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通过pyrifos介导的线粒体过载会通过ROS/AMPK/ULK1诱导EPC细胞亡

Zhiying Miao¹, Zhiruo Miao², Shuang Feng³

¹College of Life Science, Northeast Agricultural University, Harbin, 150030, People's Republic of China.

Fish & shellfish immunology

|September 3, 2023

概括

pyrifos (CPF) 杀虫剂通过破坏离子 (Ca2+) 运输,诱导鱼细胞的亡. 这导致ER压力和线粒体功能障碍,突出显示CPF.

科学领域:

环境毒理学环境毒理学
细胞生物学细胞生物学
水生毒理学水生毒理学

背景情况:

像酸 (CPF) 这样的有机酸杀虫剂对水生生态系统构成重大风险.
已知CPF会对水生动物产生严重的毒理影响.
了解CPF对鱼细胞的影响对于环境风险评估至关重要.

研究的目的:

为了研究CPF对离子 (Ca²⁺) 运输在表皮瘤皮质囊 (EPC) 细胞中的影响.
阐明鱼类细胞中CPF诱导的亡背后的机制.
探索ER压力和线粒体功能障碍在CPF毒性的作用.

主要方法:

建立暴露于CPF的EPC细胞模型.
使用AO/EB染色和Annexin V/PI测定与流细胞计的亡评估.
使用光探针 (Mag-Fluo-4 AM,Fluo-4 AM,Rhod-2 AM) 进行细胞Ca2+流量成像,并与ER-Tracker红色和Mito-Tracker绿色共同染色.
使用2-APB,4-PBA和Dorsomorphin (化合物C) 的抑制研究.

主要成果:

在EPC细胞中,CPF暴露诱导了亡,通过亡相关蛋白质 (BAX,Cyt-c,CASP3,CASP9,BCL-2) 的改变表达得到证实.
CPF导致ER中的Ca2+耗尽,随后流入线粒体,导致ER压力和线粒体功能障碍.
中介于CPF的Ca2+过载引发了ER压力,加强了线粒体活性氧物种 (Mito-ROS) 的产生,促进了AMPK酸化,并加剧了细胞死亡.

结论:

鱼细胞中CPF诱导的亡取决于Ca2+过载和随后的线粒体功能障碍.
这项研究为水生生物中CPF毒性的机制提供了新的见解.
这些发现有助于了解环境污染对水生生物的影响.

关键词:

细胞灭亡 (apoptosis) 是一种死亡的过程.水生污染物水生污染物二氧化碳平衡作用 (dishomeostasis) 的原因基基酸盐 (Chlorpyrifos) 是一种酸盐.压力ERER压力ERER压力线粒体Ca(2+) 超负荷

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