脂毒性
线粒体分裂
氧化应激
线粒体
细胞生物学
碎片(计算)
活性氧
生物
氧化磷酸化
化学
生物化学
生态学
生物技术
胰岛素抵抗
胰岛素
作者
Wei Xing,Yi-Chuang Xu,Xiao-Ying Tan,Wu-Hong Lv,Dian-Guang Zhang,Yanan He,Zhi Luo
出处
期刊:Chemosphere
[Elsevier]
日期:2023-11-01
卷期号:340: 139892-139892
被引量:1
标识
DOI:10.1016/j.chemosphere.2023.139892
摘要
Enrofloxacin (ENR) is a kind of widespread hazardous pollutant on aquatic ecosystems and causes toxic effects, such as disorders of metabolism, on aquatic animals. However, its potential mechanisms at an environmental concentration on metabolic disorders of aquatic organisms remain unclear. Herin, we found that hepatic lipotoxicity was induced by ENR exposure, which led to ENR accumulation, oxidative stress, mitochondrial fragmentation, and fatty acid transfer blockage from lipid droplets into fragmented mitochondria. ENR-induced lipotoxicity and mitochondrial β-oxidation down-regulation were mediated by reactive oxygen species (ROS). Moreover, dynamin-like protein 1 (DRP1) mediated ENR-induced mitochondrial fragmentation and changes of lipid metabolism. Mechanistically, ENR induced increment of DRP1 mitochondrial localization via dephosphorylating DRP1 at S627 and promoted its interaction with mitochondrial fission factor (MFF), leading to mitochondria fragmentation. For the first time, our study provides an innovative mechanistic link between hepatic lipotoxicity and mitochondrial fragmentation under ENR exposure, and thus identifies previously unknown mechanisms for the direct relationship between environmental ENR concentration and lipotoxicity in aquatic animals. Our study provides innovative insights for toxicological mechanisms and environmental risk assessments of antibiotics in aquatic environment.
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