perfluorooctane sulfonate (PFOS) 和其精选的类似物诱导外围血液单核细胞中的各种细胞死亡类型
Katarzyna Mokra1, Izabela Kaczmarska1, Bożena Bukowska1
1University of Lodz, Faculty of Biology and Environmental Protection, Department of Biophysics of Environmental Pollution, 141/143 Pomorska St., 90-236, Lodz, Poland.
Chemosphere
|March 14, 2024
概括
perfluorooctane sulfonate (PFOS) 触发免疫细胞中的铁和自,而像PFBS这样的短链PFAS则会诱导细胞亡. 链长度决定了人类PBMC中的PFAS毒性机制,为免疫毒性提供了洞察力.
科学领域:
- 环境毒理学环境毒理学
- 免疫毒理学 免疫毒理学
- 细胞毒理学细胞毒理学
背景情况:
- 和多醇基物质 (PFAS) 是在一般人群中广泛检测到的持久污染物.
- 由于环境问题, perfluorooctane sulfonate (PFOS) 正在被更短链的类似物如 perfluorohexane sulfonate (PFHxS) 和 perfluorobutane sulfonate (PFBS) 取代.
- 了解各种 PFAS 对人类免疫细胞的差异性毒理作用至关重要.
研究的目的:
- 研究PFOS,PFHxS和PFBS对外周血液单核细胞 (PBMC) 的影响.
- 阐明这些PFAS诱导的特定细胞死亡机制 (细胞亡,铁亡,自).
- 为了确定PFAS链的长度是否会影响激活的细胞死亡途径的类型.
主要方法:
- 人类PBMC被暴露在不同度的PFOS,PFHxS和PFBS (0.02400μM) 中24小时.
- 进行了细胞活力测试.
- 评估了亡,铁亡和自标志物,包括酶激活,细胞质水平,铁离子水平,脂质过氧化和自蛋白表达 (LC3-II,Raptor).
主要成果:
- 暴露于PFOS降低了细胞活力,并诱导了铁亡的标记物 (铁的增加,脂质过氧化) 和自 (LC3-II的增加).
- 短链PFAS (PFHxS,PFBS) 通过内在和外在途径诱导亡,特别是职业相关度的PFBS,但没有显著影响铁亡或自.
- 虽然PFOS表现出亲铁和亲自的潜力,但这些效应在较高度下被观察到,而不是PFBS的亲效应.
结论:
- PFAS的碳链长度似乎是人类PBMC中激活细胞死亡途径的关键决定因素.
- PFOS表现出明显的亲铁和亲自活动,而像PFBS这样的短链PFAS是亡的强有力的诱导剂.
- 这些发现为PFAS的免疫毒性机制提供了新的见解,强调了在风险评估中需要考虑链条长度的必要性.
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