Abstract
Abstract Recent studies in our laboratory indicated that oxidative stress plays a key role in arsenic trioxide (ATO)-induced cytotoxicity in human cancer cells. In the present investigation, we used human hepatocellular carcinoma (HepG2) cells as a model to determine whether arsenic induced DNA damage is mediated through oxidative stress. To achieve this goal, oxidative stress biomarkers were measured by lipid peroxidation, glutathione peroxidase, and catalase assays, respectively. The degree of DNA damage was estimated by the means of comet assay. The results of the lipid peroxidation showed a significant increase (p <0.05) of malondialdehyde (MDA) levels with increasing ATO concentrations. Results from the glutathione peroxidase and catalase assays showed a gradual decrease in antioxidant enzyme activity in ATO-treated cells as compared the control. In regard to the comet assay, a significant increase (p < 0.05) in comet tail-length and percentages of DNA cleavage were observed in ATO-treated cells using the comet assay. Taken together, our research demonstrated that oxidative stress modulates ATO mediated DNA damage in HepG2 cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4209. doi:10.1158/1538-7445.AM2011-4209
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