Biological Trace Element Research

, Volume 155, Issue 1, pp 119–131 | Cite as

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

  • Chengzhi Chen
  • Xuejun Jiang
  • Yanan Hu
  • ZunZhen ZhangEmail author


Sodium arsenite (NaAsO2) is a well-established environmental carcinogen that has been found to cause various human malignant tumors. Thus, how to prevent the deleterious effects caused by NaAsO2 has received widely concerns. Resveratrol (3,4′,5-trihydroxystilbene), a polyphenol found in numerous plant species, has recently been known as a natural and powerful antioxidant. However, whether resveratrol could attenuate the toxicity of NaAsO2 and its detailed mechanisms have not been reported. In this study, the protective effects of resveratrol against NaAsO2-induced oxidative and genetic damage as well as apoptosis were evaluated for the first time. We demonstrated that cotreatment of human bronchial epithelial cell with 5 μM resveratrol for 24 h effectively reduced the levels of 30 μM NaAsO2-induced reactive oxygen species, chromosomal and DNA damage, and cell apoptosis. Revseratrol was also showed to significantly elevate the concentration of glutathione (GSH) and the activities of its relevant enzymes as compared with NaAsO2 alone, indicating that resveratrol ameliorates the toxicity of NaAsO2 by modulating the process of GSH biosynthesis, recycling and utilization. Our findings further suggest that GSH homeostasis represents one of the detoxification mechanisms responding to NaAsO2 exposure, and resveratrol plays a protective role in the regulation of oxidative and genetic damage as well as apoptosis through the modulation of GSH homeostasis.


Protective role of resveratrol in NaAsO2‐induced oxidative damage


Sodium arsenite Resveratrol Oxidative damage GSH homeostasis 





2′7′-Dichlorofluorescin diacetate


γ-Glutamylcysteine synthetase


Catalytic subunit of γ-glutamylcysteine synthetase


Modifier subunit of γ-glutamylcysteine synthetase




Glutathione peroxidase


Glutathione reductase


Glutathione disulfide


Propidium iodide


Reactive oxygen species


Sodium arsenite



This work was supported by National Natural Science Foundation of China (grant number 81172632). The authors thank Prof. Ping Zhang, state key laboratory of oral diseases, West China Hospital of Stomatology, Sichuan University, for his helpful assistance on the manipulation of flow cytometry and the analysis of the original data in apoptotic assay.

Conflicts of Interest Statement

We all authors declare no potential conflict of interest relevant to this article.


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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Chengzhi Chen
    • 1
  • Xuejun Jiang
    • 1
  • Yanan Hu
    • 1
  • ZunZhen Zhang
    • 1
    Email author
  1. 1.Department of Environmental Health, West China School of Public HealthSichuan UniversityChengduPeople’s Republic of China

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