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一项关于PFAS在HepG2细胞中产生活性氧物种的亚细胞研究

V H Amstutz¹, A Mircheva², A Cengo²

¹Department of Pharmacology and Toxicology, Faculty of Medicine, Health & Life Science, Maastricht University, PO Box 616, Maastricht, 6200 MD, 6229 ER, The Netherlands. v.amstutz@maastrichtuniversity.nl.

Scientific reports

|July 2, 2025

概括

和多醇基物质 (PFAS) 通过增加活性氧物种 (ROS),可能通过抑制抗氧化剂,导致肝损伤. 不同的PFAS头组可能会触发不同的毒性路径.

科学领域:

环境毒理学环境毒理学
细胞生物学细胞生物学
生物化学生物化学

背景情况:

和多醇基物质 (PFAS) 与肝脏毒性有关,但机制尚不清楚.
了解PFAS诱导的活性氧物种 (ROS) 形成对于评估肝毒性至关重要.

研究的目的:

研究PFAS诱导的ROS的起源及其在HepG2细胞活力中的作用.
根据头组和碳链长度评估PFAS的结构-活动关系.
确定线粒体和过氧体在PFAS诱导的ROS生成中的参与.

主要方法:

暴露在各种 PFAS 的 HepG2 细胞中,具有不同的头组和链条长度.
利用奎尔素和线粒速抗氧化剂来评估ROS与细胞活力的联系.
测量过氧体和线粒体活动,溶酶体泄漏和脂质过氧化.

主要成果:

暴露于PFAS增加了ROS生成,并降低了HepG2细胞活力.
quercetin 和 mito-tempo 均降低了 PFAS 诱导的 ROS,但只有 quercetin 在 PFCA 和 PFSA 暴露后改善了细胞活力.
PFASs在24小时内没有影响过氧体或线粒体活动;溶解体泄漏和脂质过氧化是次要效应.
暴露于PFOA和PFOS降低了催化酶活性,表明内源性抗氧化剂抑制.

结论:

PFAS诱导的ROS生成可能源于抑制HepG2细胞内源性抗氧化剂.
涉及一个主群依赖的机制, perfluoroalkyl carboxylic 酸 (PFCAs) 和 perfluorosulfonic 酸 (PFSAs) 可能通过不同的途径引起肝毒性.

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