草甘驱动自依赖性铁亡,以抑制小鼠莱迪格细胞中丸激素的合成
Lu Lu1, Cai-Yu Lian1, Yan-Ting Lv1
1College of Veterinary Medicine, Shandong Provincial Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Provincial Engineering Technology Research Center of Animal Disease Control and Prevention, Shandong Agricultural University, 61 Daizong Street, Tai'an City, Shandong Province 271018, China.
The Science of the total environment
|January 10, 2024
概括
草甘除草剂暴露会触发细胞死亡途径ferroptosis,导致莱迪格细胞中受阻的丸激素合成. 准NCOA4介导的费里丁菌可能为男性生殖毒性提供治疗策略.
科学领域:
- 生殖毒理学 生殖毒理学
- 细胞死亡机制 细胞死亡机制
- 生物化学 生物化学
背景情况:
- 草药草甘 (GLY) 通过抑制丸激素合成,对男性生殖健康产生负面影响.
- 铁,一种依赖于铁的细胞死亡,与降低激素分泌有关.
- 在GLY诱导的丸激素抑制中,铁酶的具体作用仍然在很大程度上是未知的.
研究的目的:
- 为了研究铁灭菌在草甘诱导的丸莱迪格细胞中丸丸合成的抑制中的参与.
- 阐明潜在的机制,包括铁过载,谷氨酸枯竭和费里丁.
主要方法:
- 使用TM3莱迪格细胞暴露于1mM草甘,建立了体外模型.
- 评估了细胞毒性,合成,脂质过氧化和细胞内铁离子 (Fe2+) 水平.
- 研究了铁灭菌抑制剂,NCOA4 (核受体协活性剂4) 和铁类菌的作用.
主要成果:
- 暴露于草甘诱导了细胞毒性,并通过铁灭酶抑制了的合成.
- 细胞内Fe2+过载和谷氨耗尽是铁亡的关键决定因素.
- 通过释放Fe2+来促进铁亡的机制被确定为NCOA4介导的铁亡,其敲击减轻了GLY的毒性.
结论:
- 草甘诱导的男性生殖毒性是由ferroptosis介导的,由NCOA4依赖的ferritinophagy和铁积累驱动.
- 阻断铁或NCOA4介导的铁代谢显示了针对GLY生殖毒性的治疗干预的潜力.
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