The biotoxicity of perfluoroalkyl and polyfluoroalkyl substances (PFASs) to aquatic organisms has been widely concerned. However, studies on toxic effects of PFASs are usually evaluated directly by using laboratory exposure rather than laboratory validation based on data obtained in the field. In this study, wild catfish () was explored on the relationship between PFASs bioaccumulation and lipid disorders. Nine and thirteen lipid metabolites were significantly associated with perfluorooctane sulfonate (PFOS) and 6:2/8:2Cl-PFESA (trade name F-53B) exposures, respectively; and the correlated lipid metabolites were the fatty acid (FA) and conjugates, FA esters, steroids, and glycerophosphate subclasses. The effects of PFASs on lipid metabolism of fish and its mechanism were further analyzed through exposure experiments. Zebrafish () of different sexes underwent PFOS and F-53B exposures for 21 days at 100 ng/L and 100 μg/L. By determining gene expression levels, hepatic lipid contents, and histopathological change, the adverse effects order on lipid metabolism in male or female was 100 μg/L F-53B > 100 μg/L PFOS > 100 ng/L F-53B > 100 ng/L PFOS; the stress response in male was more intensive than that in female. PFOS and F-53B activated the peroxisome proliferator-activated receptor pathway, promoting the processes of FA and total cholesterol (T-CHO) transport, FA -oxidation, FA synthesis, and finally induced FA and T-CHO transportation from blood into liver, then accelerated FA to FA ester transformation, and CHO into steroids. Laboratory experiments confirmed the field analysis. This study innovatively explored the adverse effects of PFOS and F-53B on lipid metabolism and their mechanisms at field and laboratory levels, highlighting concerns regarding PFASs health risks.

中文翻译：

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全氟烷基和多氟烷基物质诱导鱼类脂质代谢损伤：现场调查和实验室研究相结合


全氟烷基和多氟烷基物质（PFASs）对水生生物的生物毒性受到广泛关注。然而，关于 PFAS 毒性作用的研究通常是通过实验室暴露直接评估，而不是根据现场获得的数据进行实验室验证。本研究以野生鲶鱼为对象，探讨了PFASs生物累积与血脂紊乱之间的关系。 9 种和 13 种脂质代谢物分别与全氟辛烷磺酸 (PFOS) 和 6:2/8:2Cl-PFESA（商品名 F-53B）暴露显着相关；相关的脂质代谢物是脂肪酸 (FA) 和结合物、FA 酯、类固醇和甘油磷酸盐亚类。通过暴露实验进一步分析了PFASs对鱼类脂质代谢的影响及其机制。不同性别的斑马鱼以 100 ng/L 和 100 μg/L 的浓度接触 PFOS 和 F-53B 21 天。通过测定基因表达水平、肝脏脂质含量和组织病理学变化，对男性或女性脂质代谢的不良影响顺序为100 μg/L F-53B > 100 μg/L PFOS > 100 ng/L F-53B > 100 ng /L 全氟辛烷磺酸；男性的应激反应比女性更强烈。 PFOS和F-53B激活过氧化物酶体增殖物激活受体途径，促进FA和总胆固醇（T-CHO）转运、FA氧化、FA合成过程，最终诱导FA和T-CHO从血液转运至肝脏，然后加速 FA 向 FA 酯的转化，以及 CHO 向类固醇的转化。实验室实验证实了现场分析。这项研究创新性地探讨了 PFOS 和 F-53B 对脂质代谢的不利影响及其在现场和实验室水平的机制，强调了对 PFAS 健康风险的担忧。