Ameliorative Potential of Selenium against Bisphenol A- Induced Hepatotoxicity in Rats

Abdel Samie, Hany A.; Nassar, Samir A.; Hussein, Youssef

Ameliorative Potential of Selenium against Bisphenol A- Induced Hepatotoxicity in Rats

Document Type : Original Article

Authors

¹ Dept. of Zoology, Faculty of Science, Menoufia University

² Zoology Department, Faculty of Science, Zagazig University, Zagazig

³ Department of Human Anatomy and Embryology, Faculty of Medicine, Zagazig University, Zagazig, Egypt

Abstract

Background: environmental pollutants affect various tissues. Bisphenol A, a compound used in making epoxy resins and polycarbonate plastics, induces many hazardous effects. Aim of the work: this work was designed to test the ameliorative potential of selenium against hepatotoxicity caused by bisphenol A.
Materials and Methods: male rats were divided into four groups. Group 1 served as control, group 2 given sodium selenite, group 3 was administered with suspension of bisphenol A that is dissolved in corn oil. Rats of group 4 were administered with selenium plus bisphenol A. Liver specimens and blood samples were inspected after 3 and 6 weeks of treatment.
Results: there was no statistical difference between control and selenium -administered rats in all parameters. Rats treated with bisphenol A suffered significant depression in weight whereas selenium administration decreased the effect on rat's weight. Bisphenol A administration induced blood vessels congestion, inflammatory infiltration, bile duct proliferation, cytoplasmic vacuolization and macrosteatosis while selenium administration improved liver histopathological criteria either after 3 or 6 weeks. Bisphenol A treatment elevated nuclear PCNA and caspase-3 expression in the cytoplasm and liver function enzymes (serum AST and ALT) and bilirubin. Again, selenium ameliorated these changes. In conclusion, bisphenolA exerted deleterious impact on rats' hepatocytes and serum biochemical parameters in a time-dependent manner. Selenium supplementation provides an extent of amelioration against bisphenol A- induced hepatotocixity.

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