Abstract 4380: Cadmium-induced toxicity in human liver carcinoma (HepG2) cells: Involvement of oxidative stress, phosphatidylserine externalization, and nucleosomal DNA fragmentation

Abstract

Abstract Human liver carcinoma (HepG2) cells were used as a test model to evaluate the in vitro cytotoxicity of cadmium and to determine whether oxidative stress plays a key role in cadmium induced apoptosis. To achieve this goal, we performed the MTT assay to measure cell viability and lipid peroxidation to determine the level of oxidative cell/tissue damage. The annexin V assay and DNA fragmentation analysis were performed for early and late apoptosis, respectively. The results of MTT assay indicated that cadmium chloride induces toxicity to HepG2 cells in a dose-dependent manner, showing a 24 h-LD50 of 3.6 µg/mL. We detected a significant increase in lipid peroxidation (malondialdehyde) concentrations in cadmium chloride-treated HepG2 cells compared to the control. Similarly, a strong dose-response relationship (p < 0.05) was obtained in connection with cadmium chloride-induced apoptosis. Cadmium chloride-induced apoptosis was characterized by a significant increase in the percentage of annexin-V positive cells (apoptotic cells), as well by the occurrence of nucleosomal DNA fragmentation. In summary, this study indicated cadmium chloride is highly cytotoxic to HepG2 cells. This cytotoxic effect may be mediated at least in part through oxidative cell/tissue damage, phosphatidylserine externalization and occurrence of nucleosomal DNA fragmentation. 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 4380.