Subchronic bisphenol S exposure affects liver function in mice involving oxidative damage.

Bisphenol S (BPS) has been widely used in the manufacturing industry as a substitute for bisphenol A (BPA). Emerging evidences, mostly from in vitro studies, suggest that BPS may exert a variety of toxicological effects and have the potential to induce oxidative stress. Nevertheless, few data are available for the in vivo effects of BPS on liver, an important target of drug toxicity. For the first time, our study systematically investigated the effects of BPS at a wide range of doses on liver function in mice upon oral administration. We found that treatment with 5000 μg/kg BPS for 8 weeks resulted in liver injury with increased plasma levels of alanine aminotransferase, aspartate aminotransferase and total bilirubin, as well as defects in hepatic morphology. Moreover, such exposure to BPS induced oxidative stress in the liver of mice by decreasing activities of antioxidant enzymes, and increasing lipid peroxidation level and expression of two biomarker genes, HO-1 and GADD45B. No significant changes were observed for treatment with lower doses (5-500 μg/kg) or shorter duration (4 weeks). In conclusion, subchronic BPS exposure could affect liver function in mice by inducing oxidative damage, indicating that BPS may be not an absolutely safe alternative to BPA.