早期的BPS暴露会通过铁灭菌诱导后代小鼠的生殖毒性
Yan Su1, Xinxin Guo1, Nuo Xu1
1Guangxi Key Laboratory of Environmental Exposomics and Entire Lifecycle Health, School of Public Health, Guilin Medical University, Guilin 541199, China; Guangxi Health Commission Key Laboratory of Entire Lifecycle Health and Care, School of Public Health, Guilin Medical University, Guilin 541199, China.
Reproductive toxicology (Elmsford, N.Y.)
|January 28, 2026
概括
早期暴露在Bisphenol S (BPS) 中会损害小鼠的男性生殖健康,导致丸损伤和精子生产受损. 细胞死亡途径铁亡被认为是这些跨代效应背后的关键机制.
科学领域:
- 环境毒理学环境毒理学
- 生殖生物学 生殖生物学
- 内分泌干扰物 干扰内分泌干扰物
背景情况:
- 双S (BPS) 是一种内分泌干扰剂,已知具有生殖毒性.
- 早期BPS暴露对男性生殖的跨代影响尚不清楚.
研究的目的:
- 调查早期BPS暴露对后代男性生殖发育的影响.
- 阐明涉及BPS诱导的生殖损伤的潜在机制,包括铁亡.
主要方法:
- 建立了一个小鼠模型,在生命早期暴露于不同剂量的BPS.
- 评估丸结构,精子参数,丸激素水平,氧化应激标志物和与铁亡相关的蛋白质.
- 在TM3莱迪格细胞中利用Fer-1治疗来验证ferroptosis的参与.
主要成果:
- 早期的BPS暴露导致丸损伤,降低了精子质量,并抑制了水平.
- 暴露于BPS导致氧化应激,丸铁积累和线粒体损伤.
- 铁亡标志物 (ACSL4,TFR1,GPX4,SLC7A11) 发生了变化,Fer-1治疗挽救了缺乏症.
结论:
- 早期的BPS暴露会以跨世代的方式引起男性的显著生殖毒性.
- 铁亡是一种关键的机制,可以调解BPS诱导的男性生殖损伤.
- 这些发现为环境内分泌干扰剂 (如BPS) 的毒理学影响提供了新的见解.
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