EFFECT OF VITAMIN C ON BISPHENOL A INDUCED HEPATO& NEPHROTOXICITY IN ALBINO RATS

Document Type : Original Article

Authors

Forensic Medicine & Clinical Toxicology Department, Faculty of Medicine, Benha University, Egypt

Abstract

Bisphenol-A (BPA) is a worldwide used endocrine disruptor that is incorporated in many plastic industries. The exposure of humans to that substance starts early during the fetal life. Many agencies raised warnings against the excessive use of such substances. The present study aimed to evaluate the oxidative stress effect of BPA on liver and kidney of albino rats, and whether co-administration of vitamin C can ameliorate this oxidative damage. Albino rats were divided into six groups: -ve control group,+ve control group,vitamin C (60mglkg) treated group, BPA treated group, BPA+ high dose of vitamin C (60mglkg) treated group, and BPA+ low dose of vitamin C (5.5mglkg) treated group The oxidative stress arising from BPA was evaluated in liver and kidney tissues. In addition, serum creatinine, uric acid levels, (AST) and (ALT) activities as markers of kidney and liver function were measured. Biochemical analysis revealed significant reduction in activities of enzymatic antioxidants in BPA treated group and BPA + vitamin C treated groups in high & low doses as compared to control group. In addition, there were significant increase in AST, ALT, uric acid, and creatinine levels in BPA treated group and reduction in their concentrations BPA + vitamin C treated groups in high & low doses as compared to control group. Histopathological and ultrastructure changes of liver and kidney were observed in BPA treated group and BPA + vitamin C treated groups as compared to control group. The present study demonstrated that BPA could induce hepato& nephrotoxicity, affecting oxidant/antioxidant balance in rat liver and kidney. In addition, Co-administration of vitamin C in low dose (5.5 mg/kg) didn't prevent this oxidative damage. While co-administration of vitamin C in high dose (60 mg/kg) augmented this oxidative damage.

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