Developmental exposure to perfluorooctane sulfonate(PFOS) impairs the endometrial receptivity.

Perfluorooctane sulfonate (PFOS) is a widely used chemical in industrial production. It can be introduced into the environment through multiple pathways and exhibits resistance to degradation. Recent research has demonstrated a significant correlation between its exposure levels in the human body and the incidence of various diseases. The expression of genes related to endometrial receptivity and the differentiation of human endometrial stromal cells (hESCs) were assessed in this study concerning PFOS. In this study, we investigated the effect of PFOS exposure on endometrial tolerance by cell and animal experiments. The activity against endometrial mesenchymal cells was significantly reduced by PFOS intervention, and the apoptosis flow assay results showed that PFOS significantly promoted cell death in a concentration-dependent manner. Transmission electron microscopy results revealed mitochondrial damage in the PFOS-intervened group, and WB results showed that the expression levels of endometrial tolerance-related proteins Homeobox A10 (HOXA10) and integrin beta3 (ITGB3) were decreased, and the expression level of Forkhead box O1 (FOXO1) protein was increased. Animal studies have shown that PFOS exposure can change uterine morphology, cause obvious damage to pinopodes morphology, change the estrous cycle of mice, and affect endometrial receptivity In the present study, we found that PFOS may synergistically affect the viability of endometrial mesenchymal stromal cells through accumulation in vivo, and that PFOS may contribute to the failure of embryo implantation by affecting mitochondrial function and consequently endometrial permissive sites.