Abstract
Classical xenoestrogenic in vivo effects of bisphenol A (2,2-bis(4-hydroxyphenyl)propane, BPA) are well-described in the literature, however the molecular mechanisms of BPA-induced hepatotoxicity are not fully characterized. The work is aimed to assess biochemical markers of BPA induced hepatotoxicity under conditions of differential supplementation with retinoids. We demonstrate that the absence of hepatic retinyl esters as the main form of vitamin A storage provides for a resistance to BPA induced liver damage. Retinoid supplementation increases the hepatotoxic effects of bisphenol A, evidenced in higher indexes of oxidative damage of lipids, proteins and non-protein thiol groups as well as increase of serum alanine aminotransferase activity and myeloperoxidase activity in liver parenchyma. The absence of hepatotoxicity signs when hepatic retinoid stores are depleted and their presence during normal or excessive retinoid supplementation suggest that hepatic retinoid availability is one of the factors determining the hepatotoxicity of bisphenol A.
Highlights
Hepatotoxicity is currently one of the pri mary targets for biomedical research due to ever increasing toxic pressure on liver as an organ of homeostasis and detoxification [1]
The adequate experimental models are indispensable for better understanding of biochemical mechanisms of hepatotoxicity progression and for development and testing of novel approaches to counteract this pathology [2]
The results of our studies demonstrate that BPA administration to wild type animals caused symptoms of hepatotoxicity to manifest on 72nd h of experiment
Summary
Hepatotoxicity is currently one of the pri mary targets for biomedical research due to ever increasing toxic pressure on liver as an organ of homeostasis and detoxification [1]. Bisphenol A (2,2-bis(4-hydroxyphe nyl)propane, BPA) is one of the potential in vivo hepatotoxicity inducer and is widely used as a monomer for polycarbonate productions [3]. Toxic xenoestrogenic effects of BPA are described in detail, the molecular mechanisms be hind BPA-induced hepatotoxicity are still poorly un derstood and require further study. The detoxifica tion of this xenobiotic, primarily in liver, generates highly reactive bisphenol metabolites and activates free-radical processes [7]. Numerous studies [9, 10] prove that retinoids control liver detoxifica tion system through regulation of expression of cyto chrome p450 isoforms by binding to nuclear retinoic acid receptor (RAR α, β, γ) and retinoid X receptors (RXR α, β, γ) [11]. The aim of this work was to evaluate the bio chemical parameters of BPA-induced hepatotoxicity under differential supplementation with retinoids
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