Vitamin D Exhibits Hepatoprotective Properties Against Bisphenol A-Induced Hepatic Injury in Rats via Mitigating Oxidative Stress, Inflammation, and Apoptosis.

Bisphenol A (BPA) is a significant synthetic xenoestrogen extensively utilized in industrial chemicals. Our objective was to assess the hepatoprotective effect of vitamin D against BPA-induced hepatic oxidative stress, liver inflammation, and apoptosis in rats. Therefore, rats were exposed to BPA alone (25 mg/kg) or treatment with vitamin D (400 IU/day) for 30 days. Vitamin D may be crucial in safeguarding the liver by functioning as an antioxidant, anti-inflammatory, and antiapoptotic agent in BPA-induced hepatic injury. The treatment of Vitamin D reversed the liver damage caused by BPA by reducing the levels of AST, ALT, and ALP in the serum. Vitamin D also improved the activity of antioxidant enzymes such as SOD and CAT, as well as the levels of liver antioxidants like GSH and TAS. Additionally, vitamin D suppressed liver inflammation and hepatic oxidative stress in rats exposed to BPA. Furthermore, vitamin D treatment alleviated the disruptions in liver structure and reduced TUNEL staining, an indicator of apoptosis, in BPA-induced liver damage. In conclusion, this study demonstrated that vitamin D treatment is a powerful protective agent against liver damage in BPA-exposed rats, achieved through the regulation of oxidant/antioxidant balance, suppression of apoptosis, and reduction of pro-inflammatory cytokine release.