Neurodevelopmental effects of exposure to environmentally relevant concentrations of perfluorooctane sulfonic acid (PFOS), perfluorobutanesulfonic acid (PFBS) and 6:2 chlorinated polyfluorinated ether sulfonate (6:2 Cl-PFESA) on larval zebrafish: Multi-omics and neuropathology perspective
文献类型： 外文期刊
作者： Cao, Xiaolong 1 ; Li, Yameng 2 ; Liu, Xiaoyu 2 ; Li, Kepiao 2 ; Hong, Shuang 2 ; Chen, Haolei 1 ; Rao, Qinxiong 2 ; Li, Huaxi 2 ; Deng, Zhongsheng 2 ; Song, Weiguo 2 ;
作者机构： 1.Univ Shanghai Sci & Technol, Sch Hlth Sci & Engn, Shanghai 200093, Peoples R China
2.Shanghai Acad Agr Sci, Inst Agrifood Stand & Testing Technol, Shanghai 201403, Peoples R China
3.Shanghai Serv Platform Agroprod Qual & Safety Eval, Shanghai 201106, Peoples R China
4.Shanghai Coelite Agrifood Testing Tech Serv Co Ltd, Shanghai 201403, Peoples R China
关键词： PFOS and its substitutes; Zebrafish; Environmentally relevant concentrations; Multi-omics analysis; Neurodevelopmental effects
期刊名称：JOURNAL OF HAZARDOUS MATERIALS （ 影响因子：11.3； 五年影响因子：12.4 ）
ISSN： 0304-3894
年卷期： 2025 年 494 卷
页码：
收录情况： SCI
摘要： Previous studies have shown that perfluorooctane sulfonic acid (PFOS) and its new substitutes perfluorobutanesulfonic acid (PFBS) and 6:2 chlorinated polyfluorinated ether sulfonate (6:2 Cl-PFESA) were associated with neurological abnormalities. However, many of these were conducted at concentrations higher than environmental levels, thus causing overt toxicity. This study employed multi-omics (transcriptomics and targeted metabolomics), morphological, behavioral and neuropathological methods to assess zebrafish embryos exposed to environmentally relevant concentrations (ERC) (10 and 100 ng/L), aiming to better elucidate the key molecular mechanisms that induce neurotoxic effects at ERC. Early development indicators and behavioral analyses showed that these three substances negatively impacted zebrafish development and inhibited locomotor behavior. Neuropathology and transcriptomics indicated that they disrupted visual phototransduction and lysosomal pathways, leading to the destruction of Nissl bodies, myelin sheaths and retinal structures, which were related to the abnormal transcription of relevant genes. Furthermore, targeted metabolomics demonstrated that they caused neurotoxicity by increasing the content of kynurenine and decreasing the content of asparagine and histidine. These findings indicated that they had similar neurotoxic effects, but the mechanisms may differ slightly. Collectively, this study will provide novel insights into understanding the mechanisms by which ERC of PFOS and its substitutes produce neurodevelopmental toxicity.
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