Abstract
Bisphenol A is an industrial chemical compound, pervasively polluting the environment and diet, classified as an endocrine disruptor because of its interference effects on the endocrine system. In zebrafish, BPA exposure induces follicular atresia. To acquire knowledge on this atretic effect, using a qualitative and quantitative histomorphological approach, we studied zebrafish ovarian follicular stage development in response to low BPA concentrations. Results show that BPA interferes with follicular progression by affecting the previtellogenic and vitellogenic phases. In particular, BPA exposure (i) increases follicular recruitment by acting on primary stage follicles, (ii) forces the follicular transition from stage III to stage IV producing enlarged stage IV follicles, and (iii) induces atresia by producing atretic follicles that are peculiarly enlarged (i.e., big atretic follicles). We suggest that BPA induces atresia by the primary effect on recruitment of stage I follicles. This forces follicular progression and produces stage IV follicles that are peculiarly enlarged that undertake the atretic development.
Highlights
Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide
We suggest that BPA forces the early follicular recruitment and peculiarly induces atresia by pushing follicular growth mechanisms associated with the vitellogenic phase
The morphological observations reported here demonstrate that BPA interferes with follicular progression affecting the previtellogenic and vitellogenic phases
Summary
Bisphenol A (BPA) is one of the highest volume chemicals produced worldwide. It is used to manufacture plastics, epoxy resins, hard plastic bottles, and metal-based food and beverage cans. We showed that 5 μg/L BPA promotes no transcriptional effect on genes involved in steroidogenesis (estrogen receptor, esr2b; steroidogenic acute regulatory protein, star; and cytochrome P450 family 11 subfamily A member, cyp11a1) and oocyte growth (follicle-stimulating hormone receptor, fshr) but significantly downregulates the expression of genes involved in ovarian development (estrogen receptors, esr and esr2a) [15], production of maturation hormone (luteinizing hormone/choriogonadotropin receptor, lhcgr), and acquisition of maturational competence (progesterone receptor membrane component, pgrmc and pgrmc2) with an increase in apoptotic gene expression (caspase and tumor protein 53) In this context, to acquire knowledge on the 5 μg/L BPA effects inducing follicular atresia, using a qualitative and quantitative histomorphological approach, we evaluated ovarian follicle stages in response to BPA exposure. The aim was to characterize the BPAinduced atresia (atretic effects) and decode the follicular stage primarily targeted by BPA exposure
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