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暴露于低氧和全氟丁烷磺酸的海洋青鳉鱼肝脏-肠道轴功能障碍。

Dysfunction of liver-gut axis in marine medaka exposed to hypoxia and perfluorobutanesulfonate.

作者信息

Li Jing, Sun Baili, Lam Paul K S, Chen Lianguo

机构信息

State Key Laboratory of Freshwater Ecology and Biotechnology, Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China; University of Chinese Academy of Sciences, Beijing 100049, China.

Department of Science, School of Science and Technology, Hong Kong Metropolitan University, Hong Kong.

出版信息

Mar Pollut Bull. 2023 Mar;188:114677. doi: 10.1016/j.marpolbul.2023.114677. Epub 2023 Jan 31.

Abstract

With objectives to explore the interactive mode on the function of liver-gut axis, adult marine medaka were exposed for 7 days to environmentally realistic concentrations of perfluorobutanesulfonate (PFBS) (0 and 10 μg/L) under normoxia or hypoxia condition. Furthermore, PFBS exposure was extended to 21 days to reveal the temporal progression in toxicity. The results showed that hypoxia exposure significantly disturbed lipid metabolism, caused oxidative damage, and induced inflammation in the livers of medaka. The composition of gut microbiota was also drastically shifted by hypoxia acute exposure. In contrast, the effect of PFBS was much milder. Hypoxia was thus the determinant of the combined toxicity. Depending on the exposure duration, a time-course recovery from PFBS innate toxicity was generally noted. Overall, the present study underlines the hypoxic and temporal variation in the dysregulation of liver-gut axis by PFBS, which is expected to support a comprehensive ecological risk assessment.

摘要

为了探究肝肠轴功能的交互模式,将成年海水青鳉在常氧或缺氧条件下暴露于环境现实浓度的全氟丁烷磺酸(PFBS)(0和10μg/L)中7天。此外,将PFBS暴露延长至21天以揭示毒性的时间进程。结果表明,缺氧暴露显著扰乱了青鳉肝脏的脂质代谢,造成氧化损伤,并诱导炎症。肠道微生物群的组成也因缺氧急性暴露而发生了巨大变化。相比之下,PFBS的影响要温和得多。因此,缺氧是联合毒性的决定因素。根据暴露持续时间,通常可观察到PFBS固有毒性的时间进程恢复。总体而言,本研究强调了PFBS对肝肠轴失调的缺氧和时间变化影响,有望支持全面的生态风险评估。

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