Perfluorooctanoic acid (PFOA) disrupts cardiac performance of thick-shell mussel by inserting into the binding pocket of proliferator-activated receptor gamma and thereby causing lipid metabolism disorders☆

文献类型： 外文期刊

第一作者： Yu, Yingying

作者： Yu, Yingying;Tong, Difei;Zhang, Weixia;Zhou, Weishang;Shi, Wei;Liu, Guangxu;Yuan, Kuankuan;Yang, Weidong;Zhao, Xinguo;Li, Weifeng

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关键词： Perfluorooctanoic acid; Cardiotoxicity; Lipotoxicity; Peroxisome proliferator-activated receptors; Mussels; Invertebrates

期刊名称：ENVIRONMENTAL POLLUTION （ 影响因子：7.3； 五年影响因子：8.1 ）

ISSN： 0269-7491

年卷期： 2025 年 376 卷

页码：

收录情况： SCI

摘要： Invertebrates constitute the largest group of animals on Earth, accounting for approximately 97 % of all animal species. Although the heart of invertebrates could be a sensitive target for environmental pollution, potential cardiotoxicity for most contaminants has received little attention. In this study, perfluorooctanoic acid (PFOA) and thick-shell mussels (Mytilus coruscus) were used to investigate the effect of PFOA on cardiac performance and the potential underlying mechanisms. Heart beat monitoring demonstrated that four-week exposure to 0.5 and 5.0 mu g/L of PFOA resulted in bradycardia and arrhythmia in thick-shell mussels. Moreover, considerably more triglyceride (TG) accumulation, higher lipoprotein lipase (LPL) and lipase (LPS) activities, and disruption of lipid metabolism-related genes were observed in the hearts of PFOA-exposed mussels. In addition, comparable adverse impacts were detected in mussels treated with proliferator-activated receptor gamma (PPAR gamma) agonist whereas the PFOA-induced effects were fully or partially alleviated by PPAR gamma antagonist. Furthermore, molecular docking and molecular dynamics simulation revealed a high binding affinity of PFOA to the PPAR gamma of 12 invertebrates, including thick-shell mussels. In general, our data suggest that PFOA may pose a severe threat to cardiac performance of invertebrate species by inserting into the binding pocket of PPAR gamma, and thereby causing cardiac lipid metabolism disorders.

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