Bisphenol A Induces Hepatotoxicity through Oxidative Stress in RatModel

Thesis
مستخلص المنشور: 

Reactive oxygen species (ROS) are cytotoxic agents that lead to significant oxidative damage. Bisphenol A (BPA) is a contaminantwith increasing exposure to it and exerts both toxic and estrogenic effects on mammalian cells. Due to limited informationconcerning the effect of BPA on liver, this study investigates whether BPA causes hepatotoxicity by induction of oxidative stress in liver. Rats were divided into five groups: The first four groups, BPA (0.1, 1, 10, 50 mg/kg/day) were administrated orally to rats forfour weeks. The fifth group was taken water with vehicle. The final body weights in the 0.1 mg group showed a significant decreasecompared to control group. Significant decreased levels of reduced glutathione, superoxide dismutase, glutathione peroxidase,glutathione-S-transferase, glutathione reductase and catalase activity were found in the 50mg BPA group compared to controlgroups. High dose of BPA (50mg/kg) significantly increased the biochemical levels of ALT, ALP and total bilirubin. BPA effect onthe activity of antioxidant genes was confirmed by real time PCR in which the expression levels of these genes in liver tissue weresignificantly decrease compared to control. Data from this study demonstrate that BPA generate ROS and reduce the tioxidantgene expression that causes hepatotoxicity.

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