Implications of early-life BPS-induced thyroid disruption on adult female reproductive disorders.

Reproductive disorders have become a growing public health concern, with early-life environmental exposures increasingly recognized as critical determinants of long-term reproductive outcomes. Among emerging endocrine disruptors, bisphenol S (BPS) raises concern due to its potential to interfere with hormone signaling during sensitive developmental windows. This study examined whether prenatal BPS exposure affects reproductive outcomes in adulthood through maternal thyroid disruption. Pregnant rats were exposed to BPS and the thyroid hormone receptor (THR) antagonist (AT 1-850). Key parameters studied included body weight, ovarian function (puberty onset, estrous cyclicity, histology, hormone levels), oxidative status, and oocyte development gene expression. Our findings support a model in which maternal thyroid disruption during critical developmental stages leads to long-term alterations in ovarian function and architecture, significantly impacting female reproductive health. This disruption is further corroborated by the striking similarity between the effects observed with BPS exposure and those induced by the THR antagonist, suggesting a common underlying mechanism. Despite a normal oxidative status, reproductive disturbances emerged as early pubertal onset, with accelerated vaginal opening and earlier first estrous. Irregular estrous cycles were noted, with prolonged estrus and metestrus phases. Folliculogenesis was impaired, marked by the accumulation of primordial, primary, and atretic follicles, and a blockade in progression to the secondary stage. Oocyte development was also altered, evidenced by elevated FIGLα and H1FOO expression. These disruptions were associated with hormonal imbalance, particularly decreased E2 levels. Altogether, these outcomes suggest that early-life BPS exposure compromises female reproductive function and efficiency in adulthood through maternal thyroid disruption.