Perinatal exposure to bisphenol A impairs the Mongolian gerbil ovarian follicle dynamics and its extracellular milieu

Abstract

Bisphenol A (BPA), a polycarbonate monomer commonly found in plastics, is an endocrine disruptor compound (EDC) that mimics the activity of steroid hormones. This study aimed to examine BPA’s effects on Mongolian gerbils’ ovary. Pregnant females (n = 5) were assigned to four groups and exposed by gavage to BPA at two doses (↓BPA, 50 µg/kg; ↑BPA, 5000 µg/kg), an oil vehicle (OC) or remained untreated (IC) from the eighth gestational day until weaning. One female from each offspring was euthanized at six months of age, and had their ovaries processed histologically. Cytochemistry was performed: HE for quantification and classification of follicles; Gomori’s Trichrome for collagen fibers; Resorcin-Fuchsin, for elastic fibers; and reticulin, for reticular fibers. Immunohistochemistry was used to analyze estrogen receptor alpha (ERα) and beta (ERβ), and the proliferative index. Results showed no significant differences in primary or secondary follicle counts among the IC, OC, ↓BPA, and ↑BPA groups. Antral follicles showed a higher incidence in the ↑BPA (6,4 ± 1,0) compared to the IC (2,7 ± 0,4) and OC (2,8 ± 0,4) groups. Collagen fiber density was significantly higher in the ↑BPA group (38,0 ± 7,5) compared to the OC group (20,7 ± 6,2). Similarly, elastic fibers were increased in the ↑BPA group (7,4 ± 0,9) relative to ↓BPA (1,8 ± 0,4), OC (2,3 ± 0,5) and IC (2,6 ± 0,9), as were reticular fibers (↑BPA: 31,5 ± 1,8; ↓BPA: 17,8 ± 2,6; OC: 14,1 ± 2,3; IC: 12,9 ± 1,2). Additionaly, BPA-exposed groups exhibited fewer interstitial glands, suggesting a reduction in steroidogenic potential. The tissue response to estrogens was elevated among animals from the ↑BPA group within activated follicles, regarding receptors alpha and beta. Higher proliferation indexes were present within activated follicles and interstitial steroidogenic glands from the ↑BPA group as well. Therefore, dysregulation of estrogenic response and establishment of fibrosis observed in our results indicate deleterious effects on the ovary’s morphophysiology, potentially leading to a pathological environment. This attests that perinatal exposure to BPA affects the offspring even in a long-term manner.