Extracts from Calendula officinalis offer in vitro protection against H2 O2 induced oxidative stress cell killing of human skin cells.

Science.gov (United States)

Alnuqaydan, Abdullah M; Lenehan, Claire E; Hughes, Rachel R; Sanderson, Barbara J

2015-01-01

The in vitro safety and antioxidant potential of Calendula officinalis flower head extracts was investigated. The effect of different concentrations (0.125, 0.5, 1.0, 2.0 and 5.0% (v/v)) of Calendula extracts on human skin cells HaCaT in vitro was explored. Doses of 1.0% (v/v) (0.88 mg dry weight/mL) or less showed no toxicity. Cells were also exposed to the Calendula extracts for either 4, 24 or 48 h before being exposed to an oxidative insult (hydrogen peroxide H2 O2 ) for 1 h. Using the MTT cytotoxicity assay, it was observed that two independent extracts of C. officinalis gave time-dependent and concentration-dependent H2 O2 protection against induced oxidative stress in vitro using human skin cells. Pre-incubation with the Calendula extracts for 24 and 48 h increased survival relative to the population without extract by 20% and 40% respectively following oxidative challenge. The antioxidant potential of the Calendula extracts was confirmed using a complimentary chemical technique, the DPPH(●) assay. Calendula extracts exhibited free radical scavenging abilities. This study demonstrates that Calendula flower extracts contain bioactive and free radical scavenging compounds that significantly protect against oxidative stress in a human skin cell culture model. Copyright © 2014 John Wiley & Sons, Ltd.

Peroxisome proliferator-activated receptor delta (PPARdelta) activation protects H9c2 cardiomyoblasts from oxidative stress-induced apoptosis.

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Pesant, Matthieu; Sueur, Stéphanie; Dutartre, Patrick; Tallandier, Mireille; Grimaldi, Paul A; Rochette, Luc; Connat, Jean-Louis

2006-02-01

Activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and PPARgamma plays beneficial roles in cardiovascular disorders such as atherosclerosis and heart reperfusion. Although PPARalpha and gamma have been documented to reduce oxidative stress in the vasculature and the heart, the role of PPARdelta remains poorly studied. We focused on PPARdelta function in the regulation of oxidative stress-induced apoptosis in the rat cardiomyoblast cell line H9c2. Using semi-quantitative reverse transcriptase-polymerase chain reaction (RT-PCR), we showed that PPARdelta is the predominantly expressed isotype whereas PPARalpha was weakly detected. By performing cell viability assays, we also showed that the selective PPARdelta agonist GW501516 protected cells from H(2)O(2)-induced cell death. The protective effect of GW501516 was due to an inhibition of H(2)O(2)-triggered apoptosis as shown by annexin-V labeling, DNA fragmentation analysis, and caspase-3 activity measurement. We demonstrated by transient transfection of a dominant negative mutant of PPARdelta that the protection induced by GW501516 was totally dependent on PPARdelta. Semi-quantitative RT-PCR and Western blotting analysis demonstrated that GW501516 treatment upregulated catalase. Moreover, forced overexpression of catalase inhibited H(2)O(2)-triggered apoptosis, as evidenced by annexin-V labeling. Taken together, our results account for an important role of PPARdelta in inhibiting the onset of oxidative stress-induced apoptosis in H9c2 cells. PPARdelta appears to be a new therapeutic target for the regulation of heart reperfusion-associated oxidative stress and stimulation of enzymatic antioxidative defences.

Pretreatment of MQA, a caffeoylquinic acid derivative compound, protects against H2O2-induced oxidative stress in SH-SY5Y cells.

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Tian, Xing; Gao, Lingyue; An, Li; Jiang, Xiaowen; Bai, Junpeng; Huang, Jian; Meng, Weihong; Zhao, Qingchun

2016-12-01

Compound MQA (1,5-O-dicaffeoyl-3-O-[4-malic acid methyl ester]-quinic acid) is a natural caffeoylquinic acid derivative isolated from Arctium lappa L. roots. This study aims to explore the neuroprotective effects of MQA against hydrogen peroxide (H 2 O 2 )-induced oxidative stress in SH-SY5Y neuroblastoma cells. The SH-SY5Y cells were divided into four groups, including control, 20 μM MQA, 200 μM H2O2, 200 μM H2O2 + 20 μM MQA groups. The effects of MQA on H 2 O 2 -induced cell death were measured by MTT and LDH assays. Hoechst 33342 and Annexin V-PI double staining were used to observed H2O2-induced apoptosis. Also, the effects of MQA on antioxidant system and mitochondrial pathway were explored. Further, steady-state phosphorylation levels of ERK1/2, Akt and GSK-3β were examined by Western blot analysis. Pretreatment with MQA prevented cell death in SH-SY5Y cells exposed to 200 μM H2O2 for 3 h. Meanwhile, Hoechst 33342 and Annexin V-PI double staining showed that MQA attenuated H 2 O 2 -induced apoptosis. These changes are related to elevation in SOD activity, reduction in MDA production and ROS formation, and increases in mitochondrial membrane potential (MMP). In addition, the potential mechanisms of MQA against H 2 O 2 -induced apoptosis are associated with increases in the Bcl-2/Bax ratio, decreases in cytochrome c release, caspase-3 and caspase-9 expressions, phosphorylation of ERK1/2, and dephosphorylation of AKT and GSK-3β. These findings suggest that protective effects of MQA against H 2 O 2 -induced apoptosis might be associated with mitochondrial apoptosis, ERK1/2 and AKT/GSK-3β pathway.

Protective effect of Dendrobium officinale polysaccharides on H2O2-induced injury in H9c2 cardiomyocytes.

Science.gov (United States)

Zhao, Xiaoyan; Dou, Mengmeng; Zhang, Zhihao; Zhang, Duoduo; Huang, Chengzhi

2017-10-01

The preliminary studies have shown that Dendrobium officinale possessed therapeutic effects on hypertension and atherosclerosis. Studies also reported that Dendrobium officinale polysaccharides showed antioxidant capabilities. However, little is known about its effects on myocardial cells under oxidative stress. The present study was designed to study the protective effect of Dendrobium officinale polysaccharides against H 2 O 2 -induced oxidative stress in H9c2 cells. MTT assay was carried out to determine the cell viability of H9c2 cells when pretreated with Dendrobium officinale polysaccharides. Fluorescent microscopy measurements were performed for evaluating the apoptosis in H9c2 cells. Furthermore, effects of Dendrobium officinale polysaccharides on the activities of antioxidative indicators (malondialdehyde, superoxide dismutase), reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP) levels were analyzed. Dendrobium officinale polysaccharides attenuated H 2 O 2 -induced cell death, as determined by the MTT assay. Dendrobium officinale polysaccharides decreased malondialdehyde levels, increased superoxide dismutase activities, and inhibited the generation of intracellular ROS. Moreover, pretreatment with Dendrobium officinale polysaccharides also inhibited apoptosis and increased the MMP levels in H9c2 cells. These results suggested the protective effects of Dendrobium officinale polysaccharides against H 2 O 2 -induced injury in H9c2 cells. The results also indicated the anti-oxidative capability of Dendrobium officinale polysaccharides. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Glucose-6-phosphate dehydrogenase deficiency does not increase the susceptibility of sperm to oxidative stress induced by H2O2.

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Roshankhah, Shiva; Rostami-Far, Zahra; Shaveisi-Zadeh, Farhad; Movafagh, Abolfazl; Bakhtiari, Mitra; Shaveisi-Zadeh, Jila

2016-12-01

Glucose-6-phosphate dehydrogenase (G6PD) deficiency is the most common human enzyme defect. G6PD plays a key role in the pentose phosphate pathway, which is a major source of nicotinamide adenine dinucleotide phosphate (NADPH). NADPH provides the reducing equivalents for oxidation-reduction reductions involved in protecting against the toxicity of reactive oxygen species such as H 2 O 2 . We hypothesized that G6PD deficiency may reduce the amount of NADPH in sperms, thereby inhibiting the detoxification of H 2 O 2 , which could potentially affect their motility and viability, resulting in an increased susceptibility to infertility. Semen samples were obtained from four males with G6PD deficiency and eight healthy males as a control. In both groups, motile sperms were isolated from the seminal fluid and incubated with 0, 10, 20, 40, 60, 80, and 120 µM concentrations of H 2 O 2 . After 1 hour incubation at 37℃, sperms were evaluated for motility and viability. Incubation of sperms with 10 and 20 µM H 2 O 2 led to very little decrease in motility and viability, but motility decreased notably in both groups in 40, 60, and 80 µM H 2 O 2 , and viability decreased in both groups in 40, 60, 80, and 120 µM H 2 O 2 . However, no statistically significant differences were found between the G6PD-deficient group and controls. G6PD deficiency does not increase the susceptibility of sperm to oxidative stress induced by H 2 O 2 , and the reducing equivalents necessary for protection against H 2 O 2 are most likely produced by other pathways. Therefore, G6PD deficiency cannot be considered as major risk factor for male infertility.

Exogenous NAD(+) decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy.

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Zhu, Ying; Zhao, Ke-Ke; Tong, Yao; Zhou, Ya-Li; Wang, Yi-Xiao; Zhao, Pei-Quan; Wang, Zhao-Yang

2016-05-31

Increased oxidative stress, which can lead to the retinal pigment epithelium (RPE) cell death by inducing ATP depletion and DNA repair, is believed to be a prominent pathology in age-related macular degeneration (AMD). In the present study, we showed that and 0.1 mM nicotinamide adenine dinucleotide (NAD(+)) administration significantly blocked RPE cell death induced by 300 μM H2O2. Further investigation showed that H2O2 resulted in increased intracellular ROS level, activation of PARP-1 and subsequently necrotic death of RPE cells. Exogenous NAD(+) administration significantly decreased intracellular and intranuclear ROS levels in H2O2-treated RPE cells. In addition, NAD(+) administration to H2O2-treated RPE cells inhibited the activation of PARP-1 and protected the RPE cells against necrotic death. Moreover, exogenous NAD(+) administration up-regulated autophagy in the H2O2-treated RPE cells. Inhibition of autophagy by LY294002 blocked the decrease of intracellular and intranuclear ROS level. Besides, inhibition of autophagy by LY294002 abolished the protection of exogenous NAD(+) against H2O2-induced cell necrotic death. Taken together, our findings indicate that that exogenous NAD(+) administration suppresses H2O2-induced oxidative stress and protects RPE cells against PARP-1 mediated necrotic death through the up-regulation of autophagy. The results suggest that exogenous NAD(+) administration might be potential value for the treatment of AMD.

Exogenous NAD+ decreases oxidative stress and protects H2O2-treated RPE cells against necrotic death through the up-regulation of autophagy

Science.gov (United States)

Zhu, Ying; Zhao, Ke-ke; Tong, Yao; Zhou, Ya-li; Wang, Yi-xiao; Zhao, Pei-quan; Wang, Zhao-yang

2016-01-01

Increased oxidative stress, which can lead to the retinal pigment epithelium (RPE) cell death by inducing ATP depletion and DNA repair, is believed to be a prominent pathology in age-related macular degeneration (AMD). In the present study, we showed that and 0.1 mM nicotinamide adenine dinucleotide (NAD+) administration significantly blocked RPE cell death induced by 300 μM H2O2. Further investigation showed that H2O2 resulted in increased intracellular ROS level, activation of PARP-1 and subsequently necrotic death of RPE cells. Exogenous NAD+ administration significantly decreased intracellular and intranuclear ROS levels in H2O2-treated RPE cells. In addition, NAD+ administration to H2O2-treated RPE cells inhibited the activation of PARP-1 and protected the RPE cells against necrotic death. Moreover, exogenous NAD+ administration up-regulated autophagy in the H2O2-treated RPE cells. Inhibition of autophagy by LY294002 blocked the decrease of intracellular and intranuclear ROS level. Besides, inhibition of autophagy by LY294002 abolished the protection of exogenous NAD+ against H2O2-induced cell necrotic death. Taken together, our findings indicate that that exogenous NAD+ administration suppresses H2O2-induced oxidative stress and protects RPE cells against PARP-1 mediated necrotic death through the up-regulation of autophagy. The results suggest that exogenous NAD+ administration might be potential value for the treatment of AMD. PMID:27240523

A unique polysaccharide purified from Hericium erinaceus mycelium prevents oxidative stress induced by H2O2 in human gastric mucosa epithelium cell.

Science.gov (United States)

Wang, Mingxing; Kanako, Nakajima; Zhang, Yanqiu; Xiao, Xulang; Gao, Qipin; Tetsuya, Konishi

2017-01-01

Hericium erinaceus (HE) has been used both as a traditional Chinese medicine and home remedy for treatment of gastric and duodenal ulcers and gastritis. EP-1, a purified polysaccharide isolated from HE mycelium, has recently been identified as the active component responsible for HE anti-gastritis activity. Because oxidative stress has been implicated as a pathogenic cause of gastritis and gastric ulcers, EP-1 antioxidant properties were systematically examined in vitro using the human gastric mucosal epithelial cell line, GES-1. Results showed that EP-1 possessed higher oxygen radical absorbance capacity (ORAC) and 2-3 times higher ability to scavenge 2,2-diphenyl-1-picrylhydrazyl (DPPH), superoxide and hydroxyl radicals than a hot water extract of commercially available HE fruiting body. A crude mycelial polysaccharide (CMPS) extract of HE, from which EP-1 was purified, showed slightly stronger radical scavenging activity and ORAC than EP-1, with the exception of DPPH-scavenging activity. Antioxidant activities of these extracts were further studied using hydrogen peroxide (H2O2)-abused GES-1 cells; EP-1 dose-dependently preserved cell viability of abused cells as assessed via MTT assay. Moreover, FACS analysis revealed that EP-1 prevented H2O2-induced apoptotic cell death by inhibiting activation of apoptotic cellular signals within mitochondria-dependent apoptotic pathways. CMPS also prevented H2O2-induced oxidative stress, but to a lesser degree than did EP-1, even though CMPS exhibited comparable or stronger in vitro antioxidant activity than did EP-1.

A unique polysaccharide purified from Hericium erinaceus mycelium prevents oxidative stress induced by H2O2 in human gastric mucosa epithelium cell.

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Mingxing Wang

Full Text Available Hericium erinaceus (HE has been used both as a traditional Chinese medicine and home remedy for treatment of gastric and duodenal ulcers and gastritis. EP-1, a purified polysaccharide isolated from HE mycelium, has recently been identified as the active component responsible for HE anti-gastritis activity. Because oxidative stress has been implicated as a pathogenic cause of gastritis and gastric ulcers, EP-1 antioxidant properties were systematically examined in vitro using the human gastric mucosal epithelial cell line, GES-1. Results showed that EP-1 possessed higher oxygen radical absorbance capacity (ORAC and 2-3 times higher ability to scavenge 2,2-diphenyl-1-picrylhydrazyl (DPPH, superoxide and hydroxyl radicals than a hot water extract of commercially available HE fruiting body. A crude mycelial polysaccharide (CMPS extract of HE, from which EP-1 was purified, showed slightly stronger radical scavenging activity and ORAC than EP-1, with the exception of DPPH-scavenging activity. Antioxidant activities of these extracts were further studied using hydrogen peroxide (H2O2-abused GES-1 cells; EP-1 dose-dependently preserved cell viability of abused cells as assessed via MTT assay. Moreover, FACS analysis revealed that EP-1 prevented H2O2-induced apoptotic cell death by inhibiting activation of apoptotic cellular signals within mitochondria-dependent apoptotic pathways. CMPS also prevented H2O2-induced oxidative stress, but to a lesser degree than did EP-1, even though CMPS exhibited comparable or stronger in vitro antioxidant activity than did EP-1.

H2O2-induced higher order chromatin degradation: A novel ...

Indian Academy of Sciences (India)

Unknown

mediator of oxidative stress, can also cause genomic damage indirectly. Thus, H2O2 at pathologically relevant concentrations rapidly induces higher order chromatin degradation (HOCD), i.e. enzymatic ... clease works through a single strand scission mechanism ... a great mutagenic risk to the surviving cells, because en-.

Anti-Ageing Effects of Sonchus oleraceus L. (pūhā) Leaf Extracts on H2O2-Induced Cell Senescence

OpenAIRE

Zong-Quan Ou; Thomas Rades; Arlene McDowell

2015-01-01

Antioxidants protect against damage from free radicals and are believed to slow the ageing process. Previously, we have reported the high antioxidant activity of 70% methanolic Sonchus oleraceus L. (Asteraceae) leaf extracts. We hypothesize that S. oleraceus extracts protect cells against H2O2-induced senescence by mediating oxidative stress. Premature senescence of young WI-38 cells was induced by application of H2O2. Cells were treated with S. oleraceus extracts before or after H2O2 stress...

Neuroprotective activity of Leontice leontopetalum extract against H2O2-stimulated oxidative stress in PC12 cells

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S. Sahranavard*

2017-11-01

Full Text Available Background and objectives: Neuronal toxicity can be induced by oxidative stress via free radicals production. In recent years, great interest has been expressed to the traditional and herbal medicines. The purpose of this study was to elucidate the neuroprotective activity of Leontice leontopetalum methanol extract against H2O2-stimulated oxidative stress in PC12 cells. Methods: The plantLeontice leontopetalum was selected based on the ethnobotanical approach, which is used traditionally for the treatment of diseases related to inflammation and pain in Turkmen Sahra, Iran. Cytotoxicity of different concentrations of the methanol extract against PC12 cells was evaluated by MTT assay. Then PC12 cells were exposed to H2O2 in the presence or absence of the extract. In the next step, the total protein concentration was measured via Bradford assay and cyclooxygenase inhibition was determined by a screening assay kit. Nitrite accumulated in culture medium of supernatant was measured by Griess reaction. Results: Our results indicated that the methanol extract of Leontice leontopetalum significantly inhibited cyclooxygenase activity in the presence of H2O2; however, it was not able to inhibit nitric oxide generation in the stimulated PC12 cells. Conclusion: The results suggested that Leontice leontopetalum may be useful in reducing risk of neurodegenerative related diseases such as Alzheimer Disease.

Anti-Ageing Effects of Sonchus oleraceus L. (pūhā) Leaf Extracts on H2O2-Induced Cell Senescence

DEFF Research Database (Denmark)

Ou, Zong-Quan; Rades, Thomas; McDowell, Arlene

2015-01-01

Antioxidants protect against damage from free radicals and are believed to slow the ageing process. Previously, we have reported the high antioxidant activity of 70% methanolic Sonchus oleraceus L. (Asteraceae) leaf extracts. We hypothesize that S. oleraceus extracts protect cells against H2O2......-induced senescence by mediating oxidative stress. Premature senescence of young WI-38 cells was induced by application of H2O2. Cells were treated with S. oleraceus extracts before or after H2O2 stress. The senescence- associated β-galactosidase (SA-β-gal) activity was used to indicate cell senescence. S....... oleraceus extracts showed higher cellular antioxidant activity than chlorogenic acid in WI-38 cells. S. oleraceus extracts suppressed H2O2 stress-induced premature senescence in a concentration-dependent manner. At 5 and 20 mg/mL, S. oleraceus extracts showed better or equivalent effects of reducing stress...

Neuroprotective and antioxidant activities of bamboo salt soy sauce against H2O2-induced oxidative stress in rat cortical neurons.

Science.gov (United States)

Jeong, Jong Hee; Noh, Min-Young; Choi, Jae-Hyeok; Lee, Haiwon; Kim, Seung Hyun

2016-04-01

Bamboo salt (BS) and soy sauce (SS) are traditional foods in Asia, which contain antioxidants that have cytoprotective effects on the body. The majority of SS products contain high levels of common salt, consumption of which has been associated with numerous detrimental effects on the body. However, BS may be considered a healthier substitute to common salt. The present study hypothesized that SS made from BS, known as bamboo salt soy sauce (BSSS), may possess enhanced cytoprotective properties; this was evaluated using a hydrogen peroxide (H 2 O 2 )-induced neuronal cell death rat model. Rat neuronal cells were pretreated with various concentrations (0.001, 0.01, 0.1, 1 and 10%) of BSSS, traditional soy sauce (TRSS) and brewed soy sauce (BRSS), and were subsequently exposed to H 2 O 2 (100 µM). The viability of neuronal cells, and the occurrence of DNA fragmentation, was subsequently examined. Pretreatment of neuronal cells with TRSS and BRSS reduced cell viability in a concentration-dependent manner, whereas neuronal cells pretreated with BSSS exhibited increased cell viability, as compared with non-treated neuronal cells. Furthermore, neuronal cells pretreated with 0.01% BSSS exhibited the greatest increase in viability. Exposure of neuronal cells to H 2 O 2 significantly increased the levels of reactive oxygen species (ROS), B-cell lymphoma 2-associated X protein, poly (ADP-ribose), cleaved poly (ADP-ribose) polymerase, cytochrome c , apoptosis-inducing factor, cleaved caspase-9 and cleaved caspase-3, in all cases. Pretreatment of neuronal cells with BSSS significantly reduced the levels of ROS generated by H 2 O 2 , and increased the levels of phosphorylated AKT and phosphorylated glycogen synthase kinase-3β. Furthermore, the observed effects of BSSS could be blocked by administration of 10 µM LY294002, a phosphatidylinositol 3-kinase inhibitor. The results of the present study suggested that BSSS may exert positive neuroprotective effects against H 2 O 2

Relationship between NaCl- and H2O2-induced cytosolic Ca2+ increases in response to stress in Arabidopsis.

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Zhonghao Jiang

Full Text Available Salinity is among the environmental factors that affect plant growth and development and constrain agricultural productivity. Salinity stress triggers increases in cytosolic free Ca(2+ concentration ([Ca(2+]i via Ca(2+ influx across the plasma membrane. Salinity stress, as well as other stresses, induces the production of reactive oxygen species (ROS. It is well established that ROS also triggers increases in [Ca(2+]i. However, the relationship and interaction between salinity stress-induced [Ca(2+]i increases and ROS-induced [Ca(2+]i increases remain poorly understood. Using an aequorin-based Ca(2+ imaging assay we have analyzed [Ca(2+]i changes in response to NaCl and H2O2 treatments in Arabidopsis thaliana. We found that NaCl and H2O2 together induced larger increases in [Ca(2+]i in Arabidopsis seedlings than either NaCl or H2O2 alone, suggesting an additive effect on [Ca(2+]i increases. Following a pre-treatment with either NaCl or H2O2, the subsequent elevation of [Ca(2+]i in response to a second treatment with either NaCl or H2O2 was significantly reduced. Furthermore, the NaCl pre-treatment suppressed the elevation of [Ca(2+]i seen with a second NaCl treatment more than that seen with a second treatment of H2O2. A similar response was seen when the initial treatment was with H2O2; subsequent addition of H2O2 led to less of an increase in [Ca(2+]i than did addition of NaCl. These results imply that NaCl-gated Ca(2+ channels and H2O2-gated Ca(2+ channels may differ, and also suggest that NaCl- and H2O2-evoked [Ca(2+]i may reduce the potency of both NaCl and H2O2 in triggering [Ca(2+]i increases, highlighting a feedback mechanism. Alternatively, NaCl and H2O2 may activate the same Ca(2+ permeable channel, which is expressed in different types of cells and/or activated via different signaling pathways.

Effects of CO, O2, NO, H2O, and irradiation temperature on the radiation-induced oxidation of SO2

International Nuclear Information System (INIS)

Tokunaga, Okihiro; Nishimura, Koichi; Suzuki, Nobutake; Washino, Masamitsu

1977-01-01

When a SO 2 -H 2 O-O 2 -N 2 gaseous mixture was irradiated by electron beams of 1.5 MeV, SO 2 was easily oxidized to H 2 SO 4 . Effects of CO, O 2 , NO, H 2 O, and irradiation temperature on the radiation-induced oxidation of SO 2 were studied by measuring the SO 2 concentration gas chromatographically. The G(-SO 2 ) increased greatly at the addition of a small amount of O 2 , and then decreased gradually with an increase in the O 2 concentration, i.e., the G(-SO 2 ) values were 0.9, 8.0, and 5.3 for the 0, 0.1, and 20% O 2 concentrations at 100 0 C, respectively (Fig.4). The G(-SO 2 ) was independent of the H 2 O concentration in the range of 0.84 to 8.4% (Fig.5). The G(-SO 2 ) decreased with a rise in the irradiation temperature (Fig.6) and an apparent activation energy of the oxidation reaction of SO 2 obtained was -4.2 kcal.mol -1 . The effects of CO, NO, and O 2 on the G(-SO 2 ) showed that SO 2 was mainly oxidized by OH and O and that the contribution of OH to the oxidation of SO 2 increased with an increase in the O 2 concentration (Table 1). The rate constants for the reactions of SO 2 with OH and O, obtained from competitive reactions of SO 2 with CO and O 2 , were 5.4 x 10 11 cm 3 .mol -1 .sec -1 and 5.0 x 10 11 cm 3 .mol -1 .sec -1 , respectively. (auth.)

Anti-Ageing Effects of Sonchus oleraceus L. (pūhā Leaf Extracts on H2O2-Induced Cell Senescence

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Zong-Quan Ou

2015-03-01

Full Text Available Antioxidants protect against damage from free radicals and are believed to slow the ageing process. Previously, we have reported the high antioxidant activity of 70% methanolic Sonchus oleraceus L. (Asteraceae leaf extracts. We hypothesize that S. oleraceus extracts protect cells against H2O2-induced senescence by mediating oxidative stress. Premature senescence of young WI-38 cells was induced by application of H2O2. Cells were treated with S. oleraceus extracts before or after H2O2 stress. The senescence- associated β-galactosidase (SA-β-gal activity was used to indicate cell senescence. S. oleraceus extracts showed higher cellular antioxidant activity than chlorogenic acid in WI-38 cells. S. oleraceus extracts suppressed H2O2 stress-induced premature senescence in a concentration-dependent manner. At 5 and 20 mg/mL, S. oleraceus extracts showed better or equivalent effects of reducing stress-induced premature senescence than the corresponding ascorbic acid treatments. These findings indicate the potential of S. oleraceus extracts to be formulated as an anti-ageing agent.

Tamarix gallica phenolics protect IEC-6 cells against H2O2 induced stress by restricting oxidative injuries and MAPKs signaling pathways.

Science.gov (United States)

Bettaib, Jamila; Talarmin, Hélène; Droguet, Mickaël; Magné, Christian; Boulaaba, Mondher; Giroux-Metges, Marie-Agnès; Ksouri, Riadh

2017-05-01

Polyphenolic compounds gained interest in the pharmaceutical research area due to their beneficial properties. Herein, antioxidant and cytoprotective capacities of T. gallica extract on H 2 O 2 -challenged rat small intestine epithelial cells were investigated. To set stress conditions, IEC-6 cultures were challenged with numerous H 2 O 2 doses and durations. Then, 40μM H 2 O 2 during 4h were selected to assess the cytoprotective effect of different T. gallica extract concentrations. Oxidative parameters, measured through CAT and SOD activities as well as MDA quantification were assessed. In addition, the expression of possibly involved MAPKs was also valued. Main results reported that T. gallica was rich in polyphenols and exhibited an important antioxidant activity (DPPH Assay, IC 50 =6μgmL -1 ; ABTS + test, IC 50 =50μgmL -1 ; Fe-reducing power, EC 50 =100μgmL -1 ). The exposure of IEC-6 cultures to 40μM H 2 O 2 during 4h caused oxidative stress manifested by (i) over 70% cell mortality, (ii) over-activity of CAT (246%), (iii) excess in MDA content (18.4nmolmg -1 ) and (iiii) a trigger of JNK phosphorylation. Pretreatment with T. gallica extract, especially when used at 0.25μgmL -1 , restored cell viability to 122%, and normal cell morphology in H 2 O 2 -chalenged cells. In addition, this extract normalized CAT activity and MDA content (100% and 14.7nmolmg -1 , respectively) to their basal levels as compared to control cells. Furthermore, stopping cell death seems to be due to dephosphorylated JNK MAPK exerted by T. gallica bioactive compounds. In all, T. gallica components provided a cross-talk between regulatory pathways leading to an efficient cytoprotection against harmful oxidative stimulus. Copyright © 2017 Elsevier Masson SAS. All rights reserved.

Porous Se@SiO2 nanospheres treated paraquat-induced acute lung injury by resisting oxidative stress

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Zhu Y

2017-09-01

Full Text Available Yong Zhu,1,* Guoying Deng,2,* Anqi Ji,2 Jiayi Yao,1 Xiaoxiao Meng,1 Jinfeng Wang,1 Qian Wang,2 Qiugen Wang,2 Ruilan Wang1 1Department of Critical Care Medicine, Shanghai General Hospital, Shanghai Jiaotong University, School of Medicine, 2Trauma Center, Shanghai General Hospital, Shanghai Jiaotong University, School of Medicine, Shanghai, China *These authors contributed equally to this work Abstract: Acute paraquat (PQ poisoning is one of the most common forms of pesticide poisoning. Oxidative stress and inflammation are thought to be important mechanisms in PQ-induced acute lung injury (ALI. Selenium (Se can scavenge intracellular free radicals directly or indirectly. In this study, we investigated whether porous Se@SiO2 nanospheres could alleviate oxidative stress and inflammation in PQ-induced ALI. Male Sprague Dawley rats and RLE-6TN cells were used in this study. Rats were categorized into 3 groups: control (n=6, PQ (n=18, and PQ + Se@SiO2 (n=18. The PQ and PQ + Se@SiO2 groups were randomly and evenly divided into 3 sub-groups according to different time points (24, 48 and 72 h after PQ treatment. Porous Se@SiO2 nanospheres 1 mg/kg (in the PQ + Se@SiO2 group were administered via intraperitoneal injection every 24 h. Expression levels of reduced glutathione, malondialdehyde, superoxide dismutase, reactive oxygen species (ROS, nuclear factor-κB (NF-κB, phosphorylated NF-κB (p-NF-κB, tumor necrosis factor-α and interleukin-1β were detected, and a histological analysis of rat lung tissues was performed. The results showed that the levels of ROS, malondialdehyde, NF-κB, p-NF-κB, tumor necrosis factor-α and interleukin-1β were markedly increased after PQ treatment. Glutathione and superoxide dismutase levels were reduced. However, treatment with porous Se@SiO2 nanospheres markedly alleviated PQ-induced oxidative stress and inflammation. Additionally, the results from histological examinations and wet-to-dry weight ratios of rat lung

Cross Talk between H2O2 and Interacting Signal Molecules under Plant Stress Response

Science.gov (United States)

Saxena, Ina; Srikanth, Sandhya; Chen, Zhong

2016-01-01

It is well established that oxidative stress is an important cause of cellular damage. During stress conditions, plants have evolved regulatory mechanisms to adapt to various environmental stresses. One of the consequences of stress is an increase in the cellular concentration of reactive oxygen species, which is subsequently converted to H2O2. H2O2 is continuously produced as the byproduct of oxidative plant aerobic metabolism. Organelles with a high oxidizing metabolic activity or with an intense rate of electron flow, such as chloroplasts, mitochondria, or peroxisomes are major sources of H2O2 production. H2O2 acts as a versatile molecule because of its dual role in cells. Under normal conditions, H2O2 immerges as an important factor during many biological processes. It has been established that it acts as a secondary messenger in signal transduction networks. In this review, we discuss potential roles of H2O2 and other signaling molecules during various stress responses. PMID:27200043

Effects of Downregulation of MicroRNA-181a on H2O2-Induced H9c2 Cell Apoptosis via the Mitochondrial Apoptotic Pathway

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Lei Wang

2014-01-01

Full Text Available Glutathione peroxidase-1 (GPx1 is a pivotal intracellular antioxidant enzyme that enzymatically reduces hydrogen peroxide to water to limit its harmful effects. This study aims to identify a microRNA (miRNA that targets GPx1 to maintain redox homeostasis. Dual luciferase assays combined with mutational analysis and immunoblotting were used to validate the bioinformatically predicted miRNAs. We sought to select miRNAs that were responsive to oxidative stress induced by hydrogen peroxide (H2O2 in the H9c2 rat cardiomyocyte cell line. Quantitative real-time PCR (qPCR demonstrated that the expression of miR-181a in H2O2-treated H9c2 cells was markedly upregulated. The downregulation of miR-181a significantly inhibited H2O2-induced cellular apoptosis, ROS production, the increase in malondialdehyde (MDA levels, the disruption of mitochondrial structure, and the activation of key signaling proteins in the mitochondrial apoptotic pathway. Our results suggest that miR-181a plays an important role in regulating the mitochondrial apoptotic pathway in cardiomyocytes challenged with oxidative stress. MiR-181a may represent a potential therapeutic target for the treatment of oxidative stress-associated cardiovascular diseases.

Identification of H2O2 induced oxidative stress associated microRNAs in HLE-B3 cells and their clinical relevance to the progression of age-related nuclear cataract.

Science.gov (United States)

Wang, Song; Guo, Chenjun; Yu, Mengsi; Ning, Xiaona; Yan, Bo; Zhao, Jing; Yang, Angang; Yan, Hong

2018-04-13

This study is aimed to screen out the microRNAs (miRNAs) associated with H 2 O 2 induced oxidative stress in human lens epithelial B3 (HLE-B3) cell lines and investigate their relations with the progression of age-related nuclear cataract. H 2 O 2 was used to induce oxidative stress in HLE-B3 cells. A genome-wide expression profiling of miRNAs in HLE-B3 cells was performed to select the differentially expressed miRNAs before and after H 2 O 2 treatment. The selected miRNAs were validated by RT-PCR and fluorescence in situ hybridization (FISH). Clinical specimens were divided into three groups according to the Lens Opacities Classification System III (LOCSIII) and the expression levels of the selected miRNAs were tested by RT-PCR in the three groups. Bioinformatics analyses were applied to predict the target genes of the miRNA hits and construct the miRNA regulatory network. The expression level of MAPK14 was analyzed by Western blot. The H 2 O 2 induced oxidative stress model of HLE-B3 cells was established. Nineteen upregulated and 30 downregulated miRNAs were identified as differentially expressed miRNAs. Seven of the total 49 were validated in the cell model. RT-PCR of the clinical samples showed that the expression levels of miR-34a-5p, miR-630 and miR-335-3p were closely related with the severity of nuclear opacity. The images taken from FISH confirmed the results of RT-PCR. There were 172 target genes of the three miRNAs clustered in the category of response to stress. The regulatory network demonstrated that 23 target genes were co-regulated by multiple miRNAs. MAPK14 was the target gene of three miRNAs and the result were verified by Western blot. Up-regulation of miR-34a-5p and miR-630 and down-regulation of miR-335-3p are related with the progression of age-related nuclear cataract and the underlying mechanism awaits further functional research to reveal.

Chlorogenic acid analogues from Gynura nepalensis protect H9c2 cardiomyoblasts against H2O2-induced apoptosis.

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Yu, Bang-Wei; Li, Jin-Long; Guo, Bin-Bin; Fan, Hui-Min; Zhao, Wei-Min; Wang, He-Yao

2016-11-01

Chlorogenic acid has shown protective effect on cardiomyocytes against oxidative stress-induced damage. Herein, we evaluated nine caffeoylquinic acid analogues (1-9) isolated from the leaves of Gynura nepalensis for their protective effect against H 2 O 2 -induced H9c2 cardiomyoblast damage and explored the underlying mechanisms. H9c2 cardiomyoblasts were exposed to H 2 O 2 (0.3 mmol/L) for 3 h, and cell viability was detected with MTT assay. Hoechst 33342 staining was performed to evaluate cell apoptosis. MMPs (mitochondrial membrane potentials) were measured using a JC-1 assay kit, and ROS (reactive oxygen species) generation was measured using CM-H 2 DCFDA. The expression levels of relevant proteins were detected using Western blot analysis. Exposure to H 2 O 2 markedly decreased the viability of H9c2 cells and catalase activity, and increased LDH release and intracellular ROS production; accompanied by a loss of MMP and increased apoptotic rate. Among the 9 chlorogenic acid analogues as well as the positive control drug epigallocatechin gallate (EGCG) tested, compound 6 (3,5-dicaffeoylquinic acid ethyl ester) was the most effective in protecting H9c2 cells from H 2 O 2 -induced cell death. Pretreatment with compound 6 (1.56-100 μmol/L) dose-dependently alleviated all the H 2 O 2 -induced detrimental effects. Moreover, exposure to H 2 O 2 significantly increased the levels of Bax, p53, cleaved caspase-8, and cleaved caspase-9, and decreased the level of Bcl-2, resulting in cell apoptosis. Exposure to H 2 O 2 also significantly increased the phosphorylation of p38, JNK and ERK in the H9c2 cells. Pretreatment with compound 6 (12.5 and 25 μmol/L) dose-dependently inhibited the H 2 O 2 -induced increase in the level of cleaved caspase-9 but not of cleaved caspase-8. It also dose-dependently suppressed the H 2 O 2 -induced phosphorylation of JNK and ERK but not that of p38. Compound 6 isolated from the leaves of Gynura nepalensis potently protects H9c2

H2S Attenuates LPS-Induced Acute Lung Injury by Reducing Oxidative/Nitrative Stress and Inflammation

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Hong-Xia Zhang

2016-12-01

Full Text Available Background: Hydrogen sulfide (H2S, known as the third endogenous gaseous transmitter, has received increasing attention because of its diverse effects, including angiogenesis, vascular relaxation and myocardial protection.We aimed to investigate the role of H2S in oxidative/nitrative stress and inflammation in acute lung injury (ALI induced by endotoxemia. Methods: Male ICR mice were divided in six groups: (1 Control group; (2 GYY4137treatment group; (3 L-NAME treatment group; (4 lipopolysaccharide (LPS treatment group; (5 LPS with GYY4137 treatment group; and (6 LPS with L-NAME treatment group. The lungs were analysed by histology, NO production in the mouse lungs determined by modified Griess (Sigma-Aldrich reaction, cytokine levels utilizing commercialkits, and protein abundance by Western blotting. Results: GYY4137, a slowly-releasing H2S donor, improved the histopathological changes in the lungs of endotoxemic mice. Treatment with NG-nitro-L-arginine methyl ester (L-NAME, a nitric oxide synthase (NOS inhibitor, increased anti-oxidant biomarkers such as thetotal antioxidant capacity (T-AOC and theactivities of catalase (CAT and superoxide dismutase (SOD but decreased a marker of peroxynitrite (ONOO- action and 3-nitrotyrosine (3-NT in endotoxemic lung. L-NAME administration also suppressed inflammation in endotoxemic lung, as evidenced by the decreased pulmonary levels of interleukin (IL-6, IL-8, and myeloperoxidase (MPO and the increased level of anti-inflammatory cytokine IL-10. GYY4137 treatment reversed endotoxin-induced oxidative/nitrative stress, as evidenced by a decrease in malondialdehyde (MDA, hydrogenperoxide (H2O2 and 3-NT and an increase in the antioxidant biomarker ratio of reduced/oxidized glutathione(GSH/GSSG ratio and T-AOC, CAT and SOD activity. GYY4137 also attenuated endotoxin-induced lung inflammation. Moreover, treatment with GYY4137 inhibited inducible NOS (iNOS expression and nitric oxide (NO production in the

Indirubin-3-Oxime Prevents H2O2-Induced Neuronal Apoptosis via Concurrently Inhibiting GSK3β and the ERK Pathway.

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Yu, Jie; Zheng, Jiacheng; Lin, Jiajia; Jin, Linlu; Yu, Rui; Mak, Shinghung; Hu, Shengquan; Sun, Hongya; Wu, Xiang; Zhang, Zaijun; Lee, Mingyuen; Tsim, Wahkeung; Su, Wei; Zhou, Wenhua; Cui, Wei; Han, Yifan; Wang, Qinwen

2017-05-01

Oxidative stress-induced neuronal apoptosis plays an important role in many neurodegenerative disorders. In this study, we have shown that indirubin-3-oxime, a derivative of indirubin originally designed for leukemia therapy, could prevent hydrogen peroxide (H 2 O 2 )-induced apoptosis in both SH-SY5Y cells and primary cerebellar granule neurons. H 2 O 2 exposure led to the increased activities of glycogen synthase kinase 3β (GSK3β) and extracellular signal-regulated kinase (ERK) in SH-SY5Y cells. Indirubin-3-oxime treatment significantly reversed the altered activity of both the PI3-K/Akt/GSK3β cascade and the ERK pathway induced by H 2 O 2 . In addition, both GSK3β and mitogen-activated protein kinase inhibitors significantly prevented H 2 O 2 -induced neuronal apoptosis. Moreover, specific inhibitors of the phosphoinositide 3-kinase (PI3-K) abolished the neuroprotective effects of indirubin-3-oxime against H 2 O 2 -induced neuronal apoptosis. These results strongly suggest that indirubin-3-oxime prevents H 2 O 2 -induced apoptosis via concurrent inhibiting GSK3β and the ERK pathway in SH-SY5Y cells, providing support for the use of indirubin-3-oxime to treat neurodegenerative disorders caused or exacerbated by oxidative stress.

Antioxidant ameliorating effects against H2O2-induced cytotoxicity in primary endometrial cells.

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Zal, F; Khademi, F; Taheri, R; Mostafavi-Pour, Z

2018-02-01

Oxidative stress and a disrupted antioxidant system are involved in a variety of pregnancy complications. In the present study, the role of vitamin E (Vit E) and folate as radical scavengers on the GSH homeostasis in stress oxidative induced in rat endometrial cells was investigated. Primary endometrial stromal cell cultures treated with 50 and 200 µM of H 2 O 2 and evaluated the cytoprotective effects of Vit E (5 µM) and folate (0.01 µM) in H 2 O 2 -treated cells for 24 h. Following the exposure of endometrial cells to H 2 O 2 alone and in the presence of Vit E and/or folate, cell survival, glutathione peroxidase (GPx) and glutathione reductase activities and the level of reduced glutathione (GSH) were measured. Cell adhesions comprise of cell attachment and spreading on collagen were determined. Flow cytometric analysis using annexin V was used to measure apoptosis. H 2 O 2 treatment showed a marked decrease in cell viability, GPx and GR activities and the level of GSH. Although Vit E or folate had some protective effect, combination therapy with Vit E and folate attenuated all the changes due to H 2 O 2 toxicity. An increasing number of alive cells was showed in the cells exposed to H 2 O 2 (50 µM) accompanied by co-treatment with Vit E and folic acid. The present findings indicate that co-administration of Vit E and folate before and during pregnancy may maintain a viable pregnancy and contribute to its clinical efficacy for the treatment of some idiopathic infertility.

Preconditioning with Gua Lou Gui Zhi decoction enhances H2O2-induced Nrf2/HO-1 activation in PC12 cells

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MAO, JINGJIE; LI, ZUANFANG; LIN, RUHUI; ZHU, XIAOQIN; LIN, JIUMAO; PENG, JUN; CHEN, LIDIAN

2015-01-01

Spasticity is common in various central neurological conditions, including after a stroke. Such spasticity may cause additional problems, and often becomes a primary concern for afflicted individuals. A number of studies have identified nuclear factor (erythroid-derived 2)-like 2 (Nrf2) as a key regulator in the adaptive survival response to oxidative stress. Elevated expression of Nrf2, combined with heme oxygenase 1 (HO-1) resistance, in the central nervous system is known to elicit key internal and external oxidation protection. Gua Lou Gui Zhi decoction (GLGZD) is a popular traditional Chinese formula with a long history of clinical use in China for the treatment of muscular spasticity following a stroke, epilepsy or a spinal cord injury. However, the mechanism underlying the efficacy of the medicine remains unclear. In the present study, the antioxidative effects of GLGZD were evaluated and the underlying molecular mechanisms were investigated, using hydrogen peroxide (H2O2)-induced rat pheochromocytoma cells (PC12 cells) as an in vitro oxidative stress model of neural cells. Upon application of different concentrations of GLGZD, a 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyltetrazolium bromide (MTT) assay and ATP measurement were conducted to assess the impact on PC12 cell proliferation. In addition, inverted microscopy observations, and the MTT and ATP assessments, revealed that GLGZD attenuated H2O2-induced oxidative damage and signaling repression in PC12 cells. Furthermore, the mRNA and protein expression levels of Nrf2 and HO-1, which are associated with oxidative stress, were analyzed using reverse transcription quantitative polymerase chain reaction (PCR) and confocal microscopy. Confocal microscopy observations, as well as the quantitative PCR assay, revealed that GLGZD exerted a neuroprotective function against H2O2-induced oxidative damage in PC12 cells. Therefore, the results demonstrated that GLGZD protected PC12 cells injured by H2O2, which may be

miR-146a down-regulation alleviates H2O2-induced cytotoxicity of PC12 cells by regulating MCL1/JAK/STAT pathway : miR-146a down-regulation relieves H2O2-induced PC12 cells cytotoxicity by MCL1/JAK/STAT.

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Yang, Xuecheng; Mao, Xin; Ding, Xuemei; Guan, Fengju; Jia, Yuefeng; Luo, Lei; Li, Bin; Tan, Hailin; Cao, Caixia

2018-02-26

Oxidative stress and miRNAs have been confirmed to play an important role in neurological diseases. The study aimed to explore the underlying effect and mechanisms of miR-146a in H 2 O 2 -induced injury of PC12 cells. Here, PC12 cells were stimulated with 200 μM of H 2 O 2 to construct oxidative injury model. Cell injury was evaluated on the basis of the changes in cell viability, migration, invasion, apoptosis, and DNA damage. Results revealed that miR-146a expression was up-regulated in H 2 O 2 -induced PC12 cells. Functional analysis showed that down-regulation of miR-146a alleviated H 2 O 2 -induced cytotoxicity in PC12 cells. Dual-luciferase reporter and western blot assay verified that MCL1 was a direct target gene of miR-146a. Moreover, anti-miR-146a-mediated suppression on cell cytotoxicity was abated following MCL1 knockdown in H 2 O 2 -induced PC12 cells. Furthermore, MCL1 activated JAK/STAT signaling pathway and MCL1 overexpression attenuated H 2 O 2 -induced cytotoxicity in PC12 cells by JAK/STAT signaling pathway. In conclusion, this study suggested that suppression of miR-146a abated H 2 O 2 -induced cytotoxicity in PC12 cells via regulating MCL1/JAK/STAT pathway.

Polysaccharide from Angelica sinensis protects H9c2 cells against oxidative injury and endoplasmic reticulum stress by activating the ATF6 pathway.

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Niu, Xiaowei; Zhang, Jingjing; Ling, Chun; Bai, Ming; Peng, Yu; Sun, Shaobo; Li, Yingdong; Zhang, Zheng

2018-01-01

Objectives Angelica sinensis exerts various pharmacological effects, such as antioxidant and anti-apoptotic activity. This study aimed to investigate the active ingredients in A. sinensis with antioxidant properties and whether A. sinensis polysaccharide (ASP) protects H9c2 cells against oxidative and endoplasmic reticulum (ER) stress. Methods The ingredients of A. sinensis and their targets and related pathways were determined using web-based databases. Markers of oxidative stress, cell viability, apoptosis, and ER stress-related signalling pathways were measured in H9c2 cells treated with hydrogen peroxide (H 2 O 2 ) and ASP. Results The ingredient-pathway-disease network showed that A. sinensis exerted protective effects against oxidative injury through its various active ingredients on regulation of multiple pathways. Subsequent experiments showed that ASP pretreatment significantly decreased H 2 O 2 -induced cytotoxicity and apoptosis in H9c2 cells. ASP pretreatment inhibited H 2 O 2 -induced reactive oxygen species generation, lactic dehydrogenase release, and malondialdehyde production. ASP exerted beneficial effects by inducing activating transcription factor 6 (ATF6) and increasing ATF6 target protein levels, which in turn attenuated ER stress and increased antioxidant activity. Conclusions Our findings indicate that ASP, a major water-soluble component of A. sinensis, exerts protective effects against H 2 O 2 -induced injury in H9c2 cells by activating the ATF6 pathway, thus ameliorating ER and oxidative stress.

The novel triterpenoid RTA 408 protects human retinal pigment epithelial cells against H2O2-induced cell injury via NF-E2-related factor 2 (Nrf2 activation

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Xiaobin Liu

2016-08-01

Full Text Available Oxidative stress-induced retinal pigment epithelial (RPE cell damage is an important factor in the pathogenesis of age-related macular degeneration (AMD. Previous studies have shown that RTA 408, a synthetic triterpenoid compound, potently activates Nrf2. This study aimed to investigate the protective effects of RTA 408 in cultured RPE cells during oxidative stress and to determine the effects of RTA 408 on Nrf2 and its downstream target genes. Primary human RPE cells were pretreated with RTA 408 and then incubated in 200 μM H2O2 for 6 h. Cell viability was measured with the WST-8 assay. Apoptosis was quantitatively measured by annexin V/propidium iodide (PI double staining and Hoechst 33342 fluorescent staining. Reduced (GSH and oxidized glutathione (GSSG were measured using colorimetric assays. Nrf2 activation and its downstream effects on phase II enzymes were examined by Western blot. Treatment of RPE cells with nanomolar ranges (10 and 100 nM of RTA 408 markedly attenuated H2O2-induced viability loss and apoptosis. RTA 408 pretreatment significantly protected cells from oxidative stress-induced GSH loss, GSSG formation and decreased ROS production. RTA 408 activated Nrf2 and increased the expression of its downstream genes, such as HO-1, NQO1, SOD2, catalase, Grx1, and Trx1. Consequently, the enzyme activities of NQO1, Grx1, and Trx1 were fully protected by RTA 408 pretreatment under oxidative stress. Moreover, knockdown of Nrf2 by siRNA significantly reduced the cytoprotective effects of RTA 408. In conclusion, our data suggest that RTA 408 protect primary human RPE cells from oxidative stress-induced damage by activating Nrf2 and its downstream genes.

Oxidative stress-induced metabolic changes in mouse C2C12 myotubes studied with high-resolution 13C, 1H, and 31P NMR spectroscopy

DEFF Research Database (Denmark)

Straadt, Ida K; Young, Jette F; Petersen, Bent O

2010-01-01

In this study, stress in relation to slaughter was investigated in a model system by the use of (13)C, (1)H, and (31)P nuclear magnetic resonance (NMR) spectroscopy for elucidating changes in the metabolites in C2C12 myotubes exposed to H(2)O(2)-induced stress. Oxidative stress resulted in lower...... to lower levels of the unlabeled ((12)C) lactate were identified in the (1)H spectra after stress exposure. These data indicate an increase in de novo synthesis of alanine, concomitant with a release of lactate from the myotubes to the medium at oxidative stress conditions. The changes in the metabolite...

The Copper Homeostasis Transcription Factor CopR Is Involved in H2O2 Stress in Lactobacillus plantarum CAUH2

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Yang Yang

2017-10-01

Full Text Available Transcriptional factors (TFs play important roles in the responses to oxidative, acid, and other environmental stresses in Gram-positive bacteria, but the regulatory mechanism of TFs involved in oxidative stress remains unknown in lactic acid bacteria. In the present work, homologous overexpression strains with 43 TFs were constructed in the Lactobacillus plantarum CAUH2 parent strain. The strain overexpressing CopR displayed the highest sensitivity and a 110-fold decrease in survival rate under H2O2 challenge. The importance of CopR in the response to H2O2 stress was further confirmed by a 10.8-fold increase in the survival of a copR insertion mutant. In silico analysis of the genes flanking copR revealed putative CopR-binding “cop box” sequences in the promoter region of the adjacent gene copB encoding a Cu2+-exporting ATPase. Electrophoretic mobility shift assay (EMSA analysis demonstrated the specific binding of CopR with copB in vitro, suggesting copB is a target gene of CopR in L. plantarum. The role of CopB involved in oxidative stress was verified by the significantly decreased survival in the copB mutant. Furthermore, a growth defect in copper-containing medium demonstrated that CopB functions as an export ATPase for copper ions. Furthermore, EMSAs revealed that CopR functions as a regulator that negatively regulates copB gene and Cu2+ serves as inducer of CopR to activate the expression of CopB in response to H2O2 stress in L. plantarum CAUH2. Our findings indicated that CopR plays an important role in enhancing oxidative resistance by regulating copB to modulate copper homeostasis.

Abscisic Acid-Induced H2O2 Accumulation Enhances Antioxidant Capacity in Pumpkin-Grafted Cucumber Leaves under Ca(NO3)2 Stress

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Shu, Sheng; Gao, Pan; Li, Lin; Yuan, Yinghui; Sun, Jin; Guo, Shirong

2016-01-01

With the aim to clarifying the role of the ABA/H2O2 signaling cascade in the regulating the antioxidant capacity of grafted cucumber plants in response to Ca(NO3)2 stress, we investigated the relationship between ABA-mediated H2O2 production and the activities of antioxidant enzymes in the leaves of pumpkin-grafted cucumber seedlings. The results showed that both ABA and H2O2 were detected in pumpkin-grafted cucumber seedlings in response to Ca(NO3)2 treatment within 0.5 h in the leaves and peaked at 3 and 6 h after Ca(NO3)2 treatment, respectively, compared to the levels under control conditions. The activities of superoxide dismutase (SOD), ascorbate peroxidase (APX), and peroxidase (POD) in pumpkin-grafted cucumber leaves gradually increased over time and peaked at 12 h of Ca(NO3)2 stress. Furthermore, in the leaves of pumpkin-grafted cucumber seedlings, the H2O2 generation, the antioxidant enzyme activities and the expression of SOD, POD and cAPX were strongly blocked by an inhibitor of ABA under Ca(NO3)2 stress, but this effect was eliminated by the addition of exogenous ABA. Moreover, the activities and gene expressions of these antioxidant enzymes in pumpkin-grafted leaves were almost inhibited under Ca(NO3)2 stress by pretreatment with ROS scavengers. These results suggest that the pumpkin grafting-induced ABA accumulation mediated H2O2 generation, resulting in the induction of antioxidant defense systems in leaves exposed to Ca(NO3)2 stress in the ABA/H2O2 signaling pathway. PMID:27746808

Proteomic and metabolomic analysis of H2O2-induced premature senescent human mesenchymal stem cells.

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Kim, Ji-Soo; Kim, Eui-Jin; Kim, Hyun-Jung; Yang, Ji-Young; Hwang, Geum-Sook; Kim, Chan-Wha

2011-06-01

Stress induced premature senescence (SIPS) occurs after exposure to many different sublethal stresses including H(2)O(2), hyperoxia, or tert-butylhydroperoxide. Human mesenchymal stem cells (hMSCs) exhibit limited proliferative potential in vitro, the so-called Hayflick limit. According to the free-radical theory, reactive oxygen species (ROS) might be the candidates responsible for senescence and age-related diseases. H(2)O(2) may be responsible for the production of high levels of ROS, in which the redox balance is disturbed and the cells shift into a state of oxidative stress, which subsequently leads to premature senescence with shortening telomeres. H(2)O(2) has been the most commonly used inducer of SIPS, which shares features of replicative senescence (RS) including a similar morphology, senescence-associated β-galactosidase activity, cell cycle regulation, etc. Therefore, in this study, the senescence of hMSC during SIPS was confirmed using a range of different analytical methods. In addition, we determined five differentially expressed spots in the 2-DE map, which were identified as Annexin A2 (ANXA2), myosin light chain 2 (MLC2), peroxisomal enoyl-CoA hydratase 1 (ECH1), prosomal protein P30-33K (PSMA1) and mutant β-actin by ESI-Q-TOF MS/MS. Also, proton ((1)H) nuclear magnetic resonance spectroscopy (NMR) was used to elucidate the difference between metabolites in the control and hMSCs treated with H(2)O(2). Among these metabolites, choline and leucine were identified by (1)H-NMR as up-regulated metabolites and glycine and proline were identified as down-regulated metabolites. Copyright © 2011 Elsevier Inc. All rights reserved.

Nuclear factor erythroid 2-related factor 2 antioxidant response element pathways protect bovine mammary epithelial cells against H2O2-induced oxidative damage in vitro.

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Ma, Y F; Wu, Z H; Gao, M; Loor, J J

2018-03-21

The experiment was conducted to determine the role of nuclear factor (erythroid-derived 2)-like factor 2 (NFE2L2, formerly Nrf2) antioxidant response element (ARE) pathway in protecting bovine mammary epithelial cells (BMEC) against H 2 O 2 -induced oxidative stress injury. An NFE2L2 small interfering RNA (siRNA) interference or a pCMV6-XL5-NFE2L2 plasmid fragment was transfected to independently downregulate or upregulate expression of NFE2L2. Isolated BMEC in triplicate were exposed to H 2 O 2 (600 μM) for 6 h to induce oxidative stress before transient transfection with scrambled siRNA, NFE2L2-siRNA, pCMV6-XL5, and pCMV6-XL5-NFE2L2. Cell proliferation, apoptosis and necrosis rates, antioxidant enzyme activities, reactive oxygen species (ROS) and malondialdehyde (MDA) production, protein and mRNA expression of NFE2L2 and downstream target genes, and fluorescence activity of ARE were measured. The results revealed that compared with the control, BMEC transfected with NFE2L2-siRNA3 had proliferation rates that were 9 or 65% lower without or with H 2 O 2 , respectively. These cells also had apoptosis and necrosis rates that were 27 and 3.5 times greater with H 2 O 2 compared with the control group, respectively. In contrast, transfected pCMV6-XL5-NFE2L2 had proliferation rates that were 64.3% greater or 17% lower without or with H 2 O 2 compared with the control group, respectively. Apoptosis rates were 1.8 times lower with H 2 O 2 compared with the control. In addition, compared with the control, production of ROS and MDA and activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase (CAT), and glutathione-S-transferase (GST) increased markedly in cells transfected with pCMV6-XL5-NFE2L2 and without H 2 O 2 . However, compared with the control, production of ROS and MDA and activity of CAT and GSH-Px increased markedly, whereas activities of SOD and GST decreased in cells transfected with pCMV6-XL5-NFE2L2 and incubated with H 2 O 2

Sources of superoxide/H2O2 during mitochondrial proline oxidation

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Renata L.S. Goncalves

2014-01-01

Full Text Available p53 Inducible gene 6 (PIG6 encodes mitochondrial proline dehydrogenase (PRODH and is up-regulated several fold upon p53 activation. Proline dehydrogenase is proposed to generate radicals that contribute to cancer cell apoptosis. However, there are at least 10 mitochondrial sites that can produce superoxide and/or H2O2, and it is unclear whether proline dehydrogenase generates these species directly, or instead drives production by other sites. Amongst six cancer cell lines, ZR75-30 human breast cancer cells had the highest basal proline dehydrogenase levels, and mitochondria isolated from ZR75-30 cells consumed oxygen and produced H2O2 with proline as sole substrate. Insects use proline oxidation to fuel flight, and mitochondria isolated from Drosophila melanogaster were even more active with proline as sole substrate than ZR75-30 mitochondria. Using mitochondria from these two models we identified the sites involved in formation of superoxide/H2O2 during proline oxidation. In mitochondria from Drosophila the main sites were respiratory complexes I and II. In mitochondria from ZR75-30 breast cancer cells the main sites were complex I and the oxoglutarate dehydrogenase complex. Even with combinations of substrates and respiratory chain inhibitors designed to minimize the contributions of other sites and maximize any superoxide/H2O2 production from proline dehydrogenase itself, there was no significant direct contribution of proline dehydrogenase to the observed H2O2 production. Thus proline oxidation by proline dehydrogenase drives superoxide/H2O2 production, but it does so mainly or exclusively by providing anaplerotic carbon for other mitochondrial dehydrogenases and not by producing superoxide/H2O2 directly.

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.

H2O2 and NADPH oxidases involve in regulation of 2-(2-phenylethyl)chromones accumulation during salt stress in Aquilaria sinensis calli.

Science.gov (United States)

Wang, Xiaohui; Dong, Xianjuan; Feng, Yingying; Liu, Xiao; Wang, Jinling; Zhang, Zhongxiu; Li, Jun; Zhao, Yunfang; Shi, Shepo; Tu, Pengfei

2018-04-01

2-(2-Phenylethyl)chromones are the main compounds responsible for the quality of agarwood, which is widely used in traditional medicines, incenses and perfumes. H 2 O 2 and NADPH oxidases (also known as respiratory burst oxidase homologs, Rbohs) mediate diverse physiological and biochemical processes in environmental stress responses. However, little is known about the function of H 2 O 2 and NADPH oxidases in 2-(2-phenylethyl)chromones accumulation. In this study, we found that salt stress induced a transient increase in content of H 2 O 2 and 2-(2-phenylethyl)chromones accumulation in Aquilaria sinensis calli. Exogenous H 2 O 2 remarkably decreased the production of 2-(2-phenylethyl)chromones, while dimethylthiourea (DMTU), a scavenger of H 2 O 2 , significantly increased 2-(2-phenylethyl)chromones accumulation in salt treated calli. Three new H 2 O 2 -generating genes, named AsRbohA-C, were isolated and characterized from A. sinensis. Salt stress also induced a transient increase in AsRbohA-C expression and NADPH oxidase activity. Furthermore, exogenous H 2 O 2 increased AsRbohA-C expression and NADPH oxidase activity, while DMTU inhibited AsRbohA-C expression and NADPH oxidase activity under salt stress. Moreover, diphenylene iodonium (DPI), the inhibitor of NADPH oxidases, reduced AsRbohA-C expression and NADPH oxidase activity, but significantly induced 2-(2-phenylethyl)chromones accumulation during salt stress. These results clearly demonstrated the central role of H 2 O 2 and NADPH oxidases in regulation of salt-induced 2-(2-phenylethyl)chromones accumulation in A. sinensis calli. Copyright © 2018 Elsevier B.V. All rights reserved.

Fucoxanthin prevents H2O2-induced neuronal apoptosis via concurrently activating the PI3-K/Akt cascade and inhibiting the ERK pathway.

Science.gov (United States)

Yu, Jie; Lin, Jia-Jia; Yu, Rui; He, Shan; Wang, Qin-Wen; Cui, Wei; Zhang, Jin-Rong

2017-01-01

Background : As a natural carotenoid abundant in chloroplasts of edible brown algae, fucoxanthin possesses various health benefits, including anti-oxidative activity in particular. Objective : In the present study, we studied whether fucoxanthin protected against hydrogen peroxide (H 2 O 2 )-induced neuronal apoptosis. Design : The neuroprotective effects of fucoxanthin on H 2 O 2 -induced toxicity were studied in both SH-SY5Y cells and primary cerebellar granule neurons. Results : Fucoxanthin significantly protected against H 2 O 2 -induced neuronal apoptosis and intracellular reactive oxygen species. H 2 O 2 treatment led to the reduced activity of phosphoinositide 3-kinase (PI3-K)/Akt cascade and the increased activity of extracellular signal-regulated kinase (ERK) pathway in SH-SY5Y cells. Moreover, fucoxanthin significantly restored the altered activities of PI3-K/Akt and ERK pathways induced by H 2 O 2 . Both specific inhibitors of glycogen synthase kinase 3β (GSK3β) and mitogen-activated protein kinase kinase (MEK) significantly protected against H 2 O 2 -induced neuronal death. Furthermore, the neuroprotective effects of fucoxanthin against H 2 O 2 -induced neuronal death were abolished by specific PI3-K inhibitors. Conclusions : Our data strongly revealed that fucoxanthin protected against H 2 O 2 -induced neurotoxicity via concurrently activating the PI3-K/Akt cascade and inhibiting the ERK pathway, providing support for the use of fucoxanthin to treat neurodegenerative disorders induced by oxidative stress.

Decreased histone deacetylase 2 impairs Nrf2 activation by oxidative stress

International Nuclear Information System (INIS)

Mercado, Nicolas; Thimmulappa, Rajesh; Thomas, Catherine M.R.; Fenwick, Peter S.; Chana, Kirandeep K.; Donnelly, Louise E.; Biswal, Shyam; Ito, Kazuhiro; Barnes, Peter J.

2011-01-01

Research highlights: → Nrf2 anti-oxidant function is impaired when HDAC activity is inhibited. → HDAC inhibition decreases Nrf2 protein stability. → HDAC2 is involved in reduced Nrf2 stability and both correlate in COPD samples. → HDAC inhibition increases Nrf2 acetylation. -- Abstract: Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a crucial role in cellular defence against oxidative stress by inducing the expression of multiple anti-oxidant genes. However, where high levels of oxidative stress are observed, such as chronic obstructive pulmonary disease (COPD), Nrf2 activity is reduced, although the molecular mechanism for this defect is uncertain. Here, we show that down-regulation of histone deacetylase (HDAC) 2 causes Nrf2 instability, resulting in reduced anti-oxidant gene expression and increase sensitivity to oxidative stress. Although Nrf2 protein was clearly stabilized after hydrogen peroxide (H 2 O 2 ) stimulation in a bronchial epithelial cell line (BEAS2B), Nrf2 stability was decreased and Nrf2 acetylation increased in the presence of an HDAC inhibitor, trichostatin A (TSA). TSA also reduced Nrf2-regulated heme-oxygenase-1 (HO-1) expression in these cells, and this was confirmed in acute cigarette-smoke exposed mice in vivo. HDAC2 knock-down by RNA interference resulted in reduced H 2 O 2 -induced Nrf2 protein stability and activity in BEAS2B cells, whereas HDAC1 knockdown had no effect. Furthermore, monocyte-derived macrophages obtained from healthy volunteers (non-smokers and smokers) and COPD patients showed a significant correlation between HDAC2 expression and Nrf2 expression (r = 0.92, p < 0.0001). Thus, reduced HDAC2 activity in COPD may account for increased Nrf2 acetylation, reduced Nrf2 stability and impaired anti oxidant defences.

Decreased histone deacetylase 2 impairs Nrf2 activation by oxidative stress

Energy Technology Data Exchange (ETDEWEB)

Mercado, Nicolas [Airway Disease Section, National Heart and Lung Institute, Imperial College, London SW3 6LY (United Kingdom); Thimmulappa, Rajesh [Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (United States); Thomas, Catherine M.R.; Fenwick, Peter S.; Chana, Kirandeep K.; Donnelly, Louise E. [Airway Disease Section, National Heart and Lung Institute, Imperial College, London SW3 6LY (United Kingdom); Biswal, Shyam [Department of Environmental Health Sciences, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD (United States); Ito, Kazuhiro [Airway Disease Section, National Heart and Lung Institute, Imperial College, London SW3 6LY (United Kingdom); Barnes, Peter J., E-mail: p.j.barnes@imperial.ac.uk [Airway Disease Section, National Heart and Lung Institute, Imperial College, London SW3 6LY (United Kingdom)

2011-03-11

Research highlights: {yields} Nrf2 anti-oxidant function is impaired when HDAC activity is inhibited. {yields} HDAC inhibition decreases Nrf2 protein stability. {yields} HDAC2 is involved in reduced Nrf2 stability and both correlate in COPD samples. {yields} HDAC inhibition increases Nrf2 acetylation. -- Abstract: Nuclear factor erythroid 2-related factor 2 (Nrf2) plays a crucial role in cellular defence against oxidative stress by inducing the expression of multiple anti-oxidant genes. However, where high levels of oxidative stress are observed, such as chronic obstructive pulmonary disease (COPD), Nrf2 activity is reduced, although the molecular mechanism for this defect is uncertain. Here, we show that down-regulation of histone deacetylase (HDAC) 2 causes Nrf2 instability, resulting in reduced anti-oxidant gene expression and increase sensitivity to oxidative stress. Although Nrf2 protein was clearly stabilized after hydrogen peroxide (H{sub 2}O{sub 2}) stimulation in a bronchial epithelial cell line (BEAS2B), Nrf2 stability was decreased and Nrf2 acetylation increased in the presence of an HDAC inhibitor, trichostatin A (TSA). TSA also reduced Nrf2-regulated heme-oxygenase-1 (HO-1) expression in these cells, and this was confirmed in acute cigarette-smoke exposed mice in vivo. HDAC2 knock-down by RNA interference resulted in reduced H{sub 2}O{sub 2}-induced Nrf2 protein stability and activity in BEAS2B cells, whereas HDAC1 knockdown had no effect. Furthermore, monocyte-derived macrophages obtained from healthy volunteers (non-smokers and smokers) and COPD patients showed a significant correlation between HDAC2 expression and Nrf2 expression (r = 0.92, p < 0.0001). Thus, reduced HDAC2 activity in COPD may account for increased Nrf2 acetylation, reduced Nrf2 stability and impaired anti oxidant defences.

Nonlinear feedback drives homeostatic plasticity in H2O2 stress response

Science.gov (United States)

Goulev, Youlian; Morlot, Sandrine; Matifas, Audrey; Huang, Bo; Molin, Mikael; Toledano, Michel B; Charvin, Gilles

2017-01-01

Homeostatic systems that rely on genetic regulatory networks are intrinsically limited by the transcriptional response time, which may restrict a cell’s ability to adapt to unanticipated environmental challenges. To bypass this limitation, cells have evolved mechanisms whereby exposure to mild stress increases their resistance to subsequent threats. However, the mechanisms responsible for such adaptive homeostasis remain largely unknown. Here, we used live-cell imaging and microfluidics to investigate the adaptive response of budding yeast to temporally controlled H2O2 stress patterns. We demonstrate that acquisition of tolerance is a systems-level property resulting from nonlinearity of H2O2 scavenging by peroxiredoxins and our study reveals that this regulatory scheme induces a striking hormetic effect of extracellular H2O2 stress on replicative longevity. Our study thus provides a novel quantitative framework bridging the molecular architecture of a cellular homeostatic system to the emergence of nonintuitive adaptive properties. DOI: http://dx.doi.org/10.7554/eLife.23971.001 PMID:28418333

Enhancing lipid productivity of Chlorella vulgaris using oxidative stress by TiO2 nanoparticles

International Nuclear Information System (INIS)

Kang, Nam Kyu; Lee, Bongsoo; Choi, Gang-Guk; Moon, Myounghoon; Park, Min S.; Yang, Ji-Won; Lim, JitKang

2014-01-01

Ability to increase the lipid production in microalgae is one of the heavily sought-after ideas to improve the economic feasibility of microalgae-derived transportation fuels for commercial applications. We used the oxidative stress by TiO 2 nanoparticles, a well-known photocatalyst, to induce lipid production in microalgae. Chlorella vulgaris UTEX 265 was cultivated under various concentrations of TiO 2 ranging from 0.1 to 5 g/L under UV-A illumination. Maximum specific growth rate was affected in responding to TiO 2 concentrations. In the presence of UV-A, chlorophyll concentration was decreased at the highest concentration of TiO 2 (5 g/L TiO 2 ) by oxidative stress. The fatty acid methyl ester (FAME) composition analysis suggested that oxidative stress causes the accumulation and decomposition of lipids. The highest FAME productivity was 18.2 g/L/d under low concentrations of TiO 2 (0.1 g/L) and a short induction time (two days). The controlled condition of TiO 2 /UV-A inducing oxidative stress (0.1 g/L TiO 2 and two days induction) could be used to increase the lipid productivity of C. vulgaris UTEX 265. Our results show the possibility of modulating the lipid induction process through oxidative stress with TiO 2 /UV-A

Assessment of cellular responses to oxidative stress using MCF-7 breast cancer cells, black seed (N. Sativa L.) extracts and H2O2.

Science.gov (United States)

Farah, Ibrahim O

2005-12-01

Black seed (N. Sativa L) is an oriental spice of the family Ranunculaceae that has long been rationally used as a natural medicine for treatment of many acute as well as chronic conditions including cardiovascular disease and immunological disorders. It has been used in the treatment of diabetes, hypertension, and dermatological conditions. There have been very few studies on the effects of N. Sativa as a chemoprevention of chronic diseases as well as in cancer prevention and/or therapy. Oxidative stress is a condition that underlies many acute as well as chronic conditions. The combination and role of oxidative stress and antioxidants in vivo is still a matter of conjecture. Our objective for the present study was to expose MCF-7 breast cancer cells in vitro (as a chronic disease example) to aqueous and alcohol extracts and in combination with H[2]O[2] as an oxidative stressor. Measurement of cell survival under various concentrations and mixtures was conducted using standard cell culture techniques, exposure protocols in 96 well plates and Fluorospectrosphotometry. Following cellular growth to 90% confluencey, exposure to water (WE) and ethanol (AE) extracts of N. sativa and H[2]O[2] was performed. Cell survival indices were calculated from percent survival using regression analysis. Results showed that the alcohol extract and its mixtures were able to influence the survival of MCF-7 cells (indices ranged from 357.15- 809.50 mug/ml in descending potency for H[2]O[2]+AE to the mix of 3). In contrast, H[2]O[2] alone reduced effectively the survival of MCF-7 cells and the least effective combinations in descending potency were AE+H[2]O[2], WE+H[2]O[2], AE+WE, and WE+AE+H[2]O[2]. Mixtures other than AE+H[2]O[2] showed possible interactions and loss of potency. In conclusion, N. Sativa alone or in combination with oxidative stress was found to be effective (in vitro) in influencing the survival of MCF-7 breast cancer cells, unveiling promising opportunities in the

Assessment of Cellular Responses to Oxidative Stress using MCF-7 Breast Cancer Cells, Black Seed (N. Sativa L. Extracts and H2O2

Directory of Open Access Journals (Sweden)

Ibrahim O. Farah

2005-12-01

Full Text Available Black seed (N. Sativa L is an oriental spice of the family Ranunculaceae that has long been rationally used as a natural medicine for treatment of many acute as well as chronic conditions including cardiovascular disease and immunological disorders. It has been used in the treatment of diabetes, hypertension, and dermatological conditions. There have been very few studies on the effects of N. Sativa as a chemoprevention of chronic diseases as well as in cancer prevention and/or therapy. Oxidative stress is a condition that underlies many acute as well as chronic conditions. The combination and role of oxidative stress and antioxidants in vivo is still a matter of conjecture. Our objective for the present study was to expose MCF-7 breast cancer cells in vitro (as a chronic disease example to aqueous and alcohol extracts and in combination with H2O2 as an oxidative stressor. Measurement of cell survival under various concentrations and mixtures was conducted using standard cell culture techniques, exposure protocols in 96 well plates and Fluorospectrosphotometry. Following cellular growth to 90% confluencey, exposure to water (WE and ethanol (AE extracts of N. sativa and H2O2 was performed. Cell survival indices were calculated from percent survival using regression analysis. Results showed that the alcohol extract and its mixtures were able to influence the survival of MCF-7 cells (indices ranged from 357.15- 809.50 Bg/ml in descending potency for H2O2+AE to the mix of 3. In contrast, H2O2 alone reduced effectively the survival of MCF-7 cells and the least effective combinations in descending potency were AE+H2O2, WE+H2O2, AE+WE, and WE+AE+H2O2. Mixtures other than AE+H2O2 showed possible interactions and loss of potency. In conclusion, N. Sativa alone or in combination with oxidative stress was found to be effective (in vitro in influencing the survival of MCF-7 breast cancer cells, unveiling promising opportunities in the field of cancer

Melandrii Herba Extract Attenuates H2O2-Induced Neurotoxicity in Human Neuroblastoma SH-SY5Y Cells and Scopolamine-Induced Memory Impairment in Mice

Directory of Open Access Journals (Sweden)

Kwang Min Lee

2017-09-01

Full Text Available Oxidative stress plays a significant role in the etiology of a variety of neurodegenerative diseases. In this study, we found that Melandrii Herba extract (ME attenuated oxidative-induced damage in cells. Mechanistically, ME exhibited protection from H2O2-induced neurotoxicity via caspase-3 inactivation, Bcl-2 downregulation, Bax upregulation, and MAPK activation (ERK 1/2, JNK 1/2, and p38 MAPK in vitro. Moreover, our in vivo data showed that ME was able to attenuate scopolamine-induced cognitive impairment. These results provide in vitro and in vivo evidence that ME exhibits neuroprotective properties against oxidative stress, which suggests that ME is worthy of further investigation as a complementary, or even as an alternative, product for preventing and treating neurodegenerative disorders.

Using H2O2 as oxidant in leaching of uranium ores. The new research on the reaction of H2O2 with Fe2+

International Nuclear Information System (INIS)

Gao Xizhen

1997-05-01

The new research on the reaction of H 2 O 2 with Fe 2+ has been studied. Through determining the electric potential, pH and O 2 release during the mutual titration between H 2 O 2 solution and FeSO 4 solution, deduced the chemical equations of H 2 O 2 (without free hydroxyl) oxidizing FeSO 4 and Fe 2 (SO 4 ) 3 oxidizing H 2 O 2 . The research results show that acid is a catalytic agent for decomposing H 2 O 2 to be O 2 and H 2 O besides iron ions. The maximum oxidizing potential is up to about 640 mV. While using H 2 O 2 as an oxidant in uranium heap leaching and in-situ leaching, controlling electric potential can be regarded as a method for adjusting the feeding speed of H 2 O 2 to keep the electric potential below 500 mV, thus the H 2 O 2 decomposition can be reduced. (13 refs., 3 tabs., 1 fig.)

Oxyhydroxide of metallic nanowires in a molecular H2O and H2O2 environment and their effects on mechanical properties.

Science.gov (United States)

Aral, Gurcan; Islam, Md Mahbubul; Wang, Yun-Jiang; Ogata, Shigenobu; Duin, Adri C T van

2018-06-14

To avoid unexpected environmental mechanical failure, there is a strong need to fully understand the details of the oxidation process and intrinsic mechanical properties of reactive metallic iron (Fe) nanowires (NWs) under various aqueous reactive environmental conditions. Herein, we employed ReaxFF reactive molecular dynamics (MD) simulations to elucidate the oxidation of Fe NWs exposed to molecular water (H2O) and hydrogen peroxide (H2O2) environment, and the influence of the oxide shell layer on the tensile mechanical deformation properties of Fe NWs. Our structural analysis shows that oxidation of Fe NWs occurs with the formation of different iron oxide and hydroxide phases in the aqueous molecular H2O and H2O2 oxidizing environments. We observe that the resulting microstructure due to pre-oxide shell layer formation reduces the mechanical stress via increasing the initial defect sites in the vicinity of the oxide region to facilitate the onset of plastic deformation during tensile loading. Specifically, the oxide layer of Fe NWs formed in the H2O2 environment has a relatively significant effect on the deterioration of the mechanical properties of Fe NWs. The weakening of the yield stress and Young modulus of H2O2 oxidized Fe NWs indicates the important role of local oxide microstructures on mechanical deformation properties of individual Fe NWs. Notably, deformation twinning is found as the primary mechanical plastic deformation mechanism of all Fe NWs, but it is initially observed at low strain and stress level for the oxidized Fe NWs.

The microbe-secreted isopeptide poly-γ-glutamic acid induces stress tolerance in Brassica napus L. seedlings by activating crosstalk between H2O2 and Ca2+

Science.gov (United States)

Lei, Peng; Pang, Xiao; Feng, Xiaohai; Li, Sha; Chi, Bo; Wang, Rui; Xu, Zongqi; Xu, Hong

2017-01-01

Poly-γ-glutamic acid (γ-PGA) is a microbe-secreted isopeptide that has been shown to promote growth and enhance stress tolerance in crops. However, its site of action and downstream signaling pathways are still unknown. In this study, we investigated γ-PGA-induced tolerance to salt and cold stresses in Brassica napus L. seedlings. Fluorescent labeling of γ-PGA was used to locate the site of its activity in root protoplasts. The relationship between γ-PGA-induced stress tolerance and two signal molecules, H2O2 and Ca2+, as well as the γ-PGA-elicited signaling pathway at the whole plant level, were explored. Fluorescent labeling showed that γ-PGA did not enter the cytoplasm but instead attached to the surface of root protoplasm. Here, it triggered a burst of H2O2 in roots by enhancing the transcription of RbohD and RbohF, and the elicited H2O2 further activated an influx of Ca2+ into root cells. Ca2+ signaling was transmitted via the stem from roots to leaves, where it elicited a fresh burst of H2O2, thus promoting plant growth and enhancing stress tolerance. On the basis of these observation, we propose that γ-PGA mediates stress tolerance in Brassica napus seedlings by activating an H2O2 burst and subsequent crosstalk between H2O2 and Ca2+ signaling. PMID:28198821

Electrochemical, H2O2-Boosted Catalytic Oxidation System

Science.gov (United States)

Akse, James R.; Thompson, John O.; Schussel, Leonard J.

2004-01-01

An improved water-sterilizing aqueous-phase catalytic oxidation system (APCOS) is based partly on the electrochemical generation of hydrogen peroxide (H2O2). This H2O2-boosted system offers significant improvements over prior dissolved-oxygen water-sterilizing systems in the way in which it increases oxidation capabilities, supplies H2O2 when needed, reduces the total organic carbon (TOC) content of treated water to a low level, consumes less energy than prior systems do, reduces the risk of contamination, and costs less to operate. This system was developed as a variant of part of an improved waste-management subsystem of the life-support system of a spacecraft. Going beyond its original intended purpose, it offers the advantage of being able to produce H2O2 on demand for surface sterilization and/or decontamination: this is a major advantage inasmuch as the benign byproducts of this H2O2 system, unlike those of systems that utilize other chemical sterilants, place no additional burden of containment control on other spacecraft air- or water-reclamation systems.

CodY Regulates Thiol Peroxidase Expression as Part of the Pneumococcal Defense Mechanism against H2O2 Stress.

Science.gov (United States)

Hajaj, Barak; Yesilkaya, Hasan; Shafeeq, Sulman; Zhi, Xiangyun; Benisty, Rachel; Tchalah, Shiran; Kuipers, Oscar P; Porat, Nurith

2017-01-01

Streptococcus pneumoniae is a facultative anaerobic pathogen. Although it maintains fermentative metabolism, during aerobic growth pneumococci produce high levels of H 2 O 2 , which can have adverse effects on cell viability and DNA, and influence pneumococcal interaction with its host. The pneumococcus is unusual in its dealing with toxic reactive oxygen species (ROS) in that it neither has catalase nor the global regulators of peroxide stress resistance. Previously, we identified pneumococcal thiol peroxidase (TpxD) as the key enzyme for enzymatic removal of H 2 O 2 , and showed that TpxD synthesis is up-regulated upon exposure to H 2 O 2 . This study aimed to reveal the mechanism controlling TpxD expression under H 2 O 2 stress. We hypothesize that H 2 O 2 activates a transcription factor which in turn up-regulates tpxD expression. Microarray analysis revealed a pneumococcal global transcriptional response to H 2 O 2 . Mutation of tpxD abolished H 2 O 2 -mediated response to high H 2 O 2 levels, signifying the need for an active TpxD under oxidative stress conditions. Bioinformatic tools, applied to search for a transcription factor modulating tpxD expression, pointed toward CodY as a potential candidate. Indeed, a putative 15-bp consensus CodY binding site was found in the proximal region of tpxD- coding sequence. Binding of CodY to this site was confirmed by EMSA, and genetic engineering techniques demonstrated that this site is essential for TpxD up-regulation under H 2 O 2 stress. Furthermore, tpxD expression was reduced in a Δ codY mutant. These data indicate that CodY is an activator of tpxD expression, triggering its up-regulation under H 2 O 2 stress. In addition we show that H 2 O 2 specifically oxidizes the 2 CodY cysteines. This oxidation may trigger a conformational change in CodY, resulting in enhanced binding to DNA. A schematic model illustrating the contribution of TpxD and CodY to pneumococcal global transcriptional response to H 2 O 2 is

Bradykinin-potentiating PEPTIDE-10C, an argininosuccinate synthetase activator, protects against H2O2-induced oxidative stress in SH-SY5Y neuroblastoma cells.

Science.gov (United States)

Querobino, Samyr Machado; Ribeiro, César Augusto João; Alberto-Silva, Carlos

2018-05-01

Bradykinin-potentiating peptides (BPPs - 5a, 7a, 9a, 10c, 11e, and 12b) of Bothrops jararaca (Bj) were described as argininosuccinate synthase (AsS) activators, improving l-arginine availability. Agmatine and polyamines, which are l-arginine metabolism products, have neuroprotective properties. Here, we investigated the neuroprotective effects of low molecular mass fraction from Bj venom (LMMF) and two synthetic BPPs (BPP-10c, BPP-12b, BPP-10c showed higher protective capacity than BPP-12b. LMMF pretreatment was unable to prevent the reduction of cell viability caused by H 2 O 2 . The neuroprotective mechanism of BPP-10c against oxidative stress was investigated. BPP-10c reduced ROS generation and lipid peroxidation in relation to cells treated only with H 2 O 2 . BBP-10c increased AsS expression and was not neuroprotective in the presence of MDLA, a specific inhibitor of AsS. BPP-10c reduced iNOS expression and nitrate levels but decreased NF-kB expression. Furthermore, BPP-10c protected the mitochondrial membrane against oxidation. Overall, we demonstrated for the first time neuroprotective mechanisms of BPPs against oxidative stress, opening new perspectives to the study and application of these peptides for the treatment of neurodegenerative diseases. Copyright © 2018 Elsevier Inc. All rights reserved.

[Mechanism and performance of styrene oxidation by O3/H2O2].

Science.gov (United States)

He, Jue-Cong; Huang, Qian-Ru; Ye, Qi-Hong; Luo, Yu-Wei; Zhang, Zai-Li; Fan, Qing-Juan; Wei, Zai-Shan

2013-10-01

It can produce a large number of free radicals in O3/H2O2, system, ozone and free radical coupling oxidation can improve the styrene removal efficiency. Styrene oxidation by O3/H2O2 was investigated. Ozone dosage, residence time, H2o2 volume fraction, spray density and molar ratio of O3/C8H8 on styrene removal were evaluated. The experimental results showed that styrene removal efficiency achieved 85.7%. The optimal residence time, H2O2, volume fraction, spray density and O3/C8H8 molar ratio were 20. 6 s, 10% , 1.72 m3.(m2.h)-1 and 0.46, respectively. The gas-phase degradation intermediate products were benzaldehyde(C6H5CHO) and benzoic acid (C6H5 COOH) , which were identified by means of gas chromatography-mass spectrometry(GC-MS). The degradation mechanism of styrene is presented.

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.

Enhancing lipid productivity of Chlorella vulgaris using oxidative stress by TiO{sub 2} nanoparticles

Energy Technology Data Exchange (ETDEWEB)

Kang, Nam Kyu; Lee, Bongsoo; Choi, Gang-Guk; Moon, Myounghoon; Park, Min S.; Yang, Ji-Won [Daejeon, Daejeon (Korea, Republic of); Lim, JitKang [Universiti Sains Malaysia, Penang (Malaysia)

2014-05-15

Ability to increase the lipid production in microalgae is one of the heavily sought-after ideas to improve the economic feasibility of microalgae-derived transportation fuels for commercial applications. We used the oxidative stress by TiO{sub 2} nanoparticles, a well-known photocatalyst, to induce lipid production in microalgae. Chlorella vulgaris UTEX 265 was cultivated under various concentrations of TiO{sub 2} ranging from 0.1 to 5 g/L under UV-A illumination. Maximum specific growth rate was affected in responding to TiO{sub 2} concentrations. In the presence of UV-A, chlorophyll concentration was decreased at the highest concentration of TiO{sub 2} (5 g/L TiO{sub 2}) by oxidative stress. The fatty acid methyl ester (FAME) composition analysis suggested that oxidative stress causes the accumulation and decomposition of lipids. The highest FAME productivity was 18.2 g/L/d under low concentrations of TiO{sub 2} (0.1 g/L) and a short induction time (two days). The controlled condition of TiO{sub 2}/UV-A inducing oxidative stress (0.1 g/L TiO{sub 2} and two days induction) could be used to increase the lipid productivity of C. vulgaris UTEX 265. Our results show the possibility of modulating the lipid induction process through oxidative stress with TiO{sub 2}/UV-A.

Inhibitory Effect of Dissolved Silica on the H2O2 Decomposition by Iron(III) and Manganese(IV) Oxides: Implications for H2O2-based In Situ Chemical Oxidation

Science.gov (United States)

Pham, Anh Le-Tuan; Doyle, Fiona M.; Sedlak, David L.

2011-01-01

The decomposition of H2O2 on iron minerals can generate •OH, a strong oxidant that can transform a wide range of contaminants. This reaction is critical to In Situ Chemical Oxidation (ISCO) processes used for soil and groundwater remediation, as well as advanced oxidation processes employed in waste treatment systems. The presence of dissolved silica at concentrations comparable to those encountered in natural waters decreases the reactivity of iron minerals toward H2O2, because silica adsorbs onto the surface of iron minerals and alters catalytic sites. At circumneutral pH values, goethite, amorphous iron oxide, hematite, iron-coated sand and montmorillonite that were pre-equilibrated with 0.05 – 1.5 mM SiO2 were significantly less reactive toward H2O2 decomposition than their original counterparts, with the H2O2 loss rates inversely proportional to the SiO2 concentration. In the goethite/H2O2 system, the overall •OH yield, defined as the percentage of decomposed H2O2 producing •OH, was almost halved in the presence of 1.5 mM SiO2. Dissolved SiO2 also slows the H2O2 decomposition on manganese(IV) oxide. The presence of dissolved SiO2 results in greater persistence of H2O2 in groundwater, lower H2O2 utilization efficiency and should be considered in the design of H2O2-based treatment systems. PMID:22129132

Modulation of notch signaling pathway to prevent H2O2/menadione-induced SK-N-MC cells death by EUK134.

Science.gov (United States)

Kamarehei, Maryam; Yazdanparast, Razieh

2014-10-01

The brain in Alzheimer's disease is under increased oxidative stress, and this may have a role in the pathogenesis and neural death in this disorder. It has been verified that numerous signaling pathways involved in neurodegenerative disorders are activated in response to reactive oxygen species (ROS). EUK134, a synthetic salen-manganese antioxidant complex, has been found to possess many interesting pharmacological activities awaiting exploration. The present study is to characterize the role of Notch signaling in apoptotic cell death of SK-N-MC cells. The cells were treated with hydrogen peroxide (H2O2) or menadione to induce oxidative stress. The free-radical scavenging capabilities of EUK134 were studied through the MTT assay, glutathione peroxidase (GPx) enzyme activity assay, and glutathione (GSH) Levels. The extents of lipid peroxidation, protein carbonyl formation, and intracellular ROS levels, as markers of oxidative stress, were also studied. Our results showed that H2O2/menadione reduced GSH levels and GPx activity. However, EUK134 protected cells against ROS-induced cell death by down-regulation of lipid peroxidation and protein carbonyl formation as well as restoration of antioxidant enzymes activity. ROS induced apoptosis and increased NICD and HES1 expression. Inhibition of NICD production proved that Notch signaling is involved in apoptosis through p53 activation. Moreover, H2O2/menadione led to Numb protein down-regulation which upon EUK134 pretreatment, its level increased and subsequently prevented Notch pathway activation. We indicated that EUK134 can be a promising candidate in designing natural-based drugs for ROS-induced neurodegenerative diseases. Collectively, ROS activated Notch signaling in SK-N-MC cells leading to cell apoptosis.

Nitroxides protect horseradish peroxidase from H2O2-induced inactivation and modulate its catalase-like activity.

Science.gov (United States)

Samuni, Amram; Maimon, Eric; Goldstein, Sara

2017-08-01

Horseradish peroxidase (HRP) catalyzes H 2 O 2 dismutation while undergoing heme inactivation. The mechanism underlying this process has not been fully elucidated. The effects of nitroxides, which protect metmyoglobin and methemoglobin against H 2 O 2 -induced inactivation, have been investigated. HRP reaction with H 2 O 2 was studied by following H 2 O 2 depletion, O 2 evolution and heme spectral changes. Nitroxide concentration was followed by EPR spectroscopy, and its reactions with the oxidized heme species were studied using stopped-flow. Nitroxide protects HRP against H 2 O 2 -induced inactivation. The rate of H 2 O 2 dismutation in the presence of nitroxide obeys zero-order kinetics and increases as [nitroxide] increases. Nitroxide acts catalytically since its oxidized form is readily reduced to the nitroxide mainly by H 2 O 2 . The nitroxide efficacy follows the order 2,2,6,6-tetramethyl-piperidine-N-oxyl (TPO)>4-OH-TPO>3-carbamoyl proxyl>4-oxo-TPO, which correlates with the order of the rate constants of nitroxide reactions with compounds I, II, and III. Nitroxide catalytically protects HRP against inactivation induced by H 2 O 2 while modulating its catalase-like activity. The protective role of nitroxide at μM concentrations is attributed to its efficient oxidation by P940, which is the precursor of the inactivated form P670. Modeling the dismutation kinetics in the presence of nitroxide adequately fits the experimental data. In the absence of nitroxide the simulation fits the observed kinetics only if it does not include the formation of a Michaelis-Menten complex. Nitroxides catalytically protect heme proteins against inactivation induced by H 2 O 2 revealing an additional role played by nitroxide antioxidants in vivo. Copyright © 2017 Elsevier B.V. All rights reserved.

Enhancement of catalase activity by repetitive low-grade H2O2 exposures protects fibroblasts from subsequent stress-induced apoptosis

International Nuclear Information System (INIS)

Sen, Prosenjit; Mukherjee, Sebanti; Bhaumik, Gayaram; Das, Pradeep; Ganguly, Sandipan; Choudhury, Nandini; Raha, Sanghamitra

2003-01-01

Exposure of Chinese hamster V79 fibroblasts to mild and repetitive H 2 O 2 doses in culture for 15 weeks produced no change in lipid peroxidation status, GSH/GSSG ratio and glutathione peroxidase activity of these cells (VST cells). In contrast, in VST cells catalase levels underwent a prominent increase which could be significantly inhibited and brought down to control levels after treatment with the catalase inhibitor 3-aminotriazole (3-AT). When control (VC) cells were exposed to UV radiation (UVC 5 J/m 2 ) or H 2 O 2 (7.5 mM, 15 min), intracellular reactive oxygen species (ROS) levels rose prominently with significant activation of caspase-3. Marked nuclear fragmentation and lower cell viability were also noted in these cells. In contrast, VST cells demonstrated a significantly lower ROS level, an absence of nuclear fragmentation and an unchanged caspase-3 activity after exposure to UVC or H 2 O 2 . Cell viability was also significantly better preserved in VST cells than VC cells after UV or H 2 O 2 exposures. Following 3-AT treatment of VST cells, UVC radiation or H 2 O 2 brought about significantly higher elevations in intracellular ROS, increases in caspase-3 activity, significantly lowered cell viability and marked nuclear fragmentation, indicating the involvement of high catalase levels in the cytoprotective effects of repetitive stress. Therefore, upregulation of the antioxidant defense after repetitive oxidative stress imparted a superior ability to cope with subsequent acute stress and escape apoptotic death and loss of viability

A polysaccharide of Dendrobium officinale ameliorates H2O2-induced apoptosis in H9c2 cardiomyocytes via PI3K/AKT and MAPK pathways.

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Zhang, Jing-Yi; Guo, Ying; Si, Jin-Ping; Sun, Xiao-Bo; Sun, Gui-Bo; Liu, Jing-Jing

2017-11-01

Dendrobium officinale is one valuable traditional Chinese medicine, which has skyscraping medicinal value. Polysaccharide is the main active ingredient in D. officinale; its antioxidant activity is a hot research topic nowadays. Oxidative stress plays an important role in the pathological progress of a variety of cardiovascular disease, as one of key factors of cardiomyocyte apoptosis. This research adopts a model of H 2 O 2 induction-H9c2 cardiomyocytes apoptosis, aiming to study the effect of Dendrobium officinale Polysaccharide (DOP-GY) for cardiomyocyte apoptosis caused by oxidative stress and its possible mechanism. Our results showed that pretreatment of DOP-GY (low dose: 6.25μg/mL, medium dose: 12.5μg/mL, high dose: 25μg/mL) followed by a 2h incubation with 200μM H 2 O 2 elevated the survival rate, cutted the LDH leakage, reduced lipid peroxidation damage, improved the activity of the endogenous antioxidant enzymes. In addition, the pretreatment of DOP-GY significantly inhibited the production of ROS, declined of the mitochondrial membrane potential, down-regulated pro-apoptosis protein and up-regulated anti-apoptosis protein. The protective effect was correlated with the PI3K/Akt and MAPK signal pathway. Collectively, these observations suggest that DOY-GY has the potential to exert cardioprotective effects against H 2 O 2 -induced H9c2 cardiomyocyte apoptosis. Copyright © 2017 Elsevier B.V. All rights reserved.

Optimization of NO oxidation by H2O2 thermal decomposition at moderate temperatures.

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Zhao, Hai-Qian; Wang, Zhong-Hua; Gao, Xing-Cun; Liu, Cheng-Hao; Qi, Han-Bing

2018-01-01

H2O2 was adopted to oxidize NO in simulated flue gas at 100-500°C. The effects of the H2O2 evaporation conditions, gas temperature, initial NO concentration, H2O2 concentration, and H2O2:NO molar ratio on the oxidation efficiency of NO were investigated. The reason for the narrow NO oxidation temperature range near 500°C was determined. The NO oxidation products were analyzed. The removal of NOx using NaOH solution at a moderate oxidation ratio was studied. It was proven that rapid evaporation of the H2O2 solution was critical to increase the NO oxidation efficiency and broaden the oxidation temperature range. the NO oxidation efficiency was above 50% at 300-500°C by contacting the outlet of the syringe needle and the stainless-steel gas pipe together to spread H2O2 solution into a thin film on the surface of the stainless-steel gas pipe, which greatly accelerated the evaporation of H2O2. The NO oxidation efficiency and the NO oxidation rate increased with increasing initial NO concentration. This method was more effective for the oxidation of NO at high concentrations. H2O2 solution with a concentration higher than 15% was more efficient in oxidizing NO. High temperatures decreased the influence of the H2O2 concentration on the NO oxidation efficiency. The oxidation efficiency of NO increased with an increase in the H2O2:NO molar ratio, but the ratio of H2O2 to oxidized NO decreased. Over 80% of the NO oxidation product was NO2, which indicated that the oxidation ratio of NO did not need to be very high. An 86.7% NO removal efficiency was obtained at an oxidation ratio of only 53.8% when combined with alkali absorption.

The roles of H2S and H2O2 in regulating AsA-GSH cycle in the leaves of wheat seedlings under drought stress.

Science.gov (United States)

Shan, Changjuan; Zhang, Shengli; Ou, Xingqi

2018-01-25

This paper investigated the roles of hydrogen sulfide (H 2 S) and hydrogen peroxide (H 2 O 2 ) and the possible relationship between them in regulating the AsA-GSH cycle in wheat leaves under drought stress (DS). Results showed that DS markedly increased the production of H 2 S and H 2 O 2 , the transcript levels and activities of ascorbate peroxidase (APX), glutathione reductase (GR), monodehydroascorbate reductase (MDHAR), and dehydroascorbate reductase (DHAR); malondialdehyde (MDA) content; and electrolyte leakage (EL). Meanwhile, DS markedly reduced plant height and biomass. Above increases induced by drought stress except MDA content and EL were all suppressed by pretreatments with H 2 S synthesis inhibitor aminooxyaceticacid (AOA) and H 2 O 2 synthesis inhibitor diphenylene iodonium (DPI). Besides, pretreatments with AOA and DPI further significantly increased MDA content and EL and significantly reduced plant height and biomass under DS. DPI reduced the production of H 2 O 2 and H 2 S induced by DS. AOA also reduced the production of H 2 S and H 2 O 2 induced by DS. Pretreatments with NaHS + AOA and H 2 O 2 + DPI reversed above effects of AOA and DPI. Our results suggested that H 2 S and H 2 O 2 all participated in the up-regulation of AsA-GSH cycle in wheat leaves by DS and possibly affected each other.

Multiple myeloma cells’ capacity to decompose H2O2 determines lenalidomide sensitivity

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Sebastian, Sinto; Zhu, Yuan X.; Braggio, Esteban; Shi, Chang-Xin; Panchabhai, Sonali C.; Van Wier, Scott A.; Ahmann, Greg J.; Chesi, Marta; Bergsagel, P. Leif; Stewart, A. Keith

2017-01-01

Lenalidomide is an immunomodulatory drug (IMiDs) with clinical efficacy in multiple myeloma (MM) and other late B-cell neoplasms. Although cereblon (CRBN) is an essential requirement for IMiD action, the complete molecular and biochemical mechanisms responsible for lenalidomide-mediated sensitivity or resistance remain unknown. Here, we report that IMiDs work primarily via inhibition of peroxidase-mediated intracellular H2O2 decomposition in MM cells. MM cells with lower H2O2-decomposition capacity were more vulnerable to lenalidomide-induced H2O2 accumulation and associated cytotoxicity. CRBN-dependent degradation of IKZF1 and IKZF3 was a consequence of H2O2-mediated oxidative stress. Lenalidomide increased intracellular H2O2 levels by inhibiting thioredoxin reductase (TrxR) in cells expressing CRBN, causing accumulation of immunoglobulin light-chain dimers, significantly increasing endoplasmic reticulum stress and inducing cytotoxicity by activation of BH3-only protein Bim in MM. Other direct inhibitors of TrxR and thioredoxin (Trx) caused similar cytotoxicity, but in a CRBN-independent fashion. Our findings could help identify patients most likely to benefit from IMiDs and suggest direct TrxR or Trx inhibitors for MM therapy. PMID:28028022

Protective effect of lavender oil on scopolamine induced cognitive deficits in mice and H2O2 induced cytotoxicity in PC12 cells.

Science.gov (United States)

Xu, Pan; Wang, Kezhu; Lu, Cong; Dong, Liming; Gao, Li; Yan, Ming; Aibai, Silafu; Liu, Xinmin

2016-12-04

Lavender essential oil (LO), an aromatic liquid extracted from Lavandula angustifolia Mill., has been traditionally used in the treatments of many nervous system diseases, and recently LO also reported to be effective for the Alzheimer's disease (AD). The improvement effect of lavender oil (LO) on the scopolamine-induced cognitive deficits in mice and H 2 O 2 induced cytotoxicity in PC12 cells have been evaluated. The relevant mechanism was also researched from the perspective of antioxidant effect and cholinergic system modulation. Cognitive deficits were induced in C57BL/6J mice treated with scopolamine (1mg/kg, i.p.) and were assessed by Morris water maze (MWM) and step-through passive avoidance tests. Then their hippocampus were removed for biochemical assays (acetylcholinesterase (AChE), superoxide dismutase (SOD), glutathione peroxidase (GPX) and malondialdehyde (MDA)). In vitro, the cytotoxicity were induced by 4h exposure to H 2 O 2 in PC12 and evaluated by cell viability (MTT), lactate dehydrogenase (LDH) level, nitric oxide (NO) release, reactive oxygen species (ROS) production and mitochondrial membrane potential (MMP). The results demonstrated that LO (100mg/kg) could improve the cognitive performance of scopolamine induced mice in behavioral tests. Meanwhile, it significantly decreased the AChE activity, MDA level, and increase SOD and GPX activities of the model. Moreover, LO (12μg/mL) protected PC12 cells from H 2 O 2 induced cytotoxicity by reducing LDH, NO release, intracellular ROS accumulation and MMP loss. It was suggested that LO could show neuroprotective effect in AD model in vivo (scopolamine-treated mice) and in vitro (H 2 O 2 induced PC12 cells) via modulating oxidative stress and AChE activity. Copyright © 2016. Published by Elsevier Ireland Ltd.

Histone peptide AKRHRK enhances H2O2-induced DNA damage and alters its site specificity

International Nuclear Information System (INIS)

Midorikawa, Kaoru; Murata, Mariko; Kawanishi, Shosuke

2005-01-01

Histone proteins are involved in compaction of DNA and the protection of cells from oxygen toxicity. However, several studies have demonstrated that the metal-binding histone reacts with H 2 O 2 , leading to oxidative damage to a nucleobase. We investigated whether histone can accelerate oxidative DNA damage, using a minimal model for the N-terminal tail of histone H4, CH 3 CO-AKRHRK-CONH 2 , which has a metal-binding site. This histone peptide enhanced DNA damage induced by H 2 O 2 and Cu(II), especially at cytosine residues, and induced additional DNA cleavage at the 5'-guanine of GGG sequences. The peptide also enhanced the formation of 8-oxo-7,8-dihydro-2'-deoxyguanosine and ESR spin-trapping signal from H 2 O 2 and Cu(II). Cyclic redox reactions involving histone-bound Cu(II) and H 2 O 2 , may give rise to multiple production of radicals leading to multiple hits in DNA. It is noteworthy that the histone H4 peptide with specific sequence AKRHRK can cause DNA damage rather than protection under metal-overloaded condition

Neuroprotective effects of corn silk maysin via inhibition of H2O2-induced apoptotic cell death in SK-N-MC cells.

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Choi, Doo Jin; Kim, Sun-Lim; Choi, Ji Won; Park, Yong Il

2014-07-25

Neuroprotective effects of maysin, which is a flavone glycoside that was isolated from the corn silk (CS, Zea mays L.) of a Korean hybrid corn Kwangpyeongok, against oxidative stress (H2O2)-induced apoptotic cell death of human neuroblastoma SK-N-MC cells were investigated. Maysin cytotoxicity was determined by measuring cell viability using MTT and lactate dehydrogenase (LDH) assays. Intracellular reactive oxygen species (ROS) were measured using a 2,7-dichlorofluorescein diacetate (DCF-DA) assay. Apoptotic cell death was monitored by annexin V-FITC/PI double staining and by a TUNEL assay. Antioxidant enzyme mRNA levels were determined by real-time PCR. The cleavage of poly (ADP-ribose) polymerase (PARP) was measured by western blotting. Maysin pretreatment reduced the cytotoxic effect of H2O2 on SK-N-MC cells, as shown by the increase in cell viability and by reduced LDH release. Maysin pretreatment also dose-dependently reduced the intracellular ROS level and inhibited PARP cleavage. In addition, DNA damage and H2O2-induced apoptotic cell death were significantly attenuated by maysin pretreatment. Moreover, maysin pretreatment (5-50 μg/ml) for 2h significantly and dose-dependently increased the mRNA levels of antioxidant enzymes (CAT, GPx-1, SOD-1, SOD-2 and HO-1) in H2O2 (200 μM)-insulted cells. These results suggest that CS maysin has neuroprotective effects against oxidative stress (H2O2)-induced apoptotic death of human brain SK-N-MC cells through its antioxidative action. This report is the first regarding neuroprotective health benefits of corn silk maysin by its anti-apoptotic action and by triggering the expression of intracellular antioxidant enzyme systems in SK-N-MC cells. Copyright © 2014 Elsevier Inc. All rights reserved.

Csk-Induced Phosphorylation of Src at Tyrosine 530 is Essential for H2O2-Mediated Suppression of ERK1/2 in Human Umbilical Vein Endothelial Cells

Science.gov (United States)

Jeon, Bo Kyung; Kwon, Kihwan; Kang, Jihee Lee; Choi, Youn-Hee

2015-01-01

Mitogen-activated protein kinases (MAPKs) are key signal transducers involved in various cellular events such as growth, proliferation, and differentiation. Previous studies have reported that H2O2 leads to phosphorylation of extracellular signal-regulated kinase (ERK), one of the MAPKs in endothelial cells. The current study shows that H2O2 suppressed ERK1/2 activation and phosphorylation at specific concentrations and times in human umbilical vein endothelial cells but not in immortalized mouse aortic endothelial cells or human astrocytoma cell line CRT-MG. Phosphorylation of other MAPK family members (i.e., p38 and JNK) was not suppressed by H2O2. The decrease in ERK1/2 phosphorylation induced by H2O2 was inversely correlated with the level of phosphorylation of Src tyrosine 530. Using siRNA, it was found that H2O2-induced suppression of ERK1/2 was dependent on Csk. Physiological laminar flow abrogated, but oscillatory flow did not affect, the H2O2-induced suppression of ERK1/2 phosphorylation. In conclusion, H2O2-induced Csk translocation to the plasma membrane leads to phosphorylation of Src at the tyrosine 530 residue resulting in a reduction of ERK1/2 phosphorylation. Physiological laminar flow abrogates this effect of H2O2 by inducing phosphorylation of Src tyrosine 419. These findings broaden our understanding of signal transduction mechanisms in the endothelial cells against oxidative stress. PMID:26234813

The role of Golgi reassembly and stacking protein 65 phosphorylation in H2O2-induced cell death and Golgi morphological changes.

Science.gov (United States)

Ji, Guang; Zhang, Weiwei; Quan, Moyuan; Chen, Yang; Qu, Hui; Hu, Zhiping

2016-12-01

This study aimed to investigate the effects of H 2 O 2 -induced oxidative stress on cell viability and survival, as well as changes in the distribution of Golgi apparatus and in the level of Golgi reassembly and stacking protein 65 (GRASP65). Cell viability of cultured N2a cells treated with H 2 O 2 was measured by the MTT assay. Apoptosis was measured by flow cytometry analyses. Cells labeled by indirect immunofluorescence were observed under confocal microscope to detect any Golgi morphological alterations; electron microscopy of Golgi apparatus was also done. Expression of GRASP65 and phospho-GRASP65 was examined by immunoblotting. H 2 O 2 treatment reduced the cell viability and raised the cell mortality of N2a cells in a time-dependent manner. Notable changes were only observed in the distribution and morphology of Golgi apparatus at 6 h after H 2 O 2 treatment. The expression of GRASP65 showed no significant changes at different time points; the phosphorylated GRASP65 level was significantly increased after H 2 O 2 treatment, peaked at 3 h, and finally dropped at 6 h. Taken together, GRASP65 phosphorylation may have a critical role in inducing cell death at the early stage after H 2 O 2 treatment, while its role in H 2 O 2 -induced Golgi morphological changes may be complex.

Alleviation of drought stress by mycorrhizas is related to increased root H2O2 efflux in trifoliate orange.

Science.gov (United States)

Huang, Yong-Ming; Zou, Ying-Ning; Wu, Qiang-Sheng

2017-02-08

The Non-invasive Micro-test Technique (NMT) is used to measure dynamic changes of specific ions/molecules non-invasively, but information about hydrogen peroxide (H 2 O 2 ) fluxes in different classes of roots by mycorrhiza is scarce in terms of NMT. Effects of Funneliformis mosseae on plant growth, H 2 O 2 , superoxide radical (O 2 ·- ), malondialdehyde (MDA) concentrations, and H 2 O 2 fluxes in the taproot (TR) and lateral roots (LRs) of trifoliate orange seedlings under well-watered (WW) and drought stress (DS) conditions were studied. DS strongly inhibited mycorrhizal colonization in the TR and LRs, whereas mycorrhizal inoculation significantly promoted plant growth and biomass production. H 2 O 2 , O 2 ·- , and MDA concentrations in leaves and roots were dramatically lower in mycorrhizal seedlings than in non-mycorrhizal seedlings under DS. Compared with non-mycorrhizal seedlings, mycorrhizal seedlings had relatively higher net root H 2 O 2 effluxes in the TR and LRs especially under WW, as well as significantly higher total root H 2 O 2 effluxes in the TR and LRs under WW and DS. Total root H 2 O 2 effluxes were significantly positively correlated with root colonization but negatively with root H 2 O 2 and MDA concentrations. It suggested that mycorrhizas induces more H 2 O 2 effluxes of the TR and LRs, thus, alleviating oxidative damage of DS in the host plant.

Oxidative stress induced lipid accumulation via SREBP1c activation in HepG2 cells

International Nuclear Information System (INIS)

Sekiya, Mika; Hiraishi, Ako; Touyama, Maiko; Sakamoto, Kazuichi

2008-01-01

SREBP1c (sterol regulatory element-binding protein 1c) is a metabolic-syndrome-associated transcription factor that controls fatty acid biosynthesis under glucose/insulin stimulation. Oxidative stress increases lipid accumulation, which promotes the generation of reactive oxygen species (ROS). However, we know little about the role of oxidative stress in fatty acid biosynthesis. To clarify the action of oxidative stress in lipid accumulation via SREBP1c, we examined SREBP1c activity in H 2 O 2 -treated mammalian cells. We introduced a luciferase reporter plasmid carrying the SREBP1c-binding site into HepG2 or COS-7 cells. With increasing H 2 O 2 dose, SREBP1c transcriptional activity increased in HepG2 cells but declined in COS-7 cells. RT-PCR analysis revealed that mRNA expression of SREBP1c gene or of SREBP1c-regulated genes rose H 2 O 2 dose-dependently in HepG2 cells but dropped in COS-7 cells. Lipid accumulation and levels of the nuclear form of SREBP1c increased in H 2 O 2 -stimulated HepG2 cells. ROS may stimulate lipid accumulation in HepG2 cells via SREBP1c activation

Protective Effects of Blueberry Anthocyanins against H2O2-Induced Oxidative Injuries in Human Retinal Pigment Epithelial Cells.

Science.gov (United States)

Huang, Wu-Yang; Wu, Han; Li, Da-Jing; Song, Jiang-Feng; Xiao, Ya-Dong; Liu, Chun-Quan; Zhou, Jian-Zhong; Sui, Zhong-Quan

2018-02-21

Blueberry anthocyanins are considered protective of eye health because of their recognized antioxidant properties. In this study, blueberry anthocyanin extract (BAE), malvidin (Mv), malvidin-3-glucoside (Mv-3-glc), and malvidin-3-galactoside (Mv-3-gal) all reduced H 2 O 2 -induced oxidative stress by decreasing the levels of reactive oxygen species and malondialdehyde and increasing the levels of superoxide dismutase, catalase, and glutathione peroxidase in human retinal pigment epithelial cells. BAE and the anthocyanin standards enhanced cell viability from 63.69 ± 3.36 to 86.57 ± 6.92% (BAE), 115.72 ± 23.41% (Mv), 98.15 ± 9.39% (Mv-3-glc), and 127.97 ± 20.09% (Mv-3-gal) and significantly inhibited cell apoptosis (P blueberry anthocyanins could inhibit the induction and progression of age-related macular degeneration (AMD) through antioxidant mechanisms.

Enhancement of catalase activity by repetitive low-grade H{sub 2}O{sub 2} exposures protects fibroblasts from subsequent stress-induced apoptosis

Energy Technology Data Exchange (ETDEWEB)

Sen, Prosenjit; Mukherjee, Sebanti; Bhaumik, Gayaram; Das, Pradeep; Ganguly, Sandipan; Choudhury, Nandini; Raha, Sanghamitra

2003-08-28

Exposure of Chinese hamster V79 fibroblasts to mild and repetitive H{sub 2}O{sub 2} doses in culture for 15 weeks produced no change in lipid peroxidation status, GSH/GSSG ratio and glutathione peroxidase activity of these cells (VST cells). In contrast, in VST cells catalase levels underwent a prominent increase which could be significantly inhibited and brought down to control levels after treatment with the catalase inhibitor 3-aminotriazole (3-AT). When control (VC) cells were exposed to UV radiation (UVC 5 J/m{sup 2}) or H{sub 2}O{sub 2} (7.5 mM, 15 min), intracellular reactive oxygen species (ROS) levels rose prominently with significant activation of caspase-3. Marked nuclear fragmentation and lower cell viability were also noted in these cells. In contrast, VST cells demonstrated a significantly lower ROS level, an absence of nuclear fragmentation and an unchanged caspase-3 activity after exposure to UVC or H{sub 2}O{sub 2}. Cell viability was also significantly better preserved in VST cells than VC cells after UV or H{sub 2}O{sub 2} exposures. Following 3-AT treatment of VST cells, UVC radiation or H{sub 2}O{sub 2} brought about significantly higher elevations in intracellular ROS, increases in caspase-3 activity, significantly lowered cell viability and marked nuclear fragmentation, indicating the involvement of high catalase levels in the cytoprotective effects of repetitive stress. Therefore, upregulation of the antioxidant defense after repetitive oxidative stress imparted a superior ability to cope with subsequent acute stress and escape apoptotic death and loss of viability.

Advanced oxidation of hypophosphite and phosphite using a UV/H2O2 process.

Science.gov (United States)

Liu, Peng; Li, Chaolin; Liang, Xingang; Xu, Jianhui; Lu, Gang; Ji, Fei

2013-01-01

The oxidation of hypophosphite and phosphite in an aqueous solution by an ultraviolet (UV)/H2O2 process was studied in this work. The reactions were performed in a lab-scale batch photoreactor. The effect of different parameters such as H2O2 dosage, H2O2 feeding mode and the initial pH of the solution on the oxidation efficiency of the process was investigated. The results indicated that the UV/H2O2 process could effectively oxidize hypophosphite and phosphite in both synthesized and real wastewater. However, neither H2O2 nor UV alone was able to appreciably oxidize the hypophosphite or phosphite. The best way of feeding H2O2 was found to be 'continuous feeding', which maximized the reaction rate. It was also found that the process presented a wide range of applicable initial pH (5-11). When treating real rinse-wastewater, which was obtained from the electroless nickel plating industry, both hypophosphite and phosphite were completely oxidized within 60 min, and by extending by another 30 min, over 90% of the chemical oxygen demand removal was obtained. Without any additional catalyst, the UV/H2O2 process can oxidize hypophosphite and phosphite to easily removable phosphate. It is really a powerful and environmentally friendly treatment method for the wastewater containing hypophosphite and phosphite.

Staphylococcus aureus Adapts to Oxidative Stress by Producing H2O2-Resistant Small-Colony Variants via the SOS Response

Science.gov (United States)

Painter, Kimberley L.; Strange, Elizabeth; Bamford, Kathleen B.; Armstrong-James, Darius

2015-01-01

The development of chronic and recurrent Staphylococcus aureus infections is associated with the emergence of slow-growing mutants known as small-colony variants (SCVs), which are highly tolerant of antibiotics and can survive inside host cells. However, the host and bacterial factors which underpin SCV emergence during infection are poorly understood. Here, we demonstrate that exposure of S. aureus to sublethal concentrations of H2O2 leads to a specific, dose-dependent increase in the population frequency of gentamicin-resistant SCVs. Time course analyses revealed that H2O2 exposure caused bacteriostasis in wild-type cells during which time SCVs appeared spontaneously within the S. aureus population. This occurred via a mutagenic DNA repair pathway that included DNA double-strand break repair proteins RexAB, recombinase A, and polymerase V. In addition to triggering SCV emergence by increasing the mutation rate, H2O2 also selected for the SCV phenotype, leading to increased phenotypic stability and further enhancing the size of the SCV subpopulation by reducing the rate of SCV reversion to the wild type. Subsequent analyses revealed that SCVs were significantly more resistant to the toxic effects of H2O2 than wild-type bacteria. With the exception of heme auxotrophs, gentamicin-resistant SCVs displayed greater catalase activity than wild-type bacteria, which contributed to their resistance to H2O2. Taken together, these data reveal a mechanism by which S. aureus adapts to oxidative stress via the production of a subpopulation of H2O2-resistant SCVs with enhanced catalase production. PMID:25690100

Carvedilol, a third-generation β-blocker prevents oxidative stress-induced neuronal death and activates Nrf2/ARE pathway in HT22 cells

Energy Technology Data Exchange (ETDEWEB)

Ouyang, Ying [Department of Pediatrics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou (China); Chen, Ziwei [Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou (China); Tan, Min [Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou (China); Department of Traditional Chinese Medicine Chemistry, College of Chinese Materia Madica, Guangzhou University of Chinese Medicine, Guangzhou 510006 (China); Liu, Anmin [Department of Neurosurgery, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou (China); Chen, Meihui [Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou (China); Liu, Jun [Department of Neurology, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou (China); Pi, Rongbiao, E-mail: pirb@mail.sysu.edu.cn [Department of Pharmacology and Toxicology, School of Pharmaceutical Sciences, Sun Yat-Sen University, Guangzhou (China); Fang, Jianpei, E-mail: jpf2005@163.com [Department of Pediatrics, Sun Yat-Sen Memorial Hospital, Sun Yat-Sen University, Guangzhou (China)

2013-11-29

Highlights: •Carvedilol significantly prevented oxidative stress-induced cell death. •Carvedilol significantly decreased the production of ROS. •Carvedilol activated Nrf2/ARE pathway. •Carvedilol increased the protein levels of HO-1 and NQO-1. -- Abstract: Carvedilol, a nonselective β-adrenoreceptor blocker with pleiotropic activities has been shown to exert neuroprotective effect due to its antioxidant property. However, the neuroprotective mechanism of carvedilol is still not fully uncovered. Nuclear factor E2-related factor 2 (Nrf2)/antioxidant response element (ARE) pathway is an important cellular stress response pathway involved in neuroprotection. Here we investigated the effect of carvedilol on oxidative stress-induced cell death (glutamate 2 mM and H{sub 2}O{sub 2} 600 μM) and the activity of Nrf2/ARE pathway in HT22 hippocampal cells. Carvedilol significantly increased cell viability and decreased ROS in HT22 cells exposed to glutamate or H{sub 2}O{sub 2}. Furthermore, carvedilol activated the Nrf2/ARE pathway in a concentration-dependent manner, and increased the protein levels of heme oxygenase-1(HO-1) and NAD(P)H quinone oxidoreductase-1(NQO-1), two downstream factors of the Nrf2/ARE pathway. Collectively, our results indicate that carvedilol protects neuronal cell against glutamate- and H{sub 2}O{sub 2}-induced neurotoxicity possibly through activating the Nrf2/ARE signaling pathway.

Generation of H2 and CO by solar thermochemical splitting of H2O and CO2 by employing metal oxides

International Nuclear Information System (INIS)

Rao, C.N.R.; Dey, Sunita

2016-01-01

Generation of H 2 and CO by splitting H 2 O and CO 2 respectively constitutes an important aspect of the present-day concerns with energy and environment. The solar thermochemical route making use of metal oxides is a viable means of accomplishing these reduction reactions. The method essentially involves reducing a metal oxide by heating and passing H 2 O or CO 2 over the nonstoichiometric oxide to cause reverse oxidation by abstracting oxygen from H 2 O or CO 2 . While ceria, perovskites and other oxides have been investigated for this purpose, recent studies have demonstrated the superior performance of perovskites of the type Ln 1−x A x Mn 1−y M y O 3 (Ln=rare earth, A=alkaline earth, M=various +2 and +3 metal ions), in the thermochemical generation of H 2 and CO. We present the important results obtained hitherto to point out how the alkaine earth and the Ln ions, specially the radius of the latter, determine the performance of the perovskites. The encouraging results obtained are exemplefied by Y 0.5 Sr 0.5 MnO 3 which releases 483 µmol/g of O 2 at 1673 K and produces 757 µmol/g of CO from CO 2 at 1173 K. The production of H 2 from H 2 O is also quite appreciable. Modification of the B site ion of the perovskite also affects the performance. In addition to perovskites, we present the generation of H 2 based on the Mn 3 O 4 /NaMnO 2 cycle briefly. - Graphical abstract: Ln 0.5 A 0.5 Mn 1−x M x O 3 (Ln=lanthanide; A=Ca, Sr; M=Al, Ga, Sc, Mg, Cr, Fe, Co) perovskites are employed for the two step thermochemical splitting of CO 2 and H 2 O for the generation of CO and H 2 . - Highlights: • Perovskite oxides based on Mn are ideal for the two-step thermochemical splitting of CO 2 and H 2 O. • In Ln 1−x A x MnO 3 perovskite (Ln=rare earth, A=alkaline earth) both Ln and A ions play major roles in the thermochemical process. • H 2 O splitting is also achieved by the use of the Mn 3 O 4 -sodium carbonate system. • Thermochemical splitting of CO 2 and H

Rat Aquaporin-5 Is pH-Gated Induced by Phosphorylation and Is Implicated in Oxidative Stress

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Claudia Rodrigues

2016-12-01

Full Text Available Aquaporin-5 (AQP5 is a membrane water channel widely distributed in human tissues that was found up-regulated in different tumors and considered implicated in carcinogenesis in different organs and systems. Despite its wide distribution pattern and physiological importance, AQP5 short-term regulation was not reported and mechanisms underlying its involvement in cancer are not well defined. In this work, we expressed rat AQP5 in yeast and investigated mechanisms of gating, as well as AQP5’s ability to facilitate H2O2 plasma membrane diffusion. We found that AQP5 can be gated by extracellular pH in a phosphorylation-dependent manner, with higher activity at physiological pH 7.4. Moreover, similar to other mammalian AQPs, AQP5 is able to increase extracellular H2O2 influx and to affect oxidative cell response with dual effects: whereas in acute oxidative stress conditions AQP5 induces an initial higher sensitivity, in chronic stress AQP5 expressing cells show improved cell survival and resistance. Our findings support the involvement of AQP5 in oxidative stress and suggest AQP5 modulation by phosphorylation as a novel tool for therapeutics.

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.

Escin activates AKT-Nrf2 signaling to protect retinal pigment epithelium cells from oxidative stress

Energy Technology Data Exchange (ETDEWEB)

Wang, Kaijun [Eye Center, The 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou (China); Zhejiang Provincial Key Lab of Ophthalmology, Hangzhou (China); Jiang, Yiqian [The First People Hospital of Xiaoshan, Hangzhou (China); Wang, Wei; Ma, Jian [Eye Center, The 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou (China); Zhejiang Provincial Key Lab of Ophthalmology, Hangzhou (China); Chen, Min, E-mail: eyedrchenminzj@163.com [Eye Center, The 2nd Affiliated Hospital, Medical College of Zhejiang University, Hangzhou (China); Zhejiang Provincial Key Lab of Ophthalmology, Hangzhou (China)

2015-12-25

Here we explored the anti-oxidative and cytoprotective potentials of escin, a natural triterpene-saponin, against hydrogen peroxide (H{sub 2}O{sub 2}) in retinal pigment epithelium (RPE) cells. We showed that escin remarkably attenuated H{sub 2}O{sub 2}-induced death and apoptosis of established (ARPE-19) and primary murine RPE cells. Meanwhile, ROS production and lipid peroxidation by H{sub 2}O{sub 2} were remarkably inhibited by escin. Escin treatment in RPE cells resulted in NF-E2-related factor 2 (Nrf2) signaling activation, evidenced by transcription of anti-oxidant-responsive element (ARE)-regulated genes, including HO-1, NQO-1 and SRXN-1. Knockdown of Nrf2 through targeted shRNAs/siRNAs alleviated escin-mediated ARE gene transcription, and almost abolished escin-mediated anti-oxidant activity and RPE cytoprotection against H{sub 2}O{sub 2}. Reversely, escin was more potent against H{sub 2}O{sub 2} damages in Nrf2-over-expressed ARPE-19 cells. Further studies showed that escin-induced Nrf2 activation in RPE cells required AKT signaling. AKT inhibitors (LY294002 and perifosine) blocked escin-induced AKT activation, and dramatically inhibited Nrf2 phosphorylation, its cytosol accumulation and nuclear translocation in RPE cells. Escin-induced RPE cytoprotection against H{sub 2}O{sub 2} was also alleviated by the AKT inhibitors. Together, these results demonstrate that escin protects RPE cells from oxidative stress possibly through activating AKT-Nrf2 signaling.

Protective Role of Nuclear Factor E2-Related Factor 2 against Acute Oxidative Stress-Induced Pancreatic β-Cell Damage

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Jingqi Fu

2015-01-01

Full Text Available Oxidative stress is implicated in the pathogenesis of pancreatic β-cell dysfunction that occurs in both type 1 and type 2 diabetes. Nuclear factor E2-related factor 2 (NRF2 is a master regulator in the cellular adaptive response to oxidative stress. The present study found that MIN6 β-cells with stable knockdown of Nrf2 (Nrf2-KD and islets isolated from Nrf2-knockout mice expressed substantially reduced levels of antioxidant enzymes in response to a variety of stressors. In scramble MIN6 cells or wild-type islets, acute exposure to oxidative stressors, including hydrogen peroxide (H2O2 and S-nitroso-N-acetylpenicillamine, resulted in cell damage as determined by decrease in cell viability, reduced ATP content, morphology changes of islets, and/or alterations of apoptotic biomarkers in a concentration- and/or time-dependent manner. In contrast, silencing of Nrf2 sensitized MIN6 cells or islets to the damage. In addition, pretreatment of MIN6 β-cells with NRF2 activators, including CDDO-Im, dimethyl fumarate (DMF, and tert-butylhydroquinone (tBHQ, protected the cells from high levels of H2O2-induced cell damage. Given that reactive oxygen species (ROS are involved in regulating glucose-stimulated insulin secretion (GSIS and persistent activation of NRF2 blunts glucose-triggered ROS signaling and GSIS, the present study highlights the distinct roles that NRF2 may play in pancreatic β-cell dysfunction that occurs in different stages of diabetes.

Protective effects of rambutan (Nephelium lappaceum) peel phenolics on H2O2-induced oxidative damages in HepG2 cells and d-galactose-induced aging mice.

Science.gov (United States)

Zhuang, Yongliang; Ma, Qingyu; Guo, Yan; Sun, Liping

2017-10-01

Rambutan peel phenolic (RPP) extracts were prepared via dynamic separation with macroporous resin. The total phenolic content and individual phenolics in RPP were determined. Results showed that the total phenolic content of RPP was 877.11 mg gallic acid equivalents (GAE)/g extract. The content of geranin (122.18 mg/g extract) was the highest among those of the 39 identified phenolic compounds. RPP protected against oxidative stress in H 2 O 2 -induced HepG2 cells in a dose-response manner. The inhibitory effects of RPP on cell apoptosis might be related to its inhibitory effects on the generation of intracellular reactive oxygen species and increased effects on superoxide dismutase activity. The in vivo anti-aging activity of RPP was evaluated using an aging mice model that was induced by d-galactose (d-gal). The results showed that RPP enhanced the antioxidative status of experimental mice. Moreover, histological analysis indicated that RPP effectively reduced d-gal-induced liver and kidney tissue damage in a dose-dependent manner. Therefore, RPP can be used as a natural antioxidant and anti-aging agent in the pharmaceutical and food industries. Copyright © 2017 Elsevier Ltd. All rights reserved.

Oxide, interface, and border traps in thermal, N2O, and N2O-nitrided oxides

International Nuclear Information System (INIS)

Fleetwood, D.M.; Saks, N.S.

1996-01-01

We have combined thermally stimulated-current (TSC) and capacitance endash voltage (C endash V) measurements to estimate oxide, interface, and effective border trap densities in 6 endash 23 nm thermal, N 2 O, and N 2 O-nitrided oxides exposed to ionizing radiation or high-field electron injection. Defect densities depend strongly on oxide processing, but radiation exposure and moderate high-field stress lead to similar trapped hole peak thermal energy distributions (between ∼1.7 and ∼2.0 eV) for all processes. This suggests that similar defects dominate the oxide charge trapping properties in these devices. Radiation-induced hole and interface trap generation efficiencies (0.1%endash 1%) in the best N 2 O and N 2 O-nitrided oxides are comparable to the best radiation hardened oxides in the literature. After ∼10 Mrad(SiO 2 ) x-ray irradiation or ∼10 mC/cm 2 constant current Fowler endash Nordheim injection, effective border trap densities as high as ∼5x10 11 cm -2 are inferred from C endash V hysteresis. These measurements suggest irradiation and high-field stress cause similar border trap energy distributions. In each case, even higher densities of compensating trapped electrons in the oxides (up to 2x10 12 cm -2 ) are inferred from combined TSC and C endash V measurements. These trapped electrons prevent conventional C endash V methods from providing accurate estimates of the total oxide trap charge density in many irradiation or high-field stress studies. Fewer compensating electrons per trapped hole (∼26%±5%) are found for irradiation of N 2 O and N 2 O-nitrided oxides than for thermal oxides (∼46%±7%). (Abstract Truncated)

Human low density lipoprotein (LDL) oxidation by metmyoglobin/H2O2: involvement of α-tocopheroxyl and phosphatidylcholine alkoxyl radicals

International Nuclear Information System (INIS)

Witting, P.K.; Willhite, C.A.; Stocker, R.; Davies, M.J.

1998-01-01

Full text: Metmyoglobin (metMb) and H 2 O 2 can oxidize low density lipoprotein (LDL) in vitro; formation of such oxidized LDL may be atherogenic. The role of α-tocopherol (α-TOH) in LDL oxidation by peroxidases, such as metMb is unclear. Herein we show that during metMb/H 2 O 2 -induced oxidation of native, α-TOH-containing, LDL, α-tocopheroxyl radical (α-TO) and hydroperoxides and hydroxides of cholesteryl esters (CE-O(O)H) and phosphatidylcholine (PC-O(O)H) accumulated concomitantly with α-TOH consumption. Accumulation of CE-O(O)H was dependent on, and correlated with, LDL's α-TOH content indicating that α-TO . acted as a chain-transfer agent and propagated LDL lipid peroxidation via tocopherol-mediated peroxidation (TMP). Further, the ratio of accumulating CE-O(O)H to PC-O(O)H remained constant in the presence α-TOH. Subsequent to α-TOH depletion, CE-O(O)H continued to accumulate, albeit at a lower rate than in the presence of α-TOH. This was accompanied by depletion of PC-OOH, a rapid increase in the CE-O(O)H/PC-O(O)H ratio, formation of lipid-derived alkoxyl radicals and phosphatidylcholine hydroxides (PC-OH), and accumulation of a second organic radical, characterized by a broad singlet EPR signal. The latter persisted for several hours at 37 deg C. We conclude that metMb/H 2 O 2 -induced peroxidation of LDL lipids is not inhibited by α-TOH and occurs initially via TMP. After α-TOH depletion, cholesteryl esters peroxidize at higher fractional rates than surface phospholipids, and this appears to be mediated via reactions involving alkoxyl radicals derived from the peroxidatic activity of metMb on PC-OO

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

5-AIQ inhibits H{sub 2}O{sub 2}-induced apoptosis through reactive oxygen species scavenging and Akt/GSK-3β signaling pathway in H9c2 cardiomyocytes

Energy Technology Data Exchange (ETDEWEB)

Park, Eun-Seok; Kang, Jun Chul; Kang, Do-Hyun; Jang, Yong Chang [Department of Applied Biochemistry, Konkuk University, Chungju, Chungbuk, 380-701 (Korea, Republic of); Yi, Kyu Yang [Bio-Organic Science Division, Korea Research Institute of Chemical Technology, Daejeon, Chungnam, 305-600 (Korea, Republic of); Chung, Hun-Jong [Industrial Medicine Department, Chungju Hospital, Konkuk Medical School, Konkuk University, Chungju, Chungbuk, 380-701 (Korea, Republic of); Park, Jong Seok [Department of Biomedical Laboratory Science, Taegu Health College, Taegu 702-722 (Korea, Republic of); Kim, Bokyung [Department of Physiology, Konkuk Medical School, Konkuk University, Chungju, Chungbuk, 380-701 (Korea, Republic of); Feng, Zhong-Ping [Department of Physiology, College of Medicine, University of Toronto, Toronto, Ont., Canada M5S 1A8 (Canada); Shin, Hwa-Sup, E-mail: hsshin@kku.ac.kr [Department of Applied Biochemistry, Konkuk University, Chungju, Chungbuk, 380-701 (Korea, Republic of)

2013-04-01

Poly(adenosine 5′-diphosphate ribose) polymerase (PARP) is a nuclear enzyme activated by DNA strand breaks and plays an important role in the tissue injury associated with ischemia and reperfusion. The aim of the present study was to investigate the protective effect of 5-aminoisoquinolinone (5-AIQ), a PARP inhibitor, against oxidative stress-induced apoptosis in H9c2 cardiomyocytes. 5-AIQ pretreatment significantly protected against H{sub 2}O{sub 2}-induced cell death, as determined by the XTT assay, cell counting, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay, and Western blot analysis of apoptosis-related proteins such as caspase-3, Bax, and Bcl-2. Upregulation of antioxidant enzymes such as manganese superoxide dismutase and catalase accompanied the protective effect of 5-AIQ on H{sub 2}O{sub 2}-induced cell death. Our data also showed that 5-AIQ pretreatment protected H9c2 cells from H{sub 2}O{sub 2}-induced apoptosis by triggering activation of Akt and glycogen synthase kinase-3β (GSK-3β), and that the protective effect of 5-AIQ was diminished by the PI3K inhibitor LY294002 at a concentration that effectively abolished 5-AIQ-induced Akt and GSK-3β activation. In addition, inhibiting the Akt/GSK-3β pathway by LY294002 significantly attenuated the 5-AIQ-mediated decrease in cleaved caspase-3 and Bax activation and H9c2 cell apoptosis induction. Taken together, these results demonstrate that 5-AIQ prevents H{sub 2}O{sub 2}-induced apoptosis in H9c2 cells by reducing intracellular reactive oxygen species production, regulating apoptosis-related proteins, and activating the Akt/GSK-3β pathway. - Highlights: ► 5-AIQ, a PARP inhibitor, decreased H{sub 2}O{sub 2}-induced H9c2 cell death and apoptosis. ► 5-AIQ upregulated antioxidant Mn-SOD and catalase, while decreasing ROS production. ► 5-AIQ decreased H{sub 2}O{sub 2}-induced increase in cleaved caspase-3 and Bax and decrease in Bcl2. ► 5-AIQ activated Akt and GSK-3�

Acute restraint stress induces endothelial dysfunction: role of vasoconstrictor prostanoids and oxidative stress.

Science.gov (United States)

Carda, Ana P P; Marchi, Katia C; Rizzi, Elen; Mecawi, André S; Antunes-Rodrigues, José; Padovan, Claudia M; Tirapelli, Carlos R

2015-01-01

We hypothesized that acute stress would induce endothelial dysfunction. Male Wistar rats were restrained for 2 h within wire mesh. Functional and biochemical analyses were conducted 24 h after the 2-h period of restraint. Stressed rats showed decreased exploration on the open arms of an elevated-plus maze (EPM) and increased plasma corticosterone concentration. Acute restraint stress did not alter systolic blood pressure, whereas it increased the in vitro contractile response to phenylephrine and serotonin in endothelium-intact rat aortas. NG-nitro-l-arginine methyl ester (l-NAME; nitric oxide synthase, NOS, inhibitor) did not alter the contraction induced by phenylephrine in aortic rings from stressed rats. Tiron, indomethacin and SQ29548 reversed the increase in the contractile response to phenylephrine induced by restraint stress. Increased systemic and vascular oxidative stress was evident in stressed rats. Restraint stress decreased plasma and vascular nitrate/nitrite (NOx) concentration and increased aortic expression of inducible (i) NOS, but not endothelial (e) NOS. Reduced expression of cyclooxygenase (COX)-1, but not COX-2, was observed in aortas from stressed rats. Restraint stress increased thromboxane (TX)B(2) (stable TXA(2) metabolite) concentration but did not affect prostaglandin (PG)F2α concentration in the aorta. Restraint reduced superoxide dismutase (SOD) activity, whereas concentrations of hydrogen peroxide (H(2)O(2)) and reduced glutathione (GSH) were not affected. The major new finding of our study is that restraint stress increases vascular contraction by an endothelium-dependent mechanism that involves increased oxidative stress and the generation of COX-derived vasoconstrictor prostanoids. Such stress-induced endothelial dysfunction could predispose to the development of cardiovascular diseases.

A study of the accelerated zircaloy-4 oxidation reaction with H2O/H2 mixture gas

International Nuclear Information System (INIS)

Kim, Y. S.; Cho, I. J.

2001-01-01

A study of the Zircaloy-4 reaction with H 2 O/H 2 mixture gas is carried out by using TGA (Thermo Gravimetric Apparatus) to estimate the hydrogen embrittlement which can possibly cause catastrophic nuclear fuel rod failure. Reaction rates are measured as a function of H 2 /H 2 O. In the experiments reaction temperature is set at 500 .deg. C and total pressure of the mixture gas is maintained at 1 atm. Experimental results reveal that hydriding and oxidation reaction are competing. In early stage, hydriding kinetics is faster than oxidation, however, oxidant in H 2 O forms oxide on the surface as steam environment is maintained, thus, this growing oxide begins to protect the zirconium base metal against hydrogen permeation. In this second stage, the total kinetic rate follows enhanced oxidation kinetics. In the final stage, it is observed that the oxide is broken down and massive hydriding takes place through the mechanical defects in the oxide, whose kinetics is similar to pure hydriding kinetics. These results are confirmed by SEM and EDX analysis along with hydrogen concentration measurements

Oxidative Stress Induces Endothelial Cell Senescence via Downregulation of Sirt6

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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.

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

Quantification and Purification of Mangiferin from Chinese Mango (Mangifera indica L.) Cultivars and Its Protective Effect on Human Umbilical Vein Endothelial Cells under H2O2-induced Stress

Science.gov (United States)

Luo, Fenglei; Lv, Qiang; Zhao, Yuqin; Hu, Guibing; Huang, Guodi; Zhang, Jiukai; Sun, Chongde; Li, Xian; Chen, Kunsong

2012-01-01

Mangiferin is a natural xanthonoid with various biological activities. Quantification of mangiferin in fruit peel, pulp, and seed kernel was carried out in 11 Chinese mango (Mangifera indica L.) cultivars. The highest mangiferin content was found in the peel of Lvpimang (LPM) fruit (7.49 mg/g DW). Efficient purification of mangiferin from mango fruit peel was then established for the first time by combination of macroporous HPD100 resin chromatography with optimized high-speed counter-current chromatography (HSCCC). Purified mangiferin was identified by both HPLC and LC-MS, and it showed higher DPPH• free-radical scavenging capacities and ferric reducing ability of plasma (FRAP) than by l-ascorbic acid (Vc) or Trolox. In addition, it showed significant protective effects on human umbilical vein endothelial cells (HUVEC) under H2O2-induced stress. Cells treated with mangiferin resulted in significant enhanced cell survival under of H2O2 stress. Therefore, mangiferin from mango fruit provides a promising perspective for the prevention of oxidative stress-associated diseases. PMID:23109851

Quantification and purification of mangiferin from Chinese Mango (Mangifera indica L.) cultivars and its protective effect on human umbilical vein endothelial cells under H(2)O(2)-induced stress.

Science.gov (United States)

Luo, Fenglei; Lv, Qiang; Zhao, Yuqin; Hu, Guibing; Huang, Guodi; Zhang, Jiukai; Sun, Chongde; Li, Xian; Chen, Kunsong

2012-01-01

Mangiferin is a natural xanthonoid with various biological activities. Quantification of mangiferin in fruit peel, pulp, and seed kernel was carried out in 11 Chinese mango (Mangifera indica L.) cultivars. The highest mangiferin content was found in the peel of Lvpimang (LPM) fruit (7.49 mg/g DW). Efficient purification of mangiferin from mango fruit peel was then established for the first time by combination of macroporous HPD100 resin chromatography with optimized high-speed counter-current chromatography (HSCCC). Purified mangiferin was identified by both HPLC and LC-MS, and it showed higher DPPH(•) free-radical scavenging capacities and ferric reducing ability of plasma (FRAP) than by l-ascorbic acid (Vc) or Trolox. In addition, it showed significant protective effects on human umbilical vein endothelial cells (HUVEC) under H(2)O(2)-induced stress. Cells treated with mangiferin resulted in significant enhanced cell survival under of H(2)O(2) stress. Therefore, mangiferin from mango fruit provides a promising perspective for the prevention of oxidative stress-associated diseases.

Piezoelectrically-induced stress-luminescence phenomenon in CaAl2O4:Eu2+

International Nuclear Information System (INIS)

Wei, Yongbin; Wu, Zheng; Jia, Yanmin; Liu, Yongsheng

2015-01-01

Piezoelectrically-induced stress-luminescence in the CaAl 2 O 4 :Eu 2+ was investigated. Blue light that was visible to the naked eye could be observed in the dark when a pulse force of ∼7.7 kN was applied to the sample. The intensity of the stress-luminescence strongly depended on the magnitude of the applied force during a pulse cycle. The intensity decreased with repetitive application of pulse stress and was completely recovered after irradiation with ultraviolet light. It is suggested that the stress-luminescence effect in CaAl 2 O 4 :Eu 2+ arises from the piezoelectrically-induced de-trapping of the charge carriers. A CaAl 2 O 4 :Eu 2+ ceramic that exhibits a stress-luminescence effect has potential applications in smart stress optically-sensing devices. - Highlights: • The strong induced stress-luminescence in CaAl 2 O 4 :Eu 2+ was observed. • The stress-luminescent intensity strongly depends on the magnitude of force. • The stress-luminescence could be completely recovered after the UV irradiation. • The strong stress-luminescent effect is potential in stress-light sensors

Sailuotong Prevents Hydrogen Peroxide (H2O2-Induced Injury in EA.hy926 Cells

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Sai Wang Seto

2017-01-01

Full Text Available Sailuotong (SLT is a standardised three-herb formulation consisting of Panax ginseng, Ginkgo biloba, and Crocus sativus designed for the management of vascular dementia. While the latest clinical trials have demonstrated beneficial effects of SLT in vascular dementia, the underlying cellular mechanisms have not been fully explored. The aim of this study was to assess the ability and mechanisms of SLT to act against hydrogen peroxide (H2O2-induced oxidative damage in cultured human vascular endothelial cells (EAhy926. SLT (1–50 µg/mL significantly suppressed the H2O2-induced cell death and abolished the H2O2-induced reactive oxygen species (ROS generation in a concentration-dependent manner. Similarly, H2O2 (0.5 mM; 24 h caused a ~2-fold increase in lactate dehydrogenase (LDH release from the EA.hy926 cells which were significantly suppressed by SLT (1–50 µg/mL in a concentration-dependent manner. Incubation of SLT (50 µg/mL increased superoxide dismutase (SOD activity and suppressed the H2O2-enhanced Bax/Bcl-2 ratio and cleaved caspase-3 expression. In conclusion, our results suggest that SLT protects EA.hy916 cells against H2O2-mediated injury via direct reduction of intracellular ROS generation and an increase in SOD activity. These protective effects are closely associated with the inhibition of the apoptotic death cascade via the suppression of caspase-3 activation and reduction of Bax/Bcl-2 ratio, thereby indicating a potential mechanism of action for the clinical effects observed.

Glutathione oxidation in response to intracellular H2O2: Key but overlapping roles for dehydroascorbate reductases.

Science.gov (United States)

Rahantaniaina, Marie-Sylviane; Li, Shengchun; Chatel-Innocenti, Gilles; Tuzet, Andrée; Mhamdi, Amna; Vanacker, Hélène; Noctor, Graham

2017-08-03

Glutathione is a pivotal molecule in oxidative stress, during which it is potentially oxidized by several pathways linked to H 2 O 2 detoxification. We have investigated the response and functional importance of 3 potential routes for glutathione oxidation pathways mediated by glutathione S-transferases (GST), glutaredoxin-dependent peroxiredoxins (PRXII), and dehydroascorbate reductases (DHAR) in Arabidopsis during oxidative stress. Loss-of-function gstU8, gstU24, gstF8, prxIIE and prxIIF mutants as well as double gstU8 gstU24, gstU8 gstF8, gstU24 gstF8, prxIIE prxIIF mutants were obtained. No mutant lines showed marked changes in their phenotype and glutathione profiles in comparison to the wild-type plants in either optimal conditions or oxidative stress triggered by catalase inhibition. By contrast, multiple loss of DHAR functions markedly decreased glutathione oxidation triggered by catalase deficiency. To assess whether this effect was mediated directly by loss of DHAR enzyme activity, or more indirectly by upregulation of other enzymes involved in glutathione and ascorbate recycling, we measured expression of glutathione reductase (GR) and expression and activity of monodehydroascorbate reductases (MDHAR). No evidence was obtained that either GRs or MDHARs were upregulated in plants lacking DHAR function. Hence, interplay between different DHARs appears to be necessary to couple ascorbate and glutathione pools and to allow glutathione-related signaling during enhanced H 2 O 2 metabolism.

Activation of ERK signalling by Src family kinases (SFKs) in DRG neurons contributes to hydrogen peroxide (H2O2)-induced thermal hyperalgesia.

Science.gov (United States)

Singh, Ajeet Kumar; Vinayak, Manjula

2017-10-01

Concomitant generation of reactive oxygen species during tissue inflammation has been recognised as a major factor for the development and the maintenance of hyperalgesia, out of which H 2 O 2 is the major player. However, molecular mechanism of H 2 O 2 induced hyperalgesia is still obscure. The aim of present study is to analyse the mechanism of H 2 O 2 -induced hyperalgesia in rats. Intraplantar injection of H 2 O 2 (5, 10 and 20 µmoles/paw) induced a significant thermal hyperalgesia in the hind paw, confirmed by increased c-Fos activity in dorsal horn of spinal cord. Onset of hyperalgesia was prior to development of oxidative stress and inflammation. Rapid increase in phosphorylation of extracellular signal regulated kinase (ERK) was observed in neurons of dorsal root ganglia after 20 min of H 2 O 2 (10 µmoles/paw) administration, which gradually returned towards normal level within 24 h, following the pattern of thermal hyperalgesia. The expression of TNFR1 followed the same pattern and colocalised with pERK. ERK phosphorylation was observed in NF-200-positive and -negative neurons, indicating the involvement of ERK in C-fibres as well as in A-fibres. Intrathecal preadministration of Src family kinases (SFKs) inhibitor (PP1) and MEK inhibitor (PD98059) prevented H 2 O 2 induced augmentation of ERK phosphorylation and thermal hyperalgesia. Pretreatment of protein tyrosine phosphatases (PTPs) inhibitor (sodium orthovanadate) also diminished hyperalgesia, although it further increased ERK phosphorylation. Combination of orthovanadate with PP1 or PD98059 did not exhibit synergistic antihyperalgesic effect. The results demonstrate SFKs-mediated ERK activation and increased TNFR1 expression in nociceptive neurons during H 2 O 2 induced hyperalgesia. However, the role of PTPs in hyperalgesic behaviour needs further molecular analysis.

Ferrous ion oxidations by ·H, ·OH and H2O2 in aerated FBX dosimetry system

International Nuclear Information System (INIS)

Gupta, B.L.; Nilekani, S.R.

1998-01-01

In the ferrous ion, benzoic acid and xylenol orange (FBX) dosimetric system, benzoic acid (BA) increases the G(Fe 3+ ) value. Xylenol orange (XO) controls the BA sensitized chain reaction as well as forms a complex with Fe 3+ . In the aerated FBX system each ·H, ·OH and H 2 O 2 oxidizes 8.5, 6.6 and 7.6 Fe 2+ ions, respectively; and these values respectively increase to 11.3, 7.6 and 8.6 in oxygenated solution. About 8% ·OH reacts with XO and the remaining with BA. The above fractional values are due to this competition. This ·OH reaction with XO oxidizes 1.8% and 2.1% ferrous ions only in aerated and oxygenated solutions, respectively. There is a competition between ·H reactions with O 2 and with BA, but both lead to the production of H 2 O 2 . The oxidation of Fe 2+ by ·OH reactions at different concentrations of H 2 O 2 is linear with absorbed dose while the ·H reactions make the oxidation of Fe 2+ non-linear with dose. This is due to competition reaction of H-adduct of BA between O 2 and Fe 3+

Removal of phenolic endocrine disrupting compounds from waste activated sludge using UV, H2O2, and UV/H2O2 oxidation processes: Effects of reaction conditions and sludge matrix

International Nuclear Information System (INIS)

Zhang, Ai; Li, Yongmei

2014-01-01

Removal of six phenolic endocrine disrupting compounds (EDCs) (estrone, 17β-estradiol, 17α-ethinylestradiol, estriol, bisphenol A, and 4-nonylphenols) from waste activated sludge (WAS) was investigated using ultraviolet light (UV), hydrogen peroxide (H 2 O 2 ), and the combined UV/H 2 O 2 processes. Effects of initial EDC concentration, H 2 O 2 dosage, and pH value were investigated. Particularly, the effects of 11 metal ions and humic acid (HA) contained in a sludge matrix on EDC degradation were evaluated. A pseudo-first-order kinetic model was used to describe the EDC degradation during UV, H 2 O 2 , and UV/H 2 O 2 treatments of WAS. The results showed that the degradation of the 6 EDCs during all the three oxidation processes fitted well with pseudo-first-order kinetics. Compared with the sole UV irradiation or H 2 O 2 oxidation process, UV/H 2 O 2 treatment was much more effective for both EDC degradation and WAS solubilization. Under their optimal conditions, the EDC degradation rate constants during UV/H 2 O 2 oxidation were 45–197 times greater than those during UV irradiation and 11–53 times greater than those during H 2 O 2 oxidation. High dosage of H 2 O 2 and low pH were favorable for the degradation of EDCs. Under the conditions of pH = 3, UV wavelength = 253.7 nm, UV fluence rate = 0.069 mW cm −2 , and H 2 O 2 dosage = 0.5 mol L −1 , the removal efficiencies of E1, E2, EE2, E3, BPA, and NP in 2 min were 97%, 92%, 95%, 94%, 89%, and 67%, respectively. The hydroxyl radical (·OH) was proved to take the most important role for the removal of EDCs. Metal ions in sludge could facilitate the removal of EDCs during UV/H 2 O 2 oxidation. Fe, Ag, and Cu ions had more obvious effects compared with other metal ions. The overall role of HA was dependent on the balance between its competition as organics and its catalysis/photosensitization effects. These indicate that the sludge matrix plays an important role in the degradation of EDCs. - Highlights: �

Kinetics of oxidation of H2 and reduction of H2O in Ni-YSZ based solid oxide cells

DEFF Research Database (Denmark)

Ebbesen, Sune Dalgaard; Mogensen, Mogens Bjerg

2012-01-01

Reduction of H2O and oxidation of H2 was studied in a Ni-YSZ electrode supported Solid Oxide Cells produced at DTU Energy conversion (former Risø DTU). Polarisation (i-V) and electrochemical impedance spectroscopic characterisation show that the kinetics for reduction of H 2O is slower compared...... to oxidation of H2. The kinetic differences cannot be explained by the reaction mechanisms which are similar in the two cases but are rather an effect of the thermodynamics. The preliminary analysis performed in this study show that the slow kinetic for reduction is partly related to the endothermic nature...... of the reaction, cooling the active electrode, thereby leading to slower kinetics at low current densities. Likewise, the increased kinetic for oxidation was found to be related to the exothermic nature of the reaction, heating the active electrode, and thereby leading to faster kinetics. At higher current...

A novel dual-ratiometric-response fluorescent probe for SO2/ClO- detection in cells and in vivo and its application in exploring the dichotomous role of SO2 under the ClO- induced oxidative stress.

Science.gov (United States)

Dou, Kun; Fu, Qiang; Chen, Guang; Yu, Fabiao; Liu, Yuxia; Cao, Ziping; Li, Guoliang; Zhao, Xianen; Xia, Lian; Chen, Lingxin; Wang, Hua; You, Jinmao

2017-07-01

Intracellular reactive sulfur species and reactive oxygen species play vital roles in immunologic mechanism. As an emerging signal transmitter, SO 2 can be generated as the anti-oxidant, while SO 2 is also a potential oxidative stress-inducer in organism. Aiming to elucidate in-depth the dichotomous role of SO 2 under oxidative stress, we designed a dual-response fluorescent probe that enabled the respective or successive detection of SO 2 and ClO - . The probe itself emits the red fluorescence (625 nm) which can largely switch to blue (410 nm) and green fluorescence (500 nm) respectively in response to SO 2 and ClO - , allowing the highly selective and accurate ratiometric quantification for both SO 2 and ClO - in cells. Moreover the ultrafast (SO 2 : <60 s; ClO - : within sec) and highly sensitive (detection limits: SO 2 : 3.5 nM; ClO - : 12.5 nM) detection were achieved. With the robust applicability, the developed probe was successfully used to quantify SO 2 and endogenous ClO - in respectively the HeLa cells and the RAW 264.7 cells, as well as to visualize the dynamic of SO 2 /ClO - in zebrafish. The fluorescent imaging studies and flow cytometry analysis confirmed the burst-and-depletion and meanwhile the oxidative-and-antioxidative effects of intracellular SO 2 under the NaClO induced oxidative stress. Copyright © 2017 Elsevier Ltd. All rights reserved.

Kinetic removal of haloacetonitrile precursors by photo-based advanced oxidation processes (UV/H2O2, UV/O3, and UV/H2O2/O3).

Science.gov (United States)

Srithep, Sirinthip; Phattarapattamawong, Songkeart

2017-06-01

The objective of the study is to evaluate the performance of conventional treatment process (i.e., coagulation, flocculation, sedimentation and sand filtration) on the removals of haloacetonitrile (HAN) precursors. In addition, the removals of HAN precursors by photo-based advanced oxidation processes (Photo-AOPs) (i.e., UV/H 2 O 2 , UV/O 3 , and UV/H 2 O 2 /O 3 ) are investigated. The conventional treatment process was ineffective to remove HAN precursors. Among Photo-AOPs, the UV/H 2 O 2 /O 3 was the most effective process for removing HAN precursors, followed by UV/H 2 O 2 , and UV/O 3 , respectively. For 20min contact time, the UV/H 2 O 2 /O 3 , UV/H 2 O 2 , and UV/O 3 suppressed the HAN formations by 54, 42, and 27% reduction. Increasing ozone doses from 1 to 5 mgL -1 in UV/O 3 systems slightly improved the removals of HAN precursors. Changes in pH (6-8) were unaffected most of processes (i.e., UV, UV/H 2 O 2 , and UV/H 2 O 2 /O 3 ), except for the UV/O 3 system that its efficiency was low in the weak acid condition. The pseudo first-order kinetic constant for removals of dichloroacetonitrile precursors (k' DCANFP ) by the UV/H 2 O 2 /O 3 , UV/H 2 O 2 and standalone UV systems were 1.4-2.8 orders magnitude higher than the UV/O 3 process. The kinetic degradation of dissolved organic nitrogen (DON) tended to be higher than the k' DCANFP value. This study firstly differentiates the kinetic degradation between DON and HAN precursors. Copyright © 2017 Elsevier Ltd. All rights reserved.

hSSB1 (NABP2/OBFC2B) is regulated by oxidative stress

OpenAIRE

Nicolas Paquet; Mark N. Adams; Nicholas W. Ashton; Christine Touma; Roland Gamsjaeger; Liza Cubeddu; Vincent Leong; Sam Beard; Emma Bolderson; Catherine H. Botting; Kenneth J. O’Byrne; Derek J. Richard

2016-01-01

The maintenance of genome stability is an essential cellular process to prevent the development of diseases including cancer. hSSB1 (NABP2/ OBFC2A) is a critical component of the DNA damage response where it participates in the repair of double-strand DNA breaks and in base excision repair of oxidized guanine residues (8-oxoguanine) by aiding the localization of the human 8-oxoguanine glycosylase (hOGG1) to damaged DNA. Here we demonstrate that following oxidative stress, hSSB1 is stabilized ...

Transcriptional regulation of Hb-α and Hb-β through nuclear factor E2-related factor-2 (Nrf2) activation in human vaginal cells: A novel mechanism of cellular adaptability to oxidative stress.

Science.gov (United States)

Saha, Debarchana; Koli, Swanand; Reddy, Kudumula Venkata Rami

2017-06-01

Hemoglobin (Hb), a major protein involved in transport of oxygen (O 2 ), is expressed by erythroid lineages. Until recently, it was not known whether non-erythroid cells express Hb. The objective was to evaluate the expression and functional significance of Hb-α and Hb-β in human primary vaginal epithelial cells (hPVECs) and decipher downstream signaling. RT-PCR, qRT-PCR, flow cytometry, Western blot, immunofluorescence were used to evaluate the expression of Hb-α, Hb-β, and nuclear factor E2-related factor-2(Nrf2) after hydrogen peroxide (H 2 O 2 ) induction. Electrophoretic mobility shift assay (EMSA) and chromatin immunoprecipitation (ChIP) assay were used to determine the binding efficiency of Nrf2 on the Hb-α promoter. Stimulation of hPVECs and human vaginal epithelial cell line, VK2/E6E7 with H 2 O 2 augmented the expression of Hb-α, Hb-β, Nrf2, heme oxygenase-1 (HO-1), and reactive oxygen species (ROS). Treatment of these cells with Nrf2 inhibitor, trigonelline (Trig) inhibited Hb-α and Hb-β expressions. Hb-α and Hb-β overexpression downregulated H 2 O 2 -induced ROS. The presence of Nrf2 binding domain was demonstrated within Hb-α promoter. The results revealed for the first time that Hb-α and Hb-β were induced by oxidative stress through the activation of Nrf2. Overexpression of Hb-α and Hb-β ameliorated H 2 O 2 -induced oxidative stress, indicating one of the possible mechanism(s) to protect hPVECS from oxidative stress. © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

Oxidative stress mediated toxicity of TiO2 nanoparticles after a concentration and time dependent exposure of the aquatic macrophyte Hydrilla verticillata.

Science.gov (United States)

Spengler, Annette; Wanninger, Lena; Pflugmacher, Stephan

2017-09-01

The present study focused on oxidative stress effects in the aquatic macrophyte Hydrilla verticillata after exposure to titanium dioxide nanoparticles (TiO 2 -NPs). Experiments were conducted with different TiO 2 -NPs and concentrations (0.1 mg/L and 10 mg/L) in a time-dependent manner (0 h, 24 h, 48 h, 96 h, 168 h). To assess various levels of the oxidative stress response in H. verticillata, the level of hydrogen peroxide (H 2 O 2 ), the ratio of reduced to oxidized glutathione (GSH/GSSG), and activities of the antioxidative enzymes catalase (CAT) and glutathione reductase (GR) were evaluated. Study results imply oxidative stress effects after TiO 2 -NP exposure as adaptations in plant metabolism became apparent to counteract increased ROS formation. All TiO 2 -NPs caused elevated activities of the enzymes CAT and GR. Moreover, decreased ratios of GSH/GSSG indicated an activation of GSH-dependent pathways counteracting ROS formation. Plants exposed to a bulk-sized control revealed a size-dependent influence on the antioxidative stress response. As H 2 O 2 level increases were solely detected after exposure to 10 mg/L TiO 2 -NPs and nano-exposed plants showed normalization in its antioxidative stress response after 168h of exposure, it can be suggested that macrophytes are able to cope with currently predicted low-level exposures to TiO 2 -NPs. Copyright © 2017 Elsevier B.V. All rights reserved.

Decolorization of methylene blue in layered manganese oxide suspension with H2O2

International Nuclear Information System (INIS)

Zhang Lili; Nie Yulun; Hu Chun; Hu Xuexiang

2011-01-01

Highlights: → Layered birnessite-type manganese oxides exhibited a well-crystallized octahedral layer (OL) structure with β-MnOOH, α-MnOOH and γ-Mn 3 O 4 . → The catalyst was highly effective for the decolorization and degradation of methylene blue in the presence of H 2 O 2 at neutral pH. → The 1 O 2 and O 2 · - were the main reactive oxygen species in the reaction. - Abstract: Layered birnessite-type manganese oxides (Na-OL-1) were prepared via a redox reaction involving MnO 4 - and Mn 2+ under markedly alkaline conditions. According to the XRD analysis, the resulting material exhibited a well-crystallized octahedral layer (OL) structure with several different phases, including β-MnOOH, α-MnOOH and γ-Mn 3 O 4 . The catalyst was highly effective for the decolorization and degradation of methylene blue (MB) in the presence of H 2 O 2 at neutral pH. The tested MB was completely decolorized in Na-OL-1 suspension by the fraction dosing of H 2 O 2 (556.5 mM at the beginning and then 183.8 mM at 40 min). Based on the studies of electron spin resonance and the effect of radical scavengers, the 1 O 2 and O 2 · - were the main reactive oxygen species (ROS) in the reaction. It was found that both oxygen and ROS were generated from the decomposition of H 2 O 2 in Na-OL-1 suspension, wherein the decomposition pathways were proposed. The generation of H 2 O 2 in Na-OL-1 suspension at air atmosphere indicated that the existence of multivalent manganese oxides greatly enhanced the interfacial electron transfer, leading to the high activity of Na-OL-1.

A Salt-Inducible Mn-Catalase (KatB) Protects Cyanobacterium from Oxidative Stress.

Science.gov (United States)

Chakravarty, Dhiman; Banerjee, Manisha; Bihani, Subhash C; Ballal, Anand

2016-02-01

Catalases, enzymes that detoxify H2O2, are widely distributed in all phyla, including cyanobacteria. Unlike the heme-containing catalases, the physiological roles of Mn-catalases remain inadequately characterized. In the cyanobacterium Anabaena, pretreatment of cells with NaCl resulted in unusually enhanced tolerance to oxidative stress. On exposure to H2O2, the NaCl-treated Anabaena showed reduced formation of reactive oxygen species, peroxides, and oxidized proteins than the control cells (i.e. not treated with NaCl) exposed to H2O2. This protective effect correlated well with the substantial increase in production of KatB, a Mn-catalase. Addition of NaCl did not safeguard the katB mutant from H2O2, suggesting that KatB was indeed responsible for detoxifying the externally added H2O2. Moreover, Anabaena deficient in KatB was susceptible to oxidative effects of salinity stress. The katB gene was strongly induced in response to osmotic stress or desiccation. Promoter-gfp analysis showed katB to be expressed only in the vegetative cells but not in heterocysts. Biochemically, KatB was an efficient, robust catalase that remained active in the presence of high concentrations of NaCl. Our findings unravel the role of Mn-catalase in acclimatization to salt/oxidative stress and demonstrate that the oxidative stress resistance of an organism can be enhanced by a simple compound such as NaCl. © 2016 American Society of Plant Biologists. All Rights Reserved.

The performance and decolourization kinetics of O3/H2O2 oxidation of reactive green 19 dye in wastewater

Science.gov (United States)

Sabri, S. N.; Abidin, C. Z. A.; Fahmi; Kow, S. H.; Razali, N. A.

2018-03-01

The degradations characteristic of azo dye Reactive Green 19 (RG19) was investigated using advanced oxidation process (AOPs). It was evaluated based on colour and chemical oxygen demand (COD) removal. The effect of operational parameters such as initial dye concentration, initial dosage of hydrogen peroxide (H2O2), contact time, and pH was also being studied. The samples were treated by ozonation (O3) and peroxone O3/H2O2 process. Advanced oxidation processes (AOPs) involve two stages of oxidation; firstly is the formation of strong oxidant and secondly the reaction of organic contaminants in water. In addition, the term advanced oxidation is referring to the processes in which oxidation of organic contaminants occurs primarily through reactions with hydroxyl radicals. There are several analyses that use to determine the efficiency of the treatment process, which are UV-Vis absorption spectra, COD, Fourier Transform Infrared (FT-IR), and pH. The results demonstrated that the ozone oxidation was efficient in decolourization and good in mineralization, based on the reduction of colour and COD. Additionally, results indicate that H2O2 is able to perform better than ozonation in order to decolourize the dye wastewater with 0.5 mL H2O2/L dye dosage of H2O2 at different initial concentration, initial pH, with contact time.

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.

Rice Bioactive Peptide Binding with TLR4 To Overcome H2O2-Induced Injury in Human Umbilical Vein Endothelial Cells through NF-κB Signaling.

Science.gov (United States)

Liang, Ying; Lin, Qinlu; Huang, Ping; Wang, Yuqian; Li, Jiajia; Zhang, Lin; Cao, Jianzhong

2018-01-17

Reactive oxygen species-induced vessel endothelium injury is crucial in cardiovascular diseases progression. Rice-derived bran bioactive peptides (RBAP) might exert antioxidant effect through unknown mechanisms. Herein, we validated the antioxidant effect and mechanism of RBAP on H 2 O 2 -induced oxidative injury in human umbilical vein endothelial cells (HUVECs). Here, HUVECs were treated with RBAP under H 2 O 2 stimulation; the effects of RBAP on HUVECs oxidative injury were evaluated. H 2 O 2 injury-induced cell morphology changes were ameliorated by RBAP. The effect of H 2 O 2 - on HUVEC apoptosis (percentage of apoptotic cell: 38.00 ± 2.00 in H 2 O 2 group vs 21.07 ± 2.06 in RBAP + H 2 O 2 group, P = 0.0013 compared to H 2 O 2 group), the protein levels of cleaved caspase-3 (relative protein expression: 2.90 ± 0.10 in H 2 O 2 group vs 1.82 ± 0.09 in RBAP + H 2 O 2 group, P < 0.0001 compared to H 2 O 2 group) and p-p65 (relative protein expression: 1.86 ± 0.09 in H 2 O 2 group vs 1.35 ± 0.08 in RBAP + H 2 O 2 group, P < 0.0001 compared to H 2 O 2 group) could be attenuated by RBAP. RBAP exerts its protective function through binding with Toll-like receptor 4 (TLR4). Taken together, RBAP protects HUVECs against H 2 O 2 -induced oxidant injury, which provided the theoretical basis for the molecular mechanism of rice deep processing and exploitation of functional peptides.

Advanced oxidation removal of hypophosphite by O3/H2O2 combined with sequential Fe(II) catalytic process.

Science.gov (United States)

Zhao, Zilong; Dong, Wenyi; Wang, Hongjie; Chen, Guanhan; Wang, Wei; Liu, Zekun; Gao, Yaguang; Zhou, Beili

2017-08-01

Elimination of hypophosphite (HP) was studied as an example of nickel plating effluents treatment by O 3 /H 2 O 2 and sequential Fe(II) catalytic oxidation process. Performance assessment performed with artificial HP solution by varying initial pH and employing various oxidation processes clearly showed that the O 3 /H 2 O 2 ─Fe(II) two-step oxidation process possessed the highest removal efficiency when operating under the same conditions. The effects of O 3 dosing, H 2 O 2 concentration, Fe(II) addition and Fe(II) feeding time on the removal efficiency of HP were further evaluated in terms of apparent kinetic rate constant. Under improved conditions (initial HP concentration of 50 mg L -1 , 75 mg L -1 O 3 , 1 mL L -1 H 2 O 2 , 150 mg L -1 Fe(II) and pH 7.0), standard discharge (<0.5 mg L -1 in China) could be achieved, and the Fe(II) feeding time was found to be the limiting factor for the evolution of apparent kinetic rate constant in the second stage. Characterization studies showed that neutralization process after oxidation treatment favored the improvement of phosphorus removal due to the formation of more metal hydroxides. Moreover, as a comparison with lab-scale Fenton approach, the O 3 /H 2 O 2 ─Fe(II) oxidation process had more competitive advantages with respect to applicable pH range, removal efficiency, sludge production as well as economic costs. Copyright © 2017 Elsevier Ltd. All rights reserved.

Role of cerium oxide nanoparticle-induced autophagy as a safeguard to exogenous H2O2-mediated DNA damage in tobacco BY-2 cells.

Science.gov (United States)

Sadhu, Abhishek; Ghosh, Ilika; Moriyasu, Yuji; Mukherjee, Anita; Bandyopadhyay, Maumita

2018-04-13

The effect of cerium oxide nanoparticle (CeNP) in plants has elicited substantial controversy. While some investigators have reported that CeNP possesses antioxidant properties, others observed CeNP to induce reactive oxygen species (ROS). In spite of considerable research carried out on the effects of CeNP in metazoans, fundamental studies that can unveil its intracellular consequences linking ROS production, autophagy and DNA damage are lacking in plants. To elucidate the impact of CeNP within plant cells, tobacco BY-2 cells were treated with 10, 50 and 250 µg ml-1 CeNP (Ce10, Ce50 and Ce250), for 24 h. Results demonstrated concentration-dependent accumulation of Ca2+ and ROS at all CeNP treatment sets. However, significant DNA damage and alteration in antioxidant defence systems were noted prominently at Ce50 and Ce250. Moreover, Ce50 and Ce250 induced DNA damage, analysed by comet assay and DNA diffusion experiments, complied with the concomitant increase in ROS. Furthermore, to evaluate the antioxidant property of CeNP, treated cells were washed after 24 h (to minimise CeNP interference) and challenged with H2O2 for 3 h. Ce10 did not induce genotoxicity and H2O2 exposure to Ce10-treated cells showed lesser DNA breakage than cells treated with H2O2 only. Interestingly, Ce10 provided better protection over N-acetyl-L-cysteine against exogenous H2O2 in BY-2 cells. CeNP exposure to transgenic BY-2 cells expressing GFP-Atg8 fusion protein exhibited formation of autophagosomes at Ce10. Application of vacuolar protease inhibitor E-64c and fluorescent basic dye acridine orange, further demonstrated accumulation of particulate matters in the vacuole and occurrence of acidic compartments, the autophagolysosomes, respectively. BY-2 cells co-treated with CeNP and autophagy inhibitor 3-methyladenine exhibited increased DNA damage in Ce10 and cell death at all assessed treatment sets. Thus, current results substantiate an alternative autophagy-mediated, antioxidant and

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.

Treatment with a JNK inhibitor increases, whereas treatment with a p38 inhibitor decreases, H2O2-induced calf pulmonary arterial endothelial cell death.

Science.gov (United States)

Park, Woo Hyun

2017-08-01

Oxidative stress induces apoptosis in endothelial cells (ECs). Reactive oxygen species (ROS) promote cell death by regulating the activity of various mitogen-activated protein kinases (MAPKs) in ECs. The present study investigated the effects of MAPK inhibitors on cell survival and glutathione (GSH) levels upon H 2 O 2 treatment in calf pulmonary artery ECs (CPAECs). H 2 O 2 treatment inhibited the growth and induced the death of CPAECs, as well as causing GSH depletion and the loss of mitochondrial membrane potential (MMP). While treatment with the MEK or JNK inhibitor impaired the growth of H 2 O 2 -treated CPAECs, treatment with the p38 inhibitor attenuated this inhibition of growth. Additionally, JNK inhibitor treatment increased the proportion of sub-G 1 phase cells in H 2 O 2 -treated CPAECs and further decreased the MMP. However, treatment with a p38 inhibitor reversed the effects of H 2 O 2 treatment on cell growth and the MMP. Similarly, JNK inhibitor treatment further increased, whereas p38 inhibitor treatment decreased, the proportion of GSH-depleted cells in H 2 O 2 -treated CPAECs. Each of the MAPK inhibitors affected cell survival, and ROS or GSH levels differently in H 2 O 2 -untreated, control CPAECs. The data suggest that the exposure of CPAECs to H 2 O 2 caused the cell growth inhibition and cell death through GSH depletion. Furthermore, JNK inhibitor treatment further enhanced, whereas p38 inhibitors attenuated, these effects. Thus, the results of the present study suggest a specific protective role for the p38 inhibitor, and not the JNK inhibitor, against H 2 O 2 -induced cell growth inhibition and cell death.

Over-expression of Trxo1 increases the viability of tobacco BY-2 cells under H2O2 treatment.

Science.gov (United States)

Ortiz-Espín, Ana; Locato, Vittoria; Camejo, Daymi; Schiermeyer, Andreas; De Gara, Laura; Sevilla, Francisca; Jiménez, Ana

2015-09-01

Reactive oxygen species (ROS), especially hydrogen peroxide, play a critical role in the regulation of plant development and in the induction of plant defence responses during stress adaptation, as well as in plant cell death. The antioxidant system is responsible for controlling ROS levels in these processes but redox homeostasis is also a key factor in plant cell metabolism under normal and stress situations. Thioredoxins (Trxs) are ubiquitous small proteins found in different cell compartments, including mitochondria and nuclei (Trxo1), and are involved in the regulation of target proteins through reduction of disulphide bonds, although their role under oxidative stress has been less well studied. This study describes over-expression of a Trxo1 for the first time, using a cell-culture model subjected to an oxidative treatment provoked by H2O2. Control and over-expressing PsTrxo1 tobacco (Nicotiana tabacum) BY-2 cells were treated with 35 mm H2O2 and the effects were analysed by studying the growth dynamics of the cultures together with oxidative stress parameters, as well as several components of the antioxidant systems involved in the metabolism of H2O2. Analysis of different hallmarks of programmed cell death was also carried out. Over-expression of PsTrxo1 caused significant differences in the response of TBY-2 cells to high concentrations of H2O2, namely higher and maintained viability in over-expressing cells, whilst the control line presented a severe decrease in viability and marked indications of oxidative stress, with generalized cell death after 3 d of treatment. In over-expressing cells, an increase in catalase activity, decreases in H2O2 and nitric oxide contents and maintenance of the glutathione redox state were observed. A decreased content of endogenous H2O2 may be responsible in part for the delayed cell death found in over-expressing cells, in which changes in oxidative parameters and antioxidants were less extended after the oxidative

Comparison of gene expression signatures of diamide, H2O2 and menadione exposed Aspergillus nidulans cultures – linking genome-wide transcriptional changes to cellular physiology

Science.gov (United States)

Pócsi, István; Miskei, Márton; Karányi, Zsolt; Emri, Tamás; Ayoubi, Patricia; Pusztahelyi, Tünde; Balla, György; Prade, Rolf A

2005-01-01

Background In addition to their cytotoxic nature, reactive oxygen species (ROS) are also signal molecules in diverse cellular processes in eukaryotic organisms. Linking genome-wide transcriptional changes to cellular physiology in oxidative stress-exposed Aspergillus nidulans cultures provides the opportunity to estimate the sizes of peroxide (O22-), superoxide (O2•-) and glutathione/glutathione disulphide (GSH/GSSG) redox imbalance responses. Results Genome-wide transcriptional changes triggered by diamide, H2O2 and menadione in A. nidulans vegetative tissues were recorded using DNA microarrays containing 3533 unique PCR-amplified probes. Evaluation of LOESS-normalized data indicated that 2499 gene probes were affected by at least one stress-inducing agent. The stress induced by diamide and H2O2 were pulse-like, with recovery after 1 h exposure time while no recovery was observed with menadione. The distribution of stress-responsive gene probes among major physiological functional categories was approximately the same for each agent. The gene group sizes solely responsive to changes in intracellular O22-, O2•- concentrations or to GSH/GSSG redox imbalance were estimated at 7.7, 32.6 and 13.0 %, respectively. Gene groups responsive to diamide, H2O2 and menadione treatments and gene groups influenced by GSH/GSSG, O22- and O2•- were only partly overlapping with distinct enrichment profiles within functional categories. Changes in the GSH/GSSG redox state influenced expression of genes coding for PBS2 like MAPK kinase homologue, PSK2 kinase homologue, AtfA transcription factor, and many elements of ubiquitin tagging, cell division cycle regulators, translation machinery proteins, defense and stress proteins, transport proteins as well as many enzymes of the primary and secondary metabolisms. Meanwhile, a separate set of genes encoding transport proteins, CpcA and JlbA amino acid starvation-responsive transcription factors, and some elements of sexual development

Intravenous infusion of H2-saline suppresses oxidative stress and elevates antioxidant potential in Thoroughbred horses after racing exercise.

Science.gov (United States)

Yamazaki, Masahiko; Kusano, Kanichi; Ishibashi, Toru; Kiuchi, Masataka; Koyama, Katsuhiro

2015-10-23

Upon intensive, exhaustive exercise, exercise-induced reactive oxygen species may exceed the antioxidant defence threshold, consequently resulting in muscular damage or late-onset chronic inflammation. Recently, the therapeutic antioxidant and anti-inflammatory effects of molecular hydrogen (H2) for human rheumatoid arthritis have been demonstrated. However, it is also important to clarify the effects of administrating H2 in large animals other than humans, as H2 is thought to reach the target organ by passive diffusion upon delivery from the blood flow, indicating that the distance from the administration point to the target is critical. However, data on the effects of H2 on oxidative stress in real-life exhaustive exercise in large animals are currently lacking. We here investigated 13 Thoroughbred horses administered intravenous 2-L saline with or without 0.6-ppm H2 (placebo, N = 6; H2, N = 7) before participating in a high-intensity simulation race. Intravenous H2-saline significantly suppressed oxidative stress immediately, 3 h, and 24 h after the race, although the antioxidant capability was not affected throughout the study. The serum creatine kinase, lactate, and uric acid levels were increased in both groups. Taken together, these results indicate that intravenous H2-saline can significantly and specifically suppress oxidative stress induced after exhaustive racing in Thoroughbred horses.

Generation of H{sub 2} and CO by solar thermochemical splitting of H{sub 2}O and CO{sub 2} by employing metal oxides

Energy Technology Data Exchange (ETDEWEB)

Rao, C.N.R., E-mail: cnrrao@jncasr.ac.in; Dey, Sunita

2016-10-15

Generation of H{sub 2} and CO by splitting H{sub 2}O and CO{sub 2} respectively constitutes an important aspect of the present-day concerns with energy and environment. The solar thermochemical route making use of metal oxides is a viable means of accomplishing these reduction reactions. The method essentially involves reducing a metal oxide by heating and passing H{sub 2}O or CO{sub 2} over the nonstoichiometric oxide to cause reverse oxidation by abstracting oxygen from H{sub 2}O or CO{sub 2}. While ceria, perovskites and other oxides have been investigated for this purpose, recent studies have demonstrated the superior performance of perovskites of the type Ln{sub 1−x}A{sub x}Mn{sub 1−y}M{sub y}O{sub 3} (Ln=rare earth, A=alkaline earth, M=various +2 and +3 metal ions), in the thermochemical generation of H{sub 2} and CO. We present the important results obtained hitherto to point out how the alkaine earth and the Ln ions, specially the radius of the latter, determine the performance of the perovskites. The encouraging results obtained are exemplefied by Y{sub 0.5}Sr{sub 0.5}MnO{sub 3} which releases 483 µmol/g of O{sub 2} at 1673 K and produces 757 µmol/g of CO from CO{sub 2} at 1173 K. The production of H{sub 2} from H{sub 2}O is also quite appreciable. Modification of the B site ion of the perovskite also affects the performance. In addition to perovskites, we present the generation of H{sub 2} based on the Mn{sub 3}O{sub 4}/NaMnO{sub 2} cycle briefly. - Graphical abstract: Ln{sub 0.5}A{sub 0.5}Mn{sub 1−x}M{sub x}O{sub 3} (Ln=lanthanide; A=Ca, Sr; M=Al, Ga, Sc, Mg, Cr, Fe, Co) perovskites are employed for the two step thermochemical splitting of CO{sub 2} and H{sub 2}O for the generation of CO and H{sub 2}. - Highlights: • Perovskite oxides based on Mn are ideal for the two-step thermochemical splitting of CO{sub 2} and H{sub 2}O. • In Ln{sub 1−x}A{sub x}MnO{sub 3} perovskite (Ln=rare earth, A=alkaline earth) both Ln and A ions play major roles

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.

Efficiency of Advanced H2O2/ZnO Oxidation Process in Ceftriaxone Antibiotic Removal from Aqueous Solutions

Directory of Open Access Journals (Sweden)

Maryam Noroozi cholcheh

2017-11-01

Full Text Available A major concern about pharmaceutical pollution is the presence of antibiotics in water resources through their release into sewers where they cause bacterial resistance and enhanced drug-resistance in human-borne pathogens and growing microbial populations in the environment. The objective of this study was to investigate the efficiency of  the advanced H2O2/ZnO oxidation process in removing ceftriaxone from aqueous solutions. For this purpose, an experimental study was conducted in which the SEM, XRD, and TEM techniques were employed to determine the size of Zinc oxide nano-particles. Additionally, the oxidation process parameters of pH (3-11, molar ratio of H2O2/ZnO (1.5-3, initial concentration of ceftriaxone (5–15 mg/L, and contact time (30-90 min were investigated. Teh data thus obntained were subjected top statistical analysis using the SPSS (ANOVA test. XRD results revealeda hexagonal crystal structure for the nano-ZnO. TEM images confirmed the spherical shape of the nanoparticles. Finally, SEM images revealed that the Zn nanoparticles used in this study were less than 30 nanometers in diameter. Based on the results, an optimum pH of 11, a contact time of 90 minutes, and a H2O2/ZnO molar ratio equal to 1.5 were the optimum conditions to achieve a ceftriaxone removal efficiency of 92%. The advance H2O2/ZnO oxidation process may thus be claimed to be highly capable of removing ceftriaxone from aqueous solutions.

[Protective effect of taxifolin on H2O2-induced 
H9C2 cell pyroptosis].

Science.gov (United States)

Ye, Yanqiong; Wang, Xiaoli; Cai, Qian; Zhuang, Jian; Tan, Xiaohua; He, Wei; Zhao, Mingyi

2017-12-28

To explore the effect of taxifolin on H2O2-induced pyroptosis in H9C2 cells and the possible mechanisms.
 Methods: The H9C2 cells was divided into 3 groups: a control group, a hydrogen peroxide (H2O2)group and a taxifolin group. The morphology of H9C2 cells was observed by inverted phase contrast microscope. The mitochondrial membrane potential was measured by JC-1 staining and flow cytometry. The alteration of the level of reactive oxygen species (ROS) was detected by specific mitochondrial probe. The protein levels of cysteinyl aspartate specific proteinase-1 (caspase-1)was determined by Western blot. The mRNA levels of interleukin-18 (IL-18), interleukin-1a (IL-1a), interleukin-1b (IL-1b), absent in melanoma 2 (AIM2), apoptosis-associated apeck-like protein (ASC), nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)and nucleotide-binding oligomerization domain-like receptor family caspase recruitment domain-containing protein 4 (NLRC4) were determined by reverse transcription-polymerase chain reaction (RT-PCR).
 Results: Compared with the control group, the morphology of H9C2 cells obviously changed in the H2O2-treated group, which was guadually improved in the presence of taxifolin. Compared with the control group, the mitochondrial membrane potential was markedly decreased in the H2O2-treated cells, accompanied by the increase ofROS (both PH2O2 group, the mitochondrial membrane potential changes in the taxifolin group was increased while the ROS was decreased, with significant difference (both PH2O2-treated group were significantly increased (all PH2O2-induced H9C2 cell pyroptosis through inhibition of AIM2, NLRP3 and NLRC4 in flammasome.

Endomembrane Ca2+-AtPases play a significant role in virus-induced adaptation to oxidative stress

DEFF Research Database (Denmark)

Shabala, Sergey; Bækgaard, Lone; Shabala, Lana

2011-01-01

Although the role of Ca2+ influx channels in oxidative stress signaling and cross-tolerance in plants is well established, little is known about the role of active Ca2+ efflux systems in this process. In our recent paper,17 we reported Potato Virus X (PVX)-induced acquired resistance to oxidative...... in adaptive responses to oxidative stress by removing excessive Ca2+ from the cytosol, and that their functional expression is significantly altered in PVX-inoculated plants. These findings highlight the crucial role of Ca2+ efflux systems in acquired tolerance to oxidative stress and open up prospects...... stress in Nicotiana benthamiana and showed the critical role of plasma membrane Ca2+/H+ exchangers in this process. The current study continues this research. Using biochemical and electrophysiological approaches, we reveal that both endomembrane P2A and P2B Ca2+-ATPases play significant roles...

Oxidative stress activates the TRPM2-Ca2+-CaMKII-ROS signaling loop to induce cell death in cancer cells.

Science.gov (United States)

Wang, Qian; Huang, Lihong; Yue, Jianbo

2017-06-01

High intracellular levels of reactive oxygen species (ROS) cause oxidative stress that results in numerous pathologies, including cell death. Transient potential receptor melastatin-2 (TRPM2), a Ca 2+ -permeable cation channel, is mainly activated by intracellular adenosine diphosphate ribose (ADPR) in response to oxidative stress. Here we studied the role and mechanisms of TRPM2-mediated Ca 2+ influx on oxidative stress-induced cell death in cancer cells. We found that oxidative stress activated the TRPM2-Ca 2+ -CaMKII cascade to inhibit early autophagy induction, which ultimately led to cell death in TRPM2 expressing cancer cells. On the other hand, TRPM2 knockdown switched cells from cell death to autophagy for survival in response to oxidative stress. Moreover, we found that oxidative stress activated the TRPM2-CaMKII cascade to further induce intracellular ROS production, which led to mitochondria fragmentation and loss of mitochondrial membrane potential. In summary, our data demonstrated that oxidative stress activates the TRPM2-Ca 2+ -CaMKII-ROS signal loop to inhibit autophagy and induce cell death. Copyright © 2016 Elsevier B.V. All rights reserved.

Tyrphostin AG-related compounds attenuate H2O2-induced TRPM2-dependent and -independent cellular responses.

Science.gov (United States)

Yamamoto, Shinichiro; Toda, Takahiro; Yonezawa, Ryo; Negoro, Takaharu; Shimizu, Shunichi

2017-05-01

TRPM2 is a Ca 2+ -permeable channel that is activated by H 2 O 2 . TRPM2-mediated Ca 2+ signaling has been implicated in the aggravation of inflammatory diseases. Therefore, the development of TRPM2 inhibitors to prevent the aggravation of these diseases is expected. We recently reported that some Tyrphostin AG-related compounds inhibited the H 2 O 2 -induced activation of TRPM2 by scavenging the intracellular hydroxyl radical. In the present study, we examined the effects of AG-related compounds on H 2 O 2 -induced cellular responses in human monocytic U937 cells, which functionally express TRPM2. The effects of AG-related compounds on H 2 O 2 -induced changes in intracellular Ca 2+ concentrations, extracellular signal-regulated kinase (ERK) activation, and CXCL8 secretion were assessed using U937 cells. Ca 2+ influxes via TRPM2 in response to H 2 O 2 were blocked by AG-related compounds. AG-related compounds also inhibited the H 2 O 2 -induced activation of ERK, and subsequent secretion of CXCL8 mediated by TRPM2-dependent and -independent mechanisms. Our results show that AG-related compounds inhibit H 2 O 2 -induced CXCL8 secretion following ERK activation, which is mediated by TRPM2-dependent and -independent mechanisms in U937 cells. We previously reported that AG-related compounds blocked H 2 O 2 -induced TRPM2 activation by scavenging the hydroxyl radical. The inhibitory effects of AG-related compounds on TRPM2-independent responses may be due to scavenging of the hydroxyl radical. Copyright © 2017 The Authors. Production and hosting by Elsevier B.V. All rights reserved.

Adsorption of CO, CO2, H2, and H2O on titania surfaces with different oxidation states

International Nuclear Information System (INIS)

Raupp, G.B.; Dumesic, J.A.

1985-01-01

The adsorptive properties of titania surfaces with different oxidation states were proved by temperature-programmed desorption (TPD) of CO, H 2 , CO 2 , and H 2 O. Auger electron spectroscopy and X-ray photoelectron spectroscopy revealed that vacuum annealing an oxidized titanium foil at temperatures from 300 to 800 K was an effective means of systematically varying the average surface oxidation state from Ti 4+ to Ti 2+ . Carbon monoxide weakly adsorbed (desorption energy of 44-49 kJ x mol -1 ) in a carbonyl fashion on coordinatively unsaturated cation sites. Titania surfaces were inert with respect to H 2 adsorption and dissociation. Carbon dioxide adsorbed in a linear molecular fashion. Water adsorbed both molecularly and dissociatively. Results are discussed in terms of the role of titania oxidation state in CO hydrogenation over titania-supported metal catalysts. 74 references, 7 figures

Removal of diethyl phthalate from water solution by adsorption, photo-oxidation, ozonation and advanced oxidation process (UV/H2O2, O3/H2O2 and O3/activated carbon)

International Nuclear Information System (INIS)

Medellin-Castillo, Nahum A.; Ocampo-Pérez, Raúl; Leyva-Ramos, Roberto; Sanchez-Polo, Manuel; Rivera-Utrilla, José; Méndez-Díaz, José D.

2013-01-01

The objective of this work was to compare the effectiveness of conventional technologies (adsorption on activated carbon, AC, and ozonation) and technologies based on advanced oxidation processes, AOPs, (UV/H 2 O 2 , O 3 /AC, O 3 /H 2 O 2 ) to remove phthalates from aqueous solution (ultrapure water, surface water and wastewater). Diethyl phthalate (DEP) was chosen as a model pollutant because of its high water solubility (1080 mg/L at 293 K) and toxicity. The activated carbons showed a high adsorption capacity to adsorb DEP in aqueous solution (up to 858 mg/g), besides the adsorption mechanism of DEP on activated carbon is governed by dispersive interactions between π electrons of its aromatic ring with π electrons of the carbon graphene planes. The photodegration process showed that the pH solution does not significantly affect the degradation kinetics of DEP and the first-order kinetic model satisfactorily fitted the experimental data. It was observed that the rate of decomposition of DEP with the O 3 /H 2 O 2 and O 3 /AC systems is faster than that with only O 3 . The technologies based on AOPs (UV/H 2 O 2 , O 3 /H 2 O 2 , O 3 /AC) significantly improve the degradation of DEP compared to conventional technologies (O 3 , UV). AC adsorption, UV/H 2 O 2 , O 3 /H 2 O 2 , and O 3 /AC showed a high yield to remove DEP; however, the disadvantage of AC adsorption is its much longer time to reach maximum removal. The best system to treat water (ultrapure and natural) polluted with DEP is the O 3 /AC one since it achieved the highest DEP degradation and TOC removal, as well as the lower water toxicity. -- Highlights: ► Activated carbons showed a high adsorption capacity (up to 858 mg/g) to remove DEP. ► The pH solution did not significantly affect the photodegradation kinetics of DEP. ► The O 3 /H 2 O 2 and O 3 /AC systems were more efficient than O 3 to degrade DEP. ► The generation of HO • from O 3 was enhanced by ACs, mainly by those of basic nature. ► O

Density functional study on the heterogeneous oxidation of NO over α-Fe_2O_3 catalyst by H_2O_2: Effect of oxygen vacancy

International Nuclear Information System (INIS)

Song, Zijian; Wang, Ben; Yu, Jie; Ma, Chuan; Zhou, Changsong; Chen, Tao; Yan, Qianqian; Wang, Ke; Sun, Lushi

2017-01-01

Highlights: • NO and H_2O_2 adsorption on perfect and oxygen defect α-Fe_2O_3 (0 0 1) surface were studied by DFT calculations. • H_2O_2 shows high chemical reactivity for its adsorption on oxygen defect α-Fe_2O_3 (0 0 1) surface. • Oxygen vacancy plays an important role of the catalytic oxidation of NO by H_2O_2 over the α-Fe_2O_3 catalyst surfaces. • Mechanism of NO oxidation over α-Fe_2O_3 (0 0 1) surface by H_2O_2 was explained. - Abstract: Catalytic oxidation with H_2O_2 is a promising method for NOx emission control in coal-fired power plants. Hematite-based catalysts are attracting increased attention because of their surface redox reactivity. To elucidate the NO oxidation mechanism on α-Fe_2O_3 surfaces, density functional theory (DFT) calculations were conducted by investigating the adsorption characteristics of nitric oxide (NO) and hydrogen peroxide (H_2O_2) on perfect and oxygen defect α-Fe_2O_3 (0 0 1) surfaces. Results show that NO was molecularly adsorbed on two kinds of surfaces. H_2O_2 adsorption on perfect surface was also in a molecular form; however, H_2O_2 dissociation occurred on oxygen defect α-Fe_2O_3 (0 0 1) surface. The adsorption intensities of the two gas molecules in perfect α-Fe_2O_3 (0 0 1) surface followed the order NO > H_2O_2, and the opposite was true for the oxygen defect α-Fe_2O_3 (0 0 1). Oxygen vacancy remarkably enhanced the adsorption intensities of NO and H_2O_2 and promoted H_2O_2 decomposition on catalyst surface. As an oxidative product of NO, HNO_2 was synthesized when NO and H_2O_2 co-adsorbed on the oxygen defect α-Fe_2O_3 (0 0 1) surface. Analyses of Mulliken population, electron density difference, and partial density of states showed that H_2O_2 decomposition followed the Haber–Weiss mechanism. The trends of equilibrium constants suggested that NO adsorption on α-Fe_2O_3 (0 0 1) surface was more favorable at low than at high temperatures, whereas H_2O_2 adsorption was favorable between 375 and

Degradation mechanism of alachlor during direct ozonation and O(3)/H(2)O(2) advanced oxidation process.

Science.gov (United States)

Qiang, Zhimin; Liu, Chao; Dong, Bingzhi; Zhang, Yalei

2010-01-01

The degradation of alachlor by direct ozonation and advanced oxidation process O(3)/H(2)O(2) was investigated in this study with focus on identification of degradation byproducts. The second-order reaction rate constant between ozone and alachlor was determined to be 2.5+/-0.1M(-1)s(-1) at pH 7.0 and 20 degrees C. Twelve and eight high-molecular-weight byproducts (with the benzene ring intact) from alachlor degradation were identified during direct ozonation and O(3)/H(2)O(2), respectively. The common degradation byproducts included N-(2,6-diethylphenyl)-methyleneamine, 8-ethyl-3,4-dihydro-quinoline, 8-ethyl-quinoline, 1-chloroacetyl-2-hydro-3-ketone-7-acetyl-indole, 2-chloro-2',6'-diacetyl-N-(methoxymethyl)acetanilide, 2-chloro-2'-acetyl-6'-ethyl-N-(methoxymethyl)-acetanilide, and two hydroxylated alachlor isomers. In direct ozonation, four more byproducts were also identified including 1-chloroacetyl-2,3-dihydro-7-ethyl-indole, 2-chloro-2',6'-ethyl-acetanilide, 2-chloro-2',6'-acetyl-acetanilide and 2-chloro-2'-ethyl-6'-acetyl-N-(methoxymethyl)-acetanilide. Degradation of alachlor by O(3) and O(3)/H(2)O(2) also led to the formation of low-molecular-weight byproducts including formic, acetic, propionic, monochloroacetic and oxalic acids as well as chloride ion (only detected in O(3)/H(2)O(2)). Nitrite and nitrate formation was negligible. Alachlor degradation occurred via oxidation of the arylethyl group, N-dealkylation, cyclization and cleavage of benzene ring. After O(3) or O(3)/H(2)O(2) treatment, the toxicity of alachlor solution examined by the Daphnia magna bioassay was slightly reduced. 2009 Elsevier Ltd. All rights reserved.

Isolation and characterization of ScGluD2, a new sugarcane beta-1,3-glucanase D family gene induced by Sporisorium scitamineum, ABA, H2O2, NaCl, and CdCl2 stresses

Directory of Open Access Journals (Sweden)

Yachun Su

2016-09-01

Full Text Available Beta-1,3-glucanases (EC 3.2.1.39, commonly known as pathogenesis-related (PR proteins, play an important role not only in plant defense against fungal pathogens but also in plant physiological and developmental processes. However, only a limited number of sugarcane beta-1,3-glucanase genes have been isolated. In the present study, we identified and characterized a new beta-1,3-glucanase gene ScGluD2 (GenBank Acc No. KF664181 from sugarcane. An X8 domain was present at the C terminal region of ScGluD2, suggesting beta-1,3-glucan-binding function. Phylogenetic analysis showed that the predicted ScGluD2 protein was classified into subfamily D beta-1,3-glucanase. Localization of the ScGluD2 protein in the plasma membrane was determined by tagging it with green fluorescent protein. The expression of ScGluD2 was more up-regulated in sugarcane smut-resistant cultivars in the early stage (1 d or 3 d than in the susceptible ones after being challenged by the smut pathogen, revealing that ScGluD2 may be involved in defense against the invasion of Sporisorium scitamineum. Transient overexpression of ScGluD2 in Nicotiana benthamiana leaves induced a defense response and exhibited antimicrobial action on the tobacco pathogens Pseudomonas solanacearum and Botrytis cinerea, further demonstrating that ScGluD2 was related to the resistance to plant pathogens. However, the transcripts of ScGluD2 partially increased (12 h under NaCl stress, and were steadily up-regulated from 6 h to 24 h upon ABA, H2O2, and CdCl2 treatments, suggesting that ABA may be a signal molecule regulating oxidative stress and play a role in the salt and heavy metal stress-induced stimulation of ScGluD2 transcripts. Taken together, ScGluD2, a novel member of subfamily D beta-1,3-glucanase, was a stress-related gene of sugarcane involved in plant defense against smut pathogen attack and salt and heavy metal stresses.

Catalase and ascorbate peroxidase-representative H2O2-detoxifying heme enzymes in plants.

Science.gov (United States)

Anjum, Naser A; Sharma, Pallavi; Gill, Sarvajeet S; Hasanuzzaman, Mirza; Khan, Ekhlaque A; Kachhap, Kiran; Mohamed, Amal A; Thangavel, Palaniswamy; Devi, Gurumayum Devmanjuri; Vasudhevan, Palanisamy; Sofo, Adriano; Khan, Nafees A; Misra, Amarendra Narayan; Lukatkin, Alexander S; Singh, Harminder Pal; Pereira, Eduarda; Tuteja, Narendra

2016-10-01

Plants have to counteract unavoidable stress-caused anomalies such as oxidative stress to sustain their lives and serve heterotrophic organisms including humans. Among major enzymatic antioxidants, catalase (CAT; EC 1.11.1.6) and ascorbate peroxidase (APX; EC 1.11.1.11) are representative heme enzymes meant for metabolizing stress-provoked reactive oxygen species (ROS; such as H2O2) and controlling their potential impacts on cellular metabolism and functions. CAT mainly occurs in peroxisomes and catalyzes the dismutation reaction without requiring any reductant; whereas, APX has a higher affinity for H2O2 and utilizes ascorbate (AsA) as specific electron donor for the reduction of H2O2 into H2O in organelles including chloroplasts, cytosol, mitochondria, and peroxisomes. Literature is extensive on the glutathione-associated H2O2-metabolizing systems in plants. However, discussion is meager or scattered in the literature available on the biochemical and genomic characterization as well as techniques for the assays of CAT and APX and their modulation in plants under abiotic stresses. This paper aims (a) to introduce oxidative stress-causative factors and highlights their relationship with abiotic stresses in plants; (b) to overview structure, occurrence, and significance of CAT and APX in plants; (c) to summarize the principles of current technologies used to assay CAT and APX in plants; (d) to appraise available literature on the modulation of CAT and APX in plants under major abiotic stresses; and finally, (e) to consider a brief cross-talk on the CAT and APX, and this also highlights the aspects unexplored so far.

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

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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.

The Effect of H2O2 Interference in Chemical Oxygen Demand Removal During Advanced Oxidation Processes

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Afsane Chavoshani

2016-07-01

Full Text Available Hydrogen peroxide (H2O2 is one of the most oxidants in AOPs. By H2O2 dissociation, hydroxyl radical with a standard oxidation potential of 2.7 is produced. It is reported H2O¬ residual in AOPs has been led to interference in chemical oxygen demand (COD test and it is able to hinder biological treatment of waste water. Because of high mixed organic load of solid waste leachate, this study investigated effect of H2O2 interference in COD removal from solid waste leachate. In this study effect of parameters such as pH (3,5,7,12, H2O2 dose (0.01, 0.02, 0.03, 0.04 mol l-1, and time reaction(10,20,30,40,50,60 min evaluated on H2O2 interference in COD removal from solid waste leachate. Optimum pH and concentration were 3 and 0.02 moll-1 respectively. With increasing reaction time, COD removal was increased. The false COD obtained between 0.49mg per 1mg of H2O2. The average of COD removal by H2O2 for 60 min was 6.57%. Also reaction rate of this process was 0.0029 min-1. The presence of H2O2 leads to overestimation of COD values after reaction time because it consumes the oxidation agent. The extent of H2O2 interference in COD analysis was proportional to the remaining H2O2 concentration at the moment of sampling.

Advanced oxidation of a reactive dyebath effluent: comparison of O3, H2O2/UV-C and TiO2/UV-A processes.

Science.gov (United States)

Alaton, Idil Arslan; Balcioglu, Isil Akmehmet; Bahnemann, Detlef W

2002-03-01

In the present study the treatment efficiency of different AOPs (O3/OH- H2O2/UV-C and TiO2/UV-A) were compared for the oxidation of simulated reactive dyebath effluent containing a mixture of monochlorotriazine type reactive dyes and various dye auxiliary chemicals at typical concentrations encountered in exhausted reactive dyebath liquors. A525 (color), UV280 (aromaticity) and TOC removal rates were assessed to screen the most appropriate oxidative process in terms of reactive dyebath effluent treatment. Special emphasis was laid on the effect of reaction pH and applied oxidant (O3, H2O2) dose on the observed reaction kinetics. It was established that the investigated AOPs were negatively affected by the Na2CO3 content (= 867 mg/L) which is always present at high concentrations in dychouse effluents since it is applied as a pH buffer and dye fixation agent during the reactive dyeing process. The ozonation reaction exhibited almost instantaneous decolorization kinetics and a reasonable TOC reduction rate. It appeared to be stable under the investigated advanced oxidation conditions and outranked the other studied AOPs based on the above mentioned criteria. Besides, the electrical energy requirements based on the EE/O parameter (the electrical energy required per order of pollutant removal in 1 m3 wastewater) was calculated for the homogenous AOPs in terms of decolorization kinetics. In view of the electrical energy efficiency, ozonation and H2O2/UV-C oxidation at the selected treatment conditions appear to be promising candidates for full-scale dyehouse effluent decolorization.

Antioxidative potential of Duranta repens (linn.) fruits against H 2 O 2 ...

African Journals Online (AJOL)

The effects of Duranta repens fruits were investigated on H2O2 induced oxidative cell death to evaluate its antioxidative potential in vitro. HEK293T cells were treated with different concentrations [0-1000 ìg/ ml] of ethanol extract (E-Ex) and methanol extract (M-Ex) of D. repens for 24h, and then treated with 100 ìM H2O2 for ...

Oxidative stress induces caveolin 1 degradation and impairs caveolae functions in skeletal muscle cells.

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Alexis Mougeolle

Full Text Available Increased level of oxidative stress, a major actor of cellular aging, impairs the regenerative capacity of skeletal muscle and leads to the reduction in the number and size of muscle fibers causing sarcopenia. Caveolin 1 is the major component of caveolae, small membrane invaginations involved in signaling and endocytic trafficking. Their role has recently expanded to mechanosensing and to the regulation of oxidative stress-induced pathways. Here, we increased the amount of reactive oxidative species in myoblasts by addition of hydrogen peroxide (H2O2 at non-toxic concentrations. The expression level of caveolin 1 was significantly decreased as early as 10 min after 500 μM H2O2 treatment. This reduction was not observed in the presence of a proteasome inhibitor, suggesting that caveolin 1 was rapidly degraded by the proteasome. In spite of caveolin 1 decrease, caveolae were still able to assemble at the plasma membrane. Their functions however were significantly perturbed by oxidative stress. Endocytosis of a ceramide analog monitored by flow cytometry was significantly diminished after H2O2 treatment, indicating that oxidative stress impaired its selective internalization via caveolae. The contribution of caveolae to the plasma membrane reservoir has been monitored after osmotic cell swelling. H2O2 treatment increased membrane fragility revealing that treated cells were more sensitive to an acute mechanical stress. Altogether, our results indicate that H2O2 decreased caveolin 1 expression and impaired caveolae functions. These data give new insights on age-related deficiencies in skeletal muscle.

CuO reduction induced formation of CuO/Cu2O hybrid oxides

Science.gov (United States)

Yuan, Lu; Yin, Qiyue; Wang, Yiqian; Zhou, Guangwen

2013-12-01

Reduction of CuO nanowires results in the formation of a unique hierarchical hybrid nanostructure, in which the parent oxide phase (CuO) works as the skeleton while the lower oxide (Cu2O) resulting from the reduction reaction forms as partially embedded nanoparticles that decorate the skeleton of the parent oxide. Using in situ transmission electron microscopy observations of the reduction process of CuO nanowires, we demonstrate that the formation of such a hierarchical hybrid oxide structure is induced by topotactic nucleation and growth of Cu2O islands on the parent CuO nanowires.

System and method to control h2o2 level in advanced oxidation processes

DEFF Research Database (Denmark)

2016-01-01

The present invention relates to a bio-electrochemical system (BES) and a method of in-situ production and removal of H2O2 using such a bio-electrochemical system (BES). Further, the invention relates to a method for in-situ control of H2O2 content in an aqueous system of advanced oxidation...

Roles of free radicals in NO oxidation by Fenton system and the enhancement on NO oxidation and H2O2 utilization efficiency.

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Zhao, Haiqian; Dong, Ming; Wang, Zhonghua; Wang, Huaiyuan; Qi, Hanbing

2018-06-20

Low H 2 O 2 utilization efficiency is the main problem when Fenton system was used to oxidize NO in flue gas. To understand the behavior of the free radicals during NO oxidation process in Fenton system is crucial to solving this problem. The oxidation capacity of ·OH and HO 2 · on NO in Fenton system was compared and the useless consumption path of ·OH and HO 2 · that caused the low utilization efficiency of H 2 O 2 were studied. A method to enhance the oxidation ability and H 2 O 2 utilization efficiency by adding reducing additives in Fenton system was proposed. The results showed that both of ·OH and HO 2 · were active substances that oxidize NO. However, the oxidation ability of ·OH radicals was stronger. The vast majority of ·OH and HO 2 · was consumed by rapid reaction ·OH+HO 2 ·→H 2 O+O 2 , which was the primary reason for the low utilization efficiency of H 2 O 2 in Fenton system. Hydroxylamine hydrochloride and ascorbic acid could accelerate the conversion of Fe 3+ to Fe 2+ , thereby increase the generation rate of ·OH and decrease the generation rate of HO 2 ·. As a result, the oxidation ability and H 2 O 2 utilization efficiency were enhanced.

JNK and NADPH Oxidase Involved in Fluoride-Induced Oxidative Stress in BV-2 Microglia Cells

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Yan, Ling; Liu, Shengnan; Wang, Chen; Wang, Fei; Song, Yingli; Yan, Nan; Xi, Shuhua; Liu, Ziyou; Sun, Guifan

2013-01-01

Excessive fluoride may cause central nervous system (CNS) dysfunction, and oxidative stress is a recognized mode of action of fluoride toxicity. In CNS, activated microglial cells can release more reactive oxygen species (ROS), and NADPH oxidase (NOX) is the major enzyme for the production of extracellular superoxide in microglia. ROS have been characterized as an important secondary messenger and modulator for various mammalian intracellular signaling pathways, including the MAPK pathways. In this study we examined ROS production and TNF-α, IL-1β inflammatory cytokines releasing, and the expression of MAPKs in BV-2 microglia cells treated with fluoride. We found that fluoride increased JNK phosphorylation level of BV-2 cells and pretreatment with JNK inhibitor SP600125 markedly reduced the levels of intracellular O2 ·− and NO. NOX inhibitor apocynin and iNOS inhibitor SMT dramatically decreased NaF-induced ROS and NO generations, respectively. Antioxidant melatonin (MEL) resulted in a reduction in JNK phosphorylation in fluoride-stimulated BV-2 microglia. The results confirmed that NOX and iNOS played an important role in fluoride inducing oxidative stress and NO production and JNK took part in the oxidative stress induced by fluoride and meanwhile also could be activated by ROS in fluoride-treated BV-2 cells. PMID:24072958

Cupriavidus pinatubonensis AEO106 deals with copper-induced oxidative stress before engaging in biodegradation of the herbicide 4-chloro-2-methylphenoxyacetic acid

DEFF Research Database (Denmark)

Svenningsen, Nanna Bygvraa; Damgaard, Mette; Rasmussen, Maria Katrine

2017-01-01

to Cu leads to accumulation of intracellular reactive oxygen species (ROS) in some bacteria, but it is not known how Cu-derived ROS and an ensuing oxidative stress affect the degradation of PA herbicides. Based on the previously proposed paradigm that bacteria deal with environmental stress before...... that it is involved in the oxidative stress response in C. pinatubonensis. The increased ROS accumulation and increased expression of the oxidative stress defense coincided with a delay in the catabolic performance, since both expression of the catabolic tfdA gene and MCPA mineralization were delayed compared...... increased accumulation of ROS measured by the oxidant sensing probe 2,7-dichlorodihydrofluorescein diacetate and flow cytometry, and resulted in upregulation of a gene encoding a protein belong to the Ohr/OsmC protein family. The ohr/osmC gene was also highly induced by H2O2 exposure suggesting...

Sequencing treatment of industrial wastewater with ultraviolet/H2O2 advanced oxidation and moving bed bioreactor

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Mohammad Mehdi Mehrabani Ardekani

2015-01-01

Full Text Available Aims: The main purpose of this study was to determine the efficiency of a sequencing treatment including ultraviolet (UV/H 2 O 2 oxidation followed by a moving bed bioreactor (MBBR. Materials and Methods: Effect of solution pH, reaction time, and H 2 O 2 concentration were investigated for an industrial wastewater sample. The effluent of the advanced oxidation processes unit was introduced to the MBBR operated for three hydraulic retention times of 4, 8, and 12 h. Results: The optimum condition for industrial wastewater treatment via advanced oxidation was solution pH: 7, H 2 O 2 dose: 1000 mg/L and 90 min reaction time. These conditions led to 74.68% chemical oxygen demand (COD removal and 66.15% biochemical oxygen demand (BOD 5 removal from presedimentation step effluent that initially had COD and BOD 5 contents of 4,400 and 1,950 mg/L, respectively. Conclusion: Combination of UV/H 2 O 2 advanced oxidation with MBBR could result in effluents that meet water quality standards for discharge to receiving waters.

SvO(2)-guided resuscitation for experimental septic shock: effects of fluid infusion and dobutamine on hemodynamics, inflammatory response, and cardiovascular oxidative stress.

Science.gov (United States)

Rosário, André Loureiro; Park, Marcelo; Brunialti, Milena Karina; Mendes, Marialice; Rapozo, Marjorie; Fernandes, Denise; Salomão, Reinaldo; Laurindo, Francisco Rafael; Schettino, Guilherme Paula; Azevedo, Luciano Cesar P

2011-12-01

The pathogenetic mechanisms associated to the beneficial effects of mixed venous oxygen saturation (SvO(2))-guided resuscitation during sepsis are unclear. Our purpose was to evaluate the effects of an algorithm of SvO(2)-driven resuscitation including fluids, norepinephrine and dobutamine on hemodynamics, inflammatory response, and cardiovascular oxidative stress during a clinically resembling experimental model of septic shock. Eighteen anesthetized and catheterized pigs (35-45 kg) were submitted to peritonitis by fecal inoculation (0.75 g/kg). After hypotension, antibiotics were administered, and the animals were randomized to two groups: control (n = 9), with hemodynamic support aiming central venous pressure 8 to 12 mmHg, urinary output 0.5 mL/kg per hour, and mean arterial pressure greater than 65 mmHg; and SvO(2) (n = 9), with the goals above, plus SvO(2) greater than 65%. The interventions lasted 12 h, and lactated Ringer's and norepinephrine (both groups) and dobutamine (SvO(2) group) were administered. Inflammatory response was evaluated by plasma concentration of cytokines, neutrophil CD14 expression, oxidant generation, and apoptosis. Oxidative stress was evaluated by plasma and myocardial nitrate concentrations, myocardial and vascular NADP(H) oxidase activity, myocardial glutathione content, and nitrotyrosine expression. Mixed venous oxygen saturation-driven resuscitation was associated with improved systolic index, oxygen delivery, and diuresis. Sepsis induced in both groups a significant increase on IL-6 concentrations and plasma nitrate concentrations and a persistent decrease in neutrophil CD14 expression. Apoptosis rate and neutrophil oxidant generation were not different between groups. Treatment strategies did not significantly modify oxidative stress parameters. Thus, an approach aiming SvO(2) during sepsis improves hemodynamics, without any significant effect on inflammatory response and oxidative stress. The beneficial effects associated

Nrf2 Inhibits Periodontal Ligament Stem Cell Apoptosis under Excessive Oxidative Stress

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Yanli Liu

2017-05-01

Full Text Available The present study aimed to analyze novel mechanisms underlying Nrf2-mediated anti-apoptosis in periodontal ligament stem cells (PDLSCs in the periodontitis oxidative microenvironment. We created an oxidative stress model with H2O2-treated PDLSCs. We used real-time PCR, Western blotting, TUNEL staining, fluorogenic assay and transfer genetics to confirm the degree of oxidative stress and apoptosis as well as the function of nuclear factor-erythroid 2-related factor 2 (Nrf2. We demonstrated that with upregulated levels of reactive oxygen species (ROS and malondialdehyde (MDA, the effect of oxidative stress was obvious under H2O2 treatment. Oxidative molecules were altered after the H2O2 exposure, whereby the signaling of Nrf2 was activated with an increase in its downstream effectors, heme oxygenase-1 (HO-1, NAD(PH:quinone oxidoreductase 1 (NQO1 and γ-glutamyl cysteine synthetase (γ-GCS. Additionally, the apoptosis levels gradually increased with oxidative stress by the upregulation of caspase-9, caspase-3, Bax and c-Fos levels in addition to the downregulation of Bcl-2. However, there was no alterations in levels of caspase-8. The enhanced antioxidant effect could not mitigate the occurrence of apoptosis. Furthermore, Nrf2 overexpression effectively improved the anti-oxidative levels and increased cell proliferation. At the same time, overexpression effectively restrained TUNEL staining and decreased the molecular levels of caspase-9, caspase-3, Bax and c-Fos, but not that of caspase-8. In contrast, silencing the expression of Nrf2 levels had the opposite effect. Collectively, Nrf2 alleviates PDLSCs via its effects on regulating oxidative stress and anti-intrinsic apoptosis by the activation of oxidative enzymes.