BISPHENOL A INDUCES HEPATOTOXICITY AND NEPHROTOXICITY THROUGHOXIDATIVE STRESS IN RAT MODEL

摘要

Bisphenol A may cause toxic effects on mammalian cells upon exposure. This study investigated the ability of bisphenol A to cause hepatotoxicity and nephrotoxicity via the aberration in the expression of apoptotic genes and oxidative stress in the liver and kidney. Four groups of male wistar rats were daily orally administered bisphenol A at a dose of 0.1, 1, 10 and 50 mg/kg/day for four weeks. The fifth group was given water with vehicle. The weights, clinical signs of toxicity were assessed and the effect of bisphenol A on the activity of apoptotsis genes was investigated by real time PCR. The final body weights in the 0.1 mg group showed a significant decrease compared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase, glutathione-S-transferase, and glutathione reductase and catalase activity were found in the 50 mg bisphenol A group compared to control groups. High dose of BPA significantly increased the biochemical levels of ALT, ALP and total bilirubin. The