Nephrotoxicity of Bisphenol A (BPA) -An Updated Review
Sivakumar J. T. Gowder.
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.
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