хлорпирифос通过激活内在和外在的亡途径来诱导巨细胞的亡
Chen-Yu Chiang1, Shin-Wu Liu1, Chun-Jung Chen2
1Department of Veterinary Medicine, National Chung Hsing University, Taichung, Taiwan.
Environmental toxicology
|March 19, 2025
概括
pyrifos农药通过内部和外部途径触发细胞亡,从而诱导巨细胞的细胞死亡. 这涉及酶激活,线粒体损伤和蛋白质表达的改变,突出显示免疫系统的毒性.
科学领域:
- 免疫毒理学 免疫毒理学
- 细胞生物学 细胞生物学
- 环境健康 环境健康
背景情况:
- pyrifos是一种广泛使用的农药,具有已知的环境和人类健康风险.
- 虽然其神经毒性和基因毒性作用已被记录,但其对免疫系统的影响尚未完全理解.
- 研究在免疫细胞中pyrifos的特定毒性机制至关重要.
研究的目的:
- 为了阐明在巨细胞中由pyrifos诱导的亡途径.
- 确定内在和外在的亡信号在pyrifos诱导的细胞毒性中的作用.
- 评估pyrifos对巨细胞活力和亡的度依赖性影响.
主要方法:
- RAW 264.7巨细胞暴露于不同度的pyrifos.
- 使用乳酸脱酶试验测量了细胞毒性.
- 通过流细胞测量和西式斑点分析分析了亡,酶激活 (酶-3, -8, -9),线粒体功能,死亡受体表达,细胞染色体c释放和Bcl2家族蛋白质.
主要成果:
- pyrifos在巨细胞中诱导了度依赖的细胞毒性和亡.
- 观察到酶-3,酶-8和酶-9的激活.
- 证实了线粒体功能障碍,细胞染色体c释放,Bcl2家族蛋白质表达的改变和死亡受体表达的增加.
结论:
- хлорпирифос通过一个依赖卡斯巴-3的机制触发巨细胞的亡.
- 内在的 (涉及酶-8,线粒体通路) 和外在的 (涉及酶-9,死亡受体) 亡通路都被pyrifos激活.
- 这些发现揭示了pyrifos的显著免疫毒性,有助于其整体健康风险.
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