聚乙烯二甲 (PET) 微和纳米塑料颗粒影响人类大脑血管细胞的线粒体效率,而不会诱导氧化应激
Sean M Gettings1, William Timbury1, Anna Dmochowska2
1UK Health Security Agency, Radiation Effects Department, Radiation Protection Science Division, Harwell Science Campus, Didcot, Oxfordshire OX11 0RQ, UK.
NanoImpact
|April 25, 2024
概括
聚乙烯二甲 (PET) 微/纳米塑料在人类大脑细胞中没有引起氧化应激. 然而,短期PET暴露损害了线粒体功能,这表明潜在的线粒体反应涉及TFAM基因表达.
科学领域:
- 环境健康科学 环境健康科学
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 塑料污染,特别是聚乙烯四甲酸盐 (PET),对环境和健康构成潜在风险.
- 人类大脑血管周细胞对于血脑屏障的完整性至关重要.
- 了解微型和纳米塑料对神经细胞的影响至关重要.
研究的目的:
- 研究PET微/纳米塑料对人类大脑血管周细胞的影响.
- 评估对线粒体功能和氧化应激的影响.
- 分析与氧化应激,铁亡和线粒体功能相关的基因表达.
主要方法:
- 在人脑血管周细胞体外暴露于PET颗粒 (50微克/毫升) 3,6和10天.
- 对氧化应激标志物的评估.
- 测量线粒体呼吸 (最大呼吸,备用呼吸能力,ATP生产).
- 分析线粒体DNA拷贝数和基因表达 (TFAM,氧化应激,铁亡标志物).
主要成果:
- 在测试度下,PET颗粒不会在皮细胞中诱导氧化应激.
- 在3天后观察到线粒体呼吸和ATP生产的短暂减少,在6天后恢复.
- 没有发现线粒体DNA拷贝数或氧化应激/铁灭基因表达的显著变化.
- 3天后,人们注意到线粒体转录因子A (TFAM) 基因的表达增加.
结论:
- PET微/纳米塑料 (50微克/毫升) 不会在人类大脑血管周细胞中诱导氧化应激.
- 短期PET暴露会损害线粒体功能,这可能表明线粒体质量反应.
- 基因TFAM可能在观察到的细胞对PET暴露的反应中发挥作用.
- 需要对线粒激进,血脑屏障完整性和细胞间相互作用进行进一步的研究.
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