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Although prior studies indicate that PFOS exposure causes female reproductive disorders, the underlying mechanism remains obscure. This study investigates the molecular mechanisms underlying PFOS\u2010induced female reproductive toxicity at human\u2010relevant exposure levels. These results demonstrate that PFOS exposure (0.2 and 20\u00a0\u00b5\n                    <jats:sc>M<\/jats:sc>\n                    ) significantly reduces polar body extrusion (PBE) and delays germinal vesicle breakdown (GVBD) in oocytes. Additionally, PFOS exposure (1\u00a0mg\u00a0kg\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00a0day\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) decreases the proportion of two\u2010cell embryos and reduces progesterone (P4) levels. Elevated O\u2010GlcNAcylation levels are observed in both ovaries and granulosa cells (GCs) under PFOS treatment. Proteomic profiling of protein O\u2010GlcNAcylation identifies that the O\u2010GlcNAcylation of forkhead box k1 (FOXK1)\u00a0at threonine (Thr) 573 cite involved in ovarian steroidogenesis. Mechanistically, co\u2010immunoprecipitation (Co\u2010IP) combined with LC\u2010MS\/MS analysis reveals a physical interaction between FOXK1\u00a0and pescadillo ribosomal biogenesis factor 1 (PES1). Increased O\u2010GlcNAcylation of FOXK1 at Thr573 inhibits the ubiquitination\u2010mediated degradation of PES1, leading to elevated PES1 expression. Furthermore, PES1 promotes aldo\u2010keto reductase family 1, member C18 (AKR1C18)\u00a0to reduce P4 levels, ultimately disrupting oocyte maturation and early embryonic development. Overall, this study provides valuable insights into the role of protein post\u2010translational modifications in oocyte maturation and embryonic development under PFOS exposure.\n                  <\/jats:p>","DOI":"10.1002\/advs.202514857","type":"journal-article","created":{"date-parts":[[2025,12,13]],"date-time":"2025-12-13T04:22:11Z","timestamp":1765599731000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["PFOS Disrupts Oocyte Maturation and Early Embryonic Development via Ovarian FOXK1 O\u2010GlcNAcylation in Mice"],"prefix":"10.1002","volume":"13","author":[{"given":"Shuwen","family":"Han","sequence":"first","affiliation":[{"name":"State Key Laboratory of Reproductive Medicine Center for Global Health School of Public Health Nanjing Medical University  Nanjing 211166 China"},{"name":"Key Laboratory of Modern Toxicology of Ministry of Education, School of Public Health Nanjing Medical University  Nanjing 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