Abstract
Abstract Arsenic is a naturally occurring element that is widely distributed in nature, air, water and soil. A well-known toxic and carcinogenic agent, arsenic has been associated with various human malignancies, including skin, lung, liver, kidney and bladder cancers. It has been shown to induce apoptosis in a variety of malignant cell lines, but the precise mechanisms involved in arsenic toxicity and carcinogenicity are not well elucidated. In this study, we used hepatocellular carcinoma (HepG2) cells as a model to determine whether DNA damage and phosphatidylserine externalization are involved in arsenic trioxide (ATO) toxicity. The MTT, single cell gel electrophoresis and annexin-V assays were used to assess cell viability, DNA damage and apoptosis, respectively. The results of the MTT assay demonstrated that ATO significantly reduced the viability of HepG2 cells in a dose-dependent fashion, showing a LD50 value of about 8.5 μg/mL, upon 24 hours of exposure. Data generated from the comet assay showed a significant time and dose-dependent increase in DNA damage, with respect to comet tail-length, tail arm and tail moment, as a result of ATO exposure. In regard to annexin V assay experiment, we observed an increase in annexin V positive cells undergoing early apoptosis in ATO-treated cells compared to the control, upon 2 hr of exposure. However, there was not a detection of annnexin V positive cells in ATO-treated cells compared to the control at 24 hr exposure. Based on the 24 hr cytotoxic effect of ATO to HepG2 cells, further studies are needed to elucidate the apoptotic potential of ATO to HepG2 cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 4379.
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