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在小鼠中,PFOS通过卵巢FOXK1O-GlcNAcylation干扰卵细胞成熟和早期胚胎发育

Shuwen Han^1,2, Qin Yuan^1,2, Zhu Wu^1,2

¹State Key Laboratory of Reproductive Medicine, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, 211166, China.

Advanced science (Weinheim, Baden-Wurttemberg, Germany)

|December 13, 2025

概括

perfluorooctane sulfonate (PFOS) 通过损害卵细胞成熟和胚胎发育来破坏雌性生殖. 这通过高O-GlcNAcylation发生,影响FOXK1和PES1等关键蛋白质,最终降低孕激素水平.

科学领域:

生殖毒理学生殖毒理学
分子内分泌学分子内分泌学
发展生物学发展生物学

背景情况:

perfluorooctane sulfonate (PFOS) 是一种持久性环境污染物,与生殖毒性有关.
PFOS诱导的女性生殖功能障碍的精确分子机制在很大程度上是未知的.

研究的目的:

阐明PFOS损害卵细胞成熟和早期胚胎发育的分子途径.
调查蛋白质O-GlcNAcylation在PFOS介导的生殖毒性中的作用.

主要方法:

卵细胞成熟测试 (极体挤出,生殖囊泡分解)
胚胎发育评估 (两细胞胚胎比例)
激素水平量的量化 (孕激素)
对O-GlcNAcylated蛋白质的蛋白质组学分析
在蛋白相互作用研究中,共免疫沉降和LC-MS/MS用于蛋白相互作用研究.

主要成果:

暴露于PFOS减少了极体挤出,并延迟了卵细胞中生殖囊泡的分解.
PFOS降低了双细胞胚胎比例和孕激素水平.
在卵巢和粒粉细胞中,PFOS增加了O-GlcNAcylation,特别是在Thr573.3的FOXK1上.
通过抑制其无化介导的降解,包括FOXK1-PES1相互作用,PFOS增加了PES1的表达.
升高的PES1促进了AKR1C18活动,降低了孕激素并扰乱了发育.

结论:

暴露于PFOS会通过O-GlcNAcylation依赖的机制破坏女性的生殖过程.
FOXK1-PES1-AKR1C18轴是PFOS毒性的关键目标,影响类固醇生成和卵细胞质量.
了解这些分子事件可以了解环境对生殖健康的影响.

关键词:

这是一种O-GlcNAcylation.在PFOS系统中,我们可以早期胚胎发育的早期发展.卵细胞成熟的过程孕激素是孕激素的一种.

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