Cytotoxicity and oxidative stress in human liver carcinoma cells exposed to arsenic trioxide (HepG(2)).

摘要: Arsenic is a trace element that occurs naturally in the earth’s crust. It has been found to be major contaminant groundwater supply several countries of world. Whether ingested or inhaled, arsenic induces both systemic (skin disorders, cardiovascular diseases, anemia, peripheral neuropathy, liver and kidney damage) carcinogenic (skin, lung, bladder neoplasms) effects. However, its molecular mechanisms toxicity are not completely understood. In this research, we used HepG2 cells as model study cytotoxicity oxidative stress associated with exposure trioxide. We hypothesized plays role trioxide induced cytotoxicity. To test hypothesis, performed MTT [3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] assay trypan blue exclusion for cell viability thiobarbituric acid lipid peroxidation. Data obtained from indicated significantly reduced cells, showing LD50 value about 23 μg/mL upon 24 h exposure, indicating dose-dependent response. Similar trend was test. generated showed significant increase (p ≤ 0.05) MDA levels trioxide-treated compared control cells. treatment increased cellular content reactive oxygen species (ROS), evidenced by peroxidation by-products. Taken together, these results indicate cytotoxic This mediated stress, biomarker injury.