Department of Pharmacology, Xiamen Institute for Food and Drug Quality Control, Xiamen 361012, Fujian, China.
Department of Pharmacology, Xiamen Institute for Food and Drug Quality Control, Xiamen 361012, Fujian, China.
Regul Toxicol Pharmacol. 2018 Feb;92:138-144. doi: 10.1016/j.yrtph.2017.11.018. Epub 2017 Dec 2.
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.
双酚 S（BPS）已被广泛应用于制造业，作为双酚 A（BPA）的替代品。越来越多的证据表明，BPS 可能具有多种毒理学作用，并具有诱导氧化应激的潜力。然而，关于 BPS 对肝脏（药物毒性的重要靶器官）的体内影响的数据却很少。本研究首次系统地研究了口服给予 BPS 在广泛剂量范围内对小鼠肝脏功能的影响。我们发现，5000μg/kg BPS 处理 8 周导致肝损伤，血浆丙氨酸氨基转移酶、天冬氨酸氨基转移酶和总胆红素水平升高，肝形态学缺陷。此外，这种 BPS 暴露通过降低抗氧化酶的活性、增加脂质过氧化水平和两种生物标志物基因 HO-1 和 GADD45B 的表达，诱导了小鼠肝脏的氧化应激。用较低剂量（5-500μg/kg）或较短时间（4 周）处理时，未观察到明显变化。总之，亚慢性 BPS 暴露可能通过诱导氧化损伤影响小鼠的肝功能，表明 BPS 可能不是 BPA 的绝对安全替代品。
