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微粒物质诱导人类肺上皮细胞的氧化应激和铁亡

Yujin Ahn^1,2, Yong-Hyeon Yim^2,3, Hee Min Yoo^1,2

¹Biometrology Group, Korea Research Institute of Standards and Science (KRISS), Daejeon 34113, Republic of Korea.

|February 23, 2024

概括

城市颗粒物 (PM) 暴露会触发反应性氧物种 (ROS) 生产,导致氧化应激和铁亡,一种细胞死亡. 这项研究证实了PM诱导的肺细胞铁,这表明了肺部疾病的新治疗点.

科学领域:

毒理学毒理学毒理学
细胞生物学细胞生物学
环境健康环境健康

背景情况:

城市颗粒物 (PM) 与呼吸道感染和肺部疾病有关.
微粒的复杂成分导致反应性氧物种 (ROS) 生产和脂质过氧化,损害肺细胞.
线粒体ROS可以通过各种途径导致器官细胞的破坏.

研究的目的:

确认通过城市PM暴露诱导铁亡.
调查ROS和氧化应激在PM诱导的肺内皮毒性中的作用.
为了确定与PM暴露相关的铁灭生物标志物.

主要方法:

使用了KRISS CRM 109-02-004,这是用于PM分析的认证参考材料.
采用RT-qPCR和信号通路分析来确认ferroptosis.
评估了细胞内线粒体潜力,ROS水平,脂质过氧化和铁灭的生物标志物.

主要成果:

暴露于颗粒物显著增加了ROS生成,并降低了线粒体潜力.
PM诱导铁亡的特征:脂质过氧化,抗氧化防御的丧失和铁的积累.
通过增加NQO1,CYP1B1,FTH1,SOD2,NRF等标志物的表达,以及关键的铁亡标志物 (xCT/SLC7A11,TRIM16,HMOX-1,FTL,CHAC1,GPX4) 的氧化应激得到证实.

结论:

城市PM诱导细胞和线粒体ROS生产,导致氧化应激和铁亡.
升高的ROS水平是触发铁亡的关键.
研究结果表明,通过准PM诱导的铁亡途径,为肺部疾病提供潜在的治疗策略.

关键词:

这就是ROSOS ROS.空气污染空气污染细胞死亡是细胞死亡.细胞毒性细胞毒性铁性化 (ferroptosis) 是一种线粒体功能障碍线粒体功能障碍颗粒物质颗粒物质颗粒物质

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