain metabolites are generated that lead to the continuous release of superoxide, as long as the capacity to reduce the resulting dions (quinones) into hydroquinones is maintained. However, the specific significance of superoxide-dependent pathways to carcinogenesis is often difficult to address, because formation of DNA adducts by mutagenic metabolites can occur in parallel. Here, we will review both mechanisms and toxicological consequences of oxidative stress triggered by metals and dietary or environmental pollutants in general. Besides causing DNA damage, ROS may further induce multiple intracellular signaling pathways, notably NF-κB, JNK/SAPK/p38, as well as Erk/MAPK. These signaling routes can lead to transcriptional induction of target genes that could promote proliferation or confer apoptosis resistance to exposed cells. The significance of these additional modes depends on tissue, cell-type and is often masked by alternate oncogenic mechanisms being activated in parallel

Analysis of genetic variation of inducible nitric oxide synthase and ...

African Journals Online (AJOL)

The genetic diversity of 100 Malaysian native chickens was investigated using polymerase chain reaction-restriction fragment polymorphism (PCR-RFLP) for two candidate genes: inducible nitric oxide synthase (INOS) and natural resistance-associated macrophage protein 1 (NRAMP1). The two genes were selected ...

Effect of magnetic field on the zero valent iron induced oxidation reaction

International Nuclear Information System (INIS)

Kim, Dong-hyo; Kim, Jungwon; Choi, Wonyong

2011-01-01

Highlights: → We investigate the zero valent iron induced oxidation in the presence of magnetic field. → The oxidative degradation of 4-chlorophenol is enhanced by the magnetic field. → ESR measurement confirms that more OH radicals are generated in the presence of magnetic field. → The magnetic field affects the mass transfer of O 2 and the recombination of radicals. - Abstract: The magnetic field (MF) effect on the zero valent iron (ZVI) induced oxidative reaction was investigated for the first time. The degradation of 4-chlorophenol (4-CP) in the ZVI system was employed as the test oxidative reaction. MF markedly enhanced the degradation of 4-CP with the concurrent production of chlorides. The consumption of dissolved O 2 by ZVI reaction was also enhanced in the presence of MF whereas the competing reaction of H 2 production from proton reduction was retarded. Since the ZVI-induced oxidation is mainly driven by the in situ generated hydroxyl radicals, the production of OH radicals was monitored by the spin trap method using electron spin resonance (ESR) spectroscopy. It was confirmed that the concentration of trapped OH radicals was enhanced in the presence of MF. Since both O 2 and Fe 0 are paramagnetic, the diffusion of O 2 onto the iron surface might be accelerated under MF. The magnetized iron can attract oxygen on itself, which makes the mass transfer process faster. As a result, the surface electrochemical reaction between Fe 0 and O 2 can be accelerated with the enhanced production of OH radicals. MF might retard the recombination of OH radicals as well.

Buffer modulation of menadione-induced oxidative stress in Saccharomyces cerevisiae.

Science.gov (United States)

Lushchak, Oleh V; Bayliak, Maria M; Korobova, Olha V; Levine, Rodney L; Lushchak, Volodymyr I

2009-01-01

The objective of this study was to compare, in vivo, the effects of bicarbonate and phosphate buffers on survival and menadione-induced oxidative stress in yeast cells. The latter were treated with different concentrations of menadione in the presence of these two buffers. At 25 mM concentration of buffers, menadione only slightly reduced yeast surviving; at 50 mM concentration, cell killing by menadione was much more pronounced in bicarbonate than in phosphate buffer. Although the content of protein carbonyl groups did not show development of oxidative stress under menadione-induced stress, inactivation of aconitase and decrease in glutathione level mirrored its induction. However, cellular glutathione and aconitase activity decrease did not correlate with yeast survival. In vitro, aconitase was more quickly inactivated in 50 mM carbonate, than in 50 mM phosphate buffer. The possible involvement of the carbonate radical in these processes is discussed.

Oxidative Damage to the Salivary Glands of Rats with Streptozotocin-Induced Diabetes-Temporal Study: Oxidative Stress and Diabetic Salivary Glands.

Science.gov (United States)

Knaś, M; Maciejczyk, M; Daniszewska, I; Klimiuk, A; Matczuk, J; Kołodziej, U; Waszkiel, D; Ładny, J R; Żendzian-Piotrowska, M; Zalewska, A

2016-01-01

Objective. This study evaluated oxidative damage caused to the salivary glands in streptozotocin-induced diabetes (DM). Materials and Methods. Rats were divided into 4 groups: groups 1 and 2, control rats, and groups 3 and 4, DM rats. 8-Hydroxy-2'-deoxyguanosine (8-OHdG), protein carbonyl (PC), 4-hydroxynonenal protein adduct (4-HNE), oxidized and/or MDA-modified LDL-cholesterol (oxy-LDL/MDA), 8-isoprostanes (8-isoP), and oxidative stress index (OSI) were measured at 7 (groups 1 and 3) and 14 (groups 2 and 4) days of experiment. Results. The unstimulated salivary flow in DM rats was reduced in the 2nd week, while the stimulated flow was decreased throughout the duration of the experiment versus control. OSI was elevated in both diabetic glands in the 1st and 2nd week, whereas 8-isoP and 8-OHdG were higher only in the parotid gland in the second week. PC and 4-HNE were increased in the 1st and 2nd week, whereas oxy-LDL/MDA was increased in the 2nd week in the diabetic parotid glands. Conclusions. Diabetes induces oxidative damage of the salivary glands, which seems to be caused by processes taking place in the salivary glands, independently of general oxidative stress. The parotid glands are more vulnerable to oxidative damage in these conditions.

Oxidative Damage to the Salivary Glands of Rats with Streptozotocin-Induced Diabetes-Temporal Study: Oxidative Stress and Diabetic Salivary Glands

Directory of Open Access Journals (Sweden)

M. Knaś

2016-01-01

Full Text Available Objective. This study evaluated oxidative damage caused to the salivary glands in streptozotocin-induced diabetes (DM. Materials and Methods. Rats were divided into 4 groups: groups 1 and 2, control rats, and groups 3 and 4, DM rats. 8-Hydroxy-2′-deoxyguanosine (8-OHdG, protein carbonyl (PC, 4-hydroxynonenal protein adduct (4-HNE, oxidized and/or MDA-modified LDL-cholesterol (oxy-LDL/MDA, 8-isoprostanes (8-isoP, and oxidative stress index (OSI were measured at 7 (groups 1 and 3 and 14 (groups 2 and 4 days of experiment. Results. The unstimulated salivary flow in DM rats was reduced in the 2nd week, while the stimulated flow was decreased throughout the duration of the experiment versus control. OSI was elevated in both diabetic glands in the 1st and 2nd week, whereas 8-isoP and 8-OHdG were higher only in the parotid gland in the second week. PC and 4-HNE were increased in the 1st and 2nd week, whereas oxy-LDL/MDA was increased in the 2nd week in the diabetic parotid glands. Conclusions. Diabetes induces oxidative damage of the salivary glands, which seems to be caused by processes taking place in the salivary glands, independently of general oxidative stress. The parotid glands are more vulnerable to oxidative damage in these conditions.

Protecting cells by protecting their vulnerable lysosomes: Identification of a new mechanism for preserving lysosomal functional integrity upon oxidative stress.

Science.gov (United States)

Pascua-Maestro, Raquel; Diez-Hermano, Sergio; Lillo, Concepción; Ganfornina, Maria D; Sanchez, Diego

2017-02-01

Environmental insults such as oxidative stress can damage cell membranes. Lysosomes are particularly sensitive to membrane permeabilization since their function depends on intraluminal acidic pH and requires stable membrane-dependent proton gradients. Among the catalog of oxidative stress-responsive genes is the Lipocalin Apolipoprotein D (ApoD), an extracellular lipid binding protein endowed with antioxidant capacity. Within the nervous system, cell types in the defense frontline, such as astrocytes, secrete ApoD to help neurons cope with the challenge. The protecting role of ApoD is known from cellular to organism level, and many of its downstream effects, including optimization of autophagy upon neurodegeneration, have been described. However, we still cannot assign a cellular mechanism to ApoD gene that explains how this protection is accomplished. Here we perform a comprehensive analysis of ApoD intracellular traffic and demonstrate its role in lysosomal pH homeostasis upon paraquat-induced oxidative stress. By combining single-lysosome in vivo pH measurements with immunodetection, we demonstrate that ApoD is endocytosed and targeted to a subset of vulnerable lysosomes in a stress-dependent manner. ApoD is functionally stable in this acidic environment, and its presence is sufficient and necessary for lysosomes to recover from oxidation-induced alkalinization, both in astrocytes and neurons. This function is accomplished by preventing lysosomal membrane permeabilization. Two lysosomal-dependent biological processes, myelin phagocytosis by astrocytes and optimization of neurodegeneration-triggered autophagy in a Drosophila in vivo model, require ApoD-related Lipocalins. Our results uncover a previously unknown biological function of ApoD, member of the finely regulated and evolutionary conserved gene family of extracellular Lipocalins. They set a lipoprotein-mediated regulation of lysosomal membrane integrity as a new mechanism at the hub of many cellular

Evaluation of radioprotective efficacy of pyrimidine-5-carboxylate derivative on radiation induced oxidative stress using Drosophila melanogaster

International Nuclear Information System (INIS)

Sarojini, B.K.; Mohan, B.J.; Narayana, B.; Sanjeev, Ganesh

2014-01-01

In the present study, radioprotection efficacy of Ethyl 4-(4-fluorophenyl)-6-methyl-2-thioxo-1,2,3,4-tetra hydropyrimidine-5-carboxylate (PYR) was evaluated against the gamma ray induced oxidative stress using drosophila melanogaster (Oregon K). The gamma ray irradiated flies were assayed for oxidative stress markers namely; Thiobarbituric acid reactive substances (TBARS) and enzymatic antioxidant SOD and CAT. The oxidative stress was induced at 6 Gy. (author)

Bursopentin (BP5 protects dendritic cells from lipopolysaccharide-induced oxidative stress for immunosuppression.

Directory of Open Access Journals (Sweden)

Tao Qin

Full Text Available Dendritic cells (DCs play a vital role in the regulation of immune-mediated inflammatory diseases. Thus, DCs have been regarded as a major target for the development of immunomodulators. However, oxidative stress could disturb inflammatory regulation in DCs. Here, we examined the effect of bursopentine (BP5, a novel pentapeptide isolated from chicken bursa of fabricius, on the protection of DCs against oxidative stress for immunosuppression. BP5 showed potent protective effects against the lipopolysaccharide (LPS-induced oxidative stress in DCs, including nitric oxide, reactive oxygen species and lipid peroxidation. Furthermore, BP5 elevated the level of cellular reductive status through increasing the reduced glutathione (GSH and the GSH/GSSG ratio. Concomitant with these, the activities of several antioxidative redox enzymes, including glutathione peroxidase (GPx, catalase (CAT and superoxide dismutase (SOD, were obviously enhanced. BP5 also suppressed submucosal DC maturation in the LPS-stimulated intestinal epithelial cells (ECs/DCs coculture system. Finally, we found that heme oxygenase 1 (HO-1 was remarkably upregulated by BP5 in the LPS-induced DCs, and played an important role in the suppression of oxidative stress and DC maturation. These results suggested that BP5 could protect the LPS-activated DCs against oxidative stress and have potential applications in DC-related inflammatory responses.