Abstract
Bisphenol-A (BP-A) is known to be toxic to mammalian cells. The present study investigated the ability of bisphenol-A to cause nephrotoxicity via aberration in the expression of apoptotic genes and oxidative stress in male rats kidney. Four groups of male Wistar rats were orally administered bisphenol-A at a dose of 0.1, 1, 10 and 50 mg kg(-1) day(-1) for 4 weeks. The fifth group was given water with vehicle. Significant increase in blood urea nitrogen and creatinine levels was observed in the group administered 50 mg kg(-1) day(-1) as compared to other groups and control. CAT activity increased insignificantly with increasing cumulative doses (10.5 +/- 0.09, 11.1 +/- 0.46, 12.6 +/- 0.34, 16.9 +/- 0.06) as compared to control (10.5 +/- 0.12). Group exposed to 50 mg BP-A (2.27 +/- 0.03*) showed significant reduction in GSH activity. Sax (1.7 +/- 0.02*) and Bad (2.1 +/- 0.01*) genes expression levels were suppressed in the group exposed to 50 mg BP-A. BclX gene expression was notaffected by BPA in all groups Bc12 gene expression was significantly up-regulated in group exposed to 50 mg BP-A(4.8 +/- 002*) as compared to control. The study showed that bisphenol-A induced nephrotoxicity through oxidative stress and by altering the apoptotic pathway involved.