хлорпирифос通过氧化应激和线粒体功能障碍在 HepG2 细胞中诱导细胞毒性
C Montanarí1, F Franco-Campos2, M Taroncher2
1Laboratory of Food Chemistry and Toxicology, Faculty of Pharmacy and Food Sciences, Universitat de València, Av. Vicent Andrés Estellés s/n, Burjassot, 46100, València, Spain.
概括
pyrifos农药通过诱导氧化应激和线粒体功能障碍,导致肝细胞受损. 需要进一步的研究来了解它对非标器官的毒性.
科学领域:
- 毒理学 毒理学 毒理学
- 细胞生物学 细胞生物学
- 生物化学 生化学
背景情况:
- pyrifos (CPF) 是一种广泛使用的有机酸盐农药,与不良健康影响有关.
- 虽然乙胆酶抑制是其主要作用,但正在研究中毒性的二次机制.
研究的目的:
- 在人类肝癌HepG2细胞中探索pyrifos诱导的急性细胞毒性的二次机制.
- 研究氧化应激和线粒体功能障碍在pyrifos毒性的作用.
主要方法:
- 暴露HepG2细胞在不同度的Chlorpyrifos.
- 评估细胞活力,活性氧物种 (ROS) 生成,脂质过氧化 (LPO) 和线粒体膜潜力 (ΔΨm).
- 对Nrf2蛋白表达的评估.
主要成果:
- хлорпирифос以度依赖的方式降低了细胞活力 (IC50 = 280.87 ± 26.63 μM).
- 二的亚毒度增加了ROS,线粒体超氧化物和LPO,同时降低了ΔΨm.
- pyrifos上调了Nrf2蛋白表达,这表明细胞对氧化应激的反应.
结论:
- хлорпирифос通过氧化应激和线粒体功能障碍诱导肝毒性.
- 这些发现强调需要进一步调查pyrifos对非标器官的毒性及其潜在机制.
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