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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^sup -1^ day^sup -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^sup -1^ day^sup -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. Bax (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 not affected by BPA in all groups. Bcl2 gene expression was significantly up-regulated in group exposed to 50 mg BP-A (4.8 ±0.02*) as compared to control. The study showed that bisphenol-A induced nephrotoxicity through oxidative stress and by altering the apoptotic pathway involved.
