The Protective Role of Resveratrol in the Sodium Arsenite-Induced Oxidative Damage via Modulation of Intracellular GSH Homeostasis

Chen, Chengzhi; Jiang, Xuejun; Hu, Yanan; Zhang, Zunzhen

doi:10.1007/s12011-013-9757-x

Cited by 32 publications

(18 citation statements)

References 31 publications

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“…In general, cytoprotection was observed with several antioxidants [12,15,22,26], including AA alone [22,29,33,58] or combined with vitamin E [22,27,28,34], thereby providing the rational for supplementing antioxidants, AA in particular, to individuals environmentally or occupationally exposed to arsenic.…”

Section: Discussionmentioning

confidence: 99%

U937 cell apoptosis induced by arsenite is prevented by low concentrations of mitochondrial ascorbic acid with hardly any effect mediated by the cytosolic fraction of the vitamin

et al. 2015

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Arsenite directly triggers cytochrome c and Smac/DIABLO release in mitochondria isolated from U937 cells. These effects were not observed in mitochondria pre-exposed for 15 min to 10 µM L-ascorbic acid (AA). In other experiments, intact cells treated for 24-72 h with arsenite were found to die by apoptosis through a mechanism involving mitochondrial permeability transition. Pre-exposure (15 min) to low micromolar concentrations of AA and dehydroascorbic acid (DHA), resulting in identical cytosolic levels of the vitamin, had a diverse impact on cell survival, as cytoprotection was only observed after treatment with AA. Also the mitochondrial accumulation of the vitamin was restricted to AA exposure. An additional indication linking cytoprotection to the mitochondrial fraction of the vitamin was obtained in experiments measuring susceptibility to arsenite in parallel with loss of mitochondrial and cytosolic AA at different times after vitamin exposure. Finally, we took advantage of our recent findings that DHA potently inhibits AA transport to demonstrate that DHA abolishes all the protective effects of AA, under the same conditions in which the mitochondrial accumulation of the vitamin is prevented without affecting the overall cellular accumulation of the vitamin.

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Section: Discussionmentioning

confidence: 99%

U937 cell apoptosis induced by arsenite is prevented by low concentrations of mitochondrial ascorbic acid with hardly any effect mediated by the cytosolic fraction of the vitamin

et al. 2015

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“…At a lower concentration, it protected human epithelial cells against SBs and MN induced by sodium arsenite [88], and rat astrocytes against SBs caused by ethanol [91]. However, a low dose enhanced the frequency of γ-H2AX foci after ionising irradiation of prostate epithelial cells [90].…”

Section: Isolated Phytochemicalsmentioning

confidence: 99%

Polyphenols and DNA Damage: A Mixed Blessing

2016

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Polyphenols are a very broad group of chemicals, widely distributed in plant foods, and endowed with antioxidant activity by virtue of their numerous phenol groups. They are widely studied as putative cancer-protective agents, potentially contributing to the cancer preventive properties of fruits and vegetables. We review recent publications relating to human trials, animal experiments and cell culture, grouping them according to whether polyphenols are investigated in whole foods and drinks, in plant extracts, or as individual compounds. A variety of assays are in use to study genetic damage endpoints. Human trials, of which there are rather few, tend to show decreases in endogenous DNA damage and protection against DNA damage induced ex vivo in blood cells. Most animal experiments have investigated the effects of polyphenols (often at high doses) in combination with known DNA-damaging agents, and generally they show protection. High concentrations can themselves induce DNA damage, as demonstrated in numerous cell culture experiments; low concentrations, on the other hand, tend to decrease DNA damage.

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“…This may be associated with its potent antioxidant function through scavenging of ROS in cells [Aggarwal et al, ; Bishayee, ]. Our previous studies showed that resveratrol relieved oxidative damage and cell death induced by sodium arsenite in both human bronchial epithelial (HBE) cells [Chen et al, ] and lung adenocarcinoma epithelial (A549) cells [Chen et al, ]. This suggests that resveratrol protects normal cells against the adverse effects of arsenite by decreasing production of ROS and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol protects against arsenic trioxide‐induced oxidative damage through maintenance of glutathione homeostasis and inhibition of apoptotic progression

Chen

Jiang

Lai

et al. 2014

Environ and Mol Mutagen

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Arsenic trioxide (As2O3) is commonly used to treat acute promyelocytic leukemia and solid tumors. However, the clinical application of the agent is limited by its cyto- and genotoxic effects on normal cells. Thus, relief of As2O3 toxicity in normal cells is essentially necessary for improvement of As2O3-mediated chemotherapy. In this study, we have identified a series of protective effects of resveratrol against As2O3-induced oxidative damage in normal human bronchial epithelial (HBE) cells. We showed that treatment of HBE cells with resveratrol significantly reduced cellular levels of DNA damage, chromosomal breakage and apoptosis induced by As2O3. The effect of resveratrol against DNA damage was associated with a decreased level of reactive oxygen species and lipid peroxidation in cells treated by As2O3, suggesting that resveratrol protects against As2O3 toxicity via a cellular anti-oxidative stress pathway. Further analysis of the roles of resveratrol demonstrated that it modulated biosynthesis, recycling and consumption of glutathione (GSH), thereby promoting GSH homeostasis in HBE cells treated by As2O3. This was further supported by results showing that resveratrol prevented an increase in the activities and levels of caspases, Fas, Fas-L and cytochrome c proteins induced by As2O3. Our study indicates that resveratrol relieves As2O3-induced oxidative damage in normal human lung cells via maintenance of GSH homeostasis and suppression of apoptosis.

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The Protective Role of Resveratrol in the Sodium Arsenite-Induced Oxidative Damage via Modulation of Intracellular GSH Homeostasis

Cited by 32 publications

References 31 publications

U937 cell apoptosis induced by arsenite is prevented by low concentrations of mitochondrial ascorbic acid with hardly any effect mediated by the cytosolic fraction of the vitamin

U937 cell apoptosis induced by arsenite is prevented by low concentrations of mitochondrial ascorbic acid with hardly any effect mediated by the cytosolic fraction of the vitamin

Polyphenols and DNA Damage: A Mixed Blessing

Resveratrol protects against arsenic trioxide‐induced oxidative damage through maintenance of glutathione homeostasis and inhibition of apoptotic progression

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