Nephrotoxicity of Bisphenol A (BPA) -An Updated Review

Bisphenol A (BPA), the highest volume chemical produced in the whole world is widely used in the production of polycarbonate plastics and epoxy resins. Polycarbonate plastics are used especially in the manufacture of consumer products. The exposure of BPA to humans occurs through food contamination from polycarbonate bottles and food and beverage cans. Dust is also a contributor to the total daily exposure of BPA. Thus, BPA has a high potential for human consumption. The U.S. Food and Drug Administration (FDA) recently announced concern about the safety of BPA and the need for more research data. This article reviews toxicity of BPA in general and kidney in particular using clinical and experimental literature. BPA is toxic to aquatic organisms, animals and humans. BPA is cytotoxic and mutagenic and exerts various adverse effects on immune, endocrine, reproductive, developmental and nervous systems in animals and human and exhibits toxicity by all routes of exposure. Metabolism of BPA is much more rapid in humans than in rodents. BPA increases estrogen metabolism in the kidney and upregulates cytochrome p-450 aromatase activity by means of steroidogenesis. BPA acts as biomarker for renal disease and exhibits nephrotoxicity. BPA toxicity with reference to human exposure level and also carcinogenicity are lacking. While focusing on kidney, this review suggests that further research is required to evaluate the molecular mechanism of BPA induced nephrotoxicity. Protective role of antioxidants against BPA induced toxicity / nephrotoxicity is discussed in this literature. Keywords: Antioxidants, bisphenol A (BPA), environmental estrogen, kidney, oxidative stress, toxicity.