全氟辛烷磺酰胺 (PFOSA) 通过激活斑马鱼芳基烃受体诱导心脏毒性,Environmental Science & Technology

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全氟辛烷磺酰胺 (PFOSA) 通过激活斑马鱼芳基烃受体诱导心脏毒性
Environmental Science & Technology ( IF 10.8 ) Pub Date : 2022-06-02 , DOI: 10.1021/acs.est.1c08875
Honghong Chen _{1,

2} , Wenhui Qiu _{1,

2} , Xuanjun Yang _{3,

4} , Fangyi Chen ₅ , Jiaying Chen ₅ , Liang Tang ₆ , Hanbing Zhong ₃ , Jason T Magnuson ₇ , Chunmiao Zheng ₁ , Elvis Genbo Xu ₈

Affiliation

全氟辛烷磺酰胺 (PFOSA) 是全氟辛烷磺酸 (PFOS) 的前体，在工业过程中广泛使用，但对其毒性知之甚少，特别是对于通常对外源暴露敏感的早期生命阶段生物体。在此，在暴露于 0.01、0.1、1、10 和 100 μg/L PFOSA 浓度后，使用转录、形态、生理和生化测定来评估对水生生物的潜在影响。暴露斑马鱼中最重要的Tox功能与通过基因本体论(GO)、京都基因和基因组百科全书(KEGG)途径和独创性途径分析(IPA)分析预测的心脏病有关。与转录变化预测的影响一致，暴露于 0.1、1、10 或 100 μg/L PFOSA 后观察到心脏形态异常、心跳信号紊乱以及心率和心输出量降低。此外，通过补充芳基碳氢化合物受体 (AHR) 拮抗剂或ahr2-吗啉敲低，可以预防或减轻这些 PFOSA 诱导的心脏效应，揭示了 AHR 在 PFOSA 诱导的心脏毒性中的重要作用。我们的研究结果首次提供了鱼类证据，证明 PFOSA 会损害正常的心脏发育和功能，并引起人们对自然环境中 PFOSA 类似物的关注。

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Perfluorooctane Sulfonamide (PFOSA) Induces Cardiotoxicity via Aryl Hydrocarbon Receptor Activation in Zebrafish

Perfluorooctane sulfonamide (PFOSA), a precursor of perfluorooctanesulfonate (PFOS), is widely used during industrial processes, though little is known about its toxicity, particularly to early life stage organisms that are generally sensitive to xenobiotic exposure. Here, following exposure to concentrations of 0.01, 0.1, 1, 10, and 100 μg/L PFOSA, transcriptional, morphological, physiological, and biochemical assays were used to evaluate the potential effects on aquatic organisms. The top Tox functions in exposed zebrafish were related to cardiac diseases predicted by Gene Ontology (GO), Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway, and Ingenuity Pathway Analysis (IPA) analysis. Consistent with impacts predicted by transcriptional changes, abnormal cardiac morphology, disordered heartbeat signals, as well as reduced heart rate and cardiac output were observed following the exposure of 0.1, 1, 10, or 100 μg/L PFOSA. Furthermore, these PFOSA-induced cardiac effects were either prevented or alleviated by supplementation with an aryl hydrocarbon receptor (AHR) antagonist or ahr2-morpholino knock-down, uncovering a seminal role of AHR in PFOSA-induced cardiotoxicity. Our results provide the first evidence in fish that PFOSA can impair proper heart development and function and raises concern for PFOSA analogues in the natural environment.

更新日期：2022-06-02

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