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首页> 外文期刊>Regulatory Toxicology and Pharmacology: RTP >Subchronic bisphenol S exposure affects liver function in mice involving oxidative damage
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Subchronic bisphenol S exposure affects liver function in mice involving oxidative damage

机译：副铬双酚的暴露会影响涉及氧化损伤的小鼠中的肝功能

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摘要

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 mu g/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 mu g/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.
机译：双酚S（BPS）已广泛用于制造业作为双酚A（BPA）的替代品。新兴的证据主要来自体外研究，表明BPS可能发挥各种毒理学作用，并且具有诱导氧化应激的可能性。然而，很少有数据对于肝脏的BPS体内效应，是药物毒性的重要目标。我们的研究首次系统地研究了BPS在口服给药时小鼠肝功能上的各种剂量的影响。我们发现，用5000μg/ kg bps治疗8周，导致肝损伤，随着丙氨酸氨基转移酶，天冬氨酸氨基转移酶和总胆红素的增加，以及肝脏形态的缺陷。此外，通过降低抗氧化剂酶的活性，增加脂质过氧化水平和两个生物标志物基因，HO-1和GADD45B的脂质过氧化水平和表达，使BPS在小鼠肝脏诱导氧化应激。未观察到较低剂量（5-500μg/ kg）或更短的持续时间（4周）治疗的显着变化。总之，通过诱导氧化损伤，亚温度BPS暴露可能影响小鼠中的肝功能，表明BPS可能不是BPA的绝对安全的替代品。

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