青基会以ROS依赖的方式加剧RSL3诱导的铁亡
Xiuhao Yu1, Shaokun Chen2, Hailin Wang1,2,3
1Sino-Danish College, University of Chinese Academy of Sciences, Beijing 100049, P. R. China.
Chemical research in toxicology
|May 21, 2024
概括
青基 (CBQs),新出现的水污染物,通过诱导铁亡,加剧细胞死亡. 这种细胞死亡机制涉及铁的积累,GPX4的失活,和反应性氧物种,影响哺乳动物的细胞.
科学领域:
- 环境化学环境化学
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
背景情况:
- 子基 (CBQs) 是新出现的水中的消毒副产品.
- 这些化合物由于其毒性,对公众健康构成潜在风险.
研究的目的:
- 研究三个特定的CBQs (四-1,4-二,2,5-二-1,4-二和2--1,4-二) 的毒性机制.
- 为了确定CBQ是否诱导铁亡,一种调节细胞死亡的形式.
主要方法:
- 哺乳动物细胞单独暴露于CBQ和与Ras选择性致命小分子3 (RSL3) 结合.
- 评估细胞死亡,铁积累,谷氨过氧化酶4 (GPX4) 活性和活性氧物种 (ROS) 水平.
主要成果:
- CBQs显著加剧RSL3诱导的细胞死亡.
- 由CBQs诱导的细胞死亡与铁积累增加和GPX4无活化有关,这是铁亡的特征.
- 反应性氧物种在铁死过程中扮演中介CBQ毒性的角色.
结论:
- CBQs可以诱导哺乳动物细胞中的铁亡,单独或与RSL3.3协同.
- 铁积累,GPX4无活化和ROS是CBQ毒性的关键媒介.
- 了解这些机制对于评估CBQ的健康风险至关重要.
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