通过Endoplasmic网膜应激和PERK-eIF2α-CHOP信号通路在TM3细胞中的色素诱导的细胞亡
Mi Tian1, Hongting Cao2, Haoxuan Gao1
1School of Public Health, Ningxia Medical University, Yinchuan, Ningxia 750004, China.
Ecotoxicology and environmental safety
|September 4, 2024
概括
暴露于罗农药会引起男性生殖毒性,原因是通过Endoplasmic reticulum (ER) 应激和PERK-eIF2α-CHOP通路诱导莱迪格细胞亡. 抑制ER压力或PERK活动可以减轻这些有害影响.
科学领域:
- 毒理学 毒理学 毒理学
- 生殖生物学 生殖生物学
- 细胞生物学 细胞生物学
背景情况:
- 轮 (ROT) 是一种具有不确定的生殖毒性天然杀虫剂.
- 男人生殖健康至关重要,了解农药的影响至关重要.
研究的目的:
- 为了研究罗特诺对男性生殖毒性的影响.
- 阐明内质网膜 (ER) 应激和亡在罗农诱导的丸损伤中的作用.
主要方法:
- 在28天的时间里,小鼠接受了不同剂量的罗诺 (0,2,4,8毫克/公斤/天) 治疗.
- 鼠标的莱迪格 (TM3) 细胞用罗特 (0.250,500,1000 nM) 进行治疗.
- 分析了ER应激和亡途径 (PERK-eIF2α-CHOP),使用4-酸 (4-PBA) 和GSK2606414.
主要成果:
- 罗坦诱导丸损伤,受损的精子生成,降低丸激素,以及莱迪格细胞亡.
- 轮破坏了ER的超结构,导致雷迪格细胞中的ER应激.
- 轮通过ER压力和PERK-eIF2α-CHOP通路触发了TM3细胞亡,而这被4-PBA和GSK2606414缓解了.
结论:
- 轮激素诱导的男性生殖毒性是由莱迪格细胞亡介导的.
- ER应激和PERK-eIF2α-CHOP信号通路是罗诺毒性的关键机制.
- 准ER应激通路可能提供治疗策略,防止罗农诱导的生殖损伤.
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