Bisphenol S (BPS) is extensively utilized in various industries such as plastic manufacturing, food packaging, and electronics. The release of BPS into aquatic environments has been observed to have negative impacts on aquatic ecosystems. Research has shown that exposure to BPS can have adverse effects on the health of aquatic animals. This study aimed to explore the mechanism of oxidative stress and endoplasmic reticulum stress induced in freshwater crayfish () by exposure to BPS (0 µg/L, 1 µg/L, 10 µg/L, and 100 µg/L) for 14 days. The results showed that BPS exposure resulted in elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA) and severe intestinal histological damage. In addition, oxidative stress can occur in the body by inhibiting the activity of antioxidant enzymes and the expression of related genes. BPS exposure induced a significant increase in the relative mRNA expression levels of inflammatory cytokines ( and ) and key unfolded protein response (UPR) related genes (, and ). At the same time, BPS exposure also induced up-regulation of apoptosis genes ( and ), suggesting that UPR and signaling pathways may play a protective role in the process of apoptosis and oxidative stress. In conclusion, Our findings present the initial evidence that exposure to environmentally relevant levels of BPS can lead to intestinal injury through various pathways, highlighting concerns about the potential harm at a population level from BPS and other bisphenol analogs.

中文翻译：

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探索双酚 S 引起淡水小龙虾（克氏原螯虾）肠道损伤的机制：分子和生化方法


双酚 S (BPS) 广泛应用于塑料制造、食品包装和电子等各个行业。据观察，BPS 释放到水生环境中会对水生生态系统产生负面影响。研究表明，接触 BPS 会对水生动物的健康产生不利影响。本研究旨在探讨淡水小龙虾暴露于 BPS（0 µg/L、1 µg/L、10 µg/L 和 100 µg/L）14 天诱导氧化应激和内质网应激的机制。结果表明，BPS 暴露导致活性氧 (ROS) 和丙二醛 (MDA) 水平升高以及严重的肠道组织学损伤。此外，通过抑制抗氧化酶的活性和相关基因的表达，体内会出现氧化应激。 BPS 暴露诱导炎症细胞因子 ( 和 ) 和关键未折叠蛋白反应 (UPR) 相关基因 ( 和 ) 的相对 mRNA 表达水平显着增加。同时，BPS暴露还诱导凋亡基因(和)上调，提示UPR和信号通路可能在细胞凋亡和氧化应激过程中发挥保护作用。总之，我们的研究结果提供了初步证据，表明接触环境相关水平的 BPS 可通过各种途径导致肠道损伤，凸显了人们对 BPS 和其他双酚类似物对人群潜在危害的担忧。