在性成熟之前接触双S会通过Cathepsin L介导的颗粒状细胞死亡损害卵泡发育
Fei Li1, Fuhai Shen2, Yuxia Zhou3
1Clinical Research Center for Obstetrics and Gynecology, Key Laboratory of Maternal & Fetal Medicine of National Health Commission of China, Shandong Provincial Maternal and Child Health Care Hospital Affiliated to Qingdao University, Jinan 250001, China; Jinan (Preparatory) Key Laboratory of Women's Diseases and Fertility Preservation, Jinan 250014, China; School of Public Health, North China University of Science and Technology, Tangshan, Hebei 063210, China.
在青春期前暴露于Bisphenol S (BPS) 损害了卵巢储备和卵泡发育,因为它会导致颗粒状细胞死亡. 这种生殖毒性是由素S (CTSL) 介导的,它是亡途径中的关键酶.
科学领域:
- 生殖毒理学 生殖毒理学
- 环境健康 环境健康
- 分子生物学分子生物学
背景情况:
- 双S (BPS) 是一种环境污染物,可疑存在生殖风险.
- 青春期前BPS暴露对女性生殖发育的影响及其机制尚不清楚.
研究的目的:
- 为了研究早期BPS暴露与卵泡发育不良之间的关联.
- 阐明BPS诱导的生殖毒性背后的分子机制.
主要方法:
- 对3至16岁女孩尿液BPS水平的分析.
- 在前青春期大鼠模型中评估BPS对毛囊发育的影响.
- 在体外研究中使用颗粒细胞来检查分子通路.
主要成果:
- 在女性尿样中检测到BPS的高检测率 (95.7%).
- 在大鼠中,BPS暴露减少了卵巢储备,增加了异常毛囊.
- 在颗粒细胞中,BPS上调了甲素家族表达 (CTSL,CTSD,CTSB),激活了酶3并诱导了亡.
- 鉴定出CTSL是BPS诱导的粒状细胞死亡的关键调解者.
结论:
- 青春期前BPS暴露会损害卵泡发育和卵巢储备.
- BPS通过甲素S介导的亡诱导颗粒状细胞的死亡.
- 这些发现提供了对环境污染物诱导的女性生殖功能障碍的机制性见解.
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