Neonatal exposure to bisphenol A reduces the pool of primordial follicles in the rat ovary

RODRÍGUEZ HORACIO ADOLFO; SANTAMBROSIO NE; SANTAMARÍA, CG; MUÑOZ DE TORO MM; LUQUE EH

REPRODUCTIVE TOXICOLOGY (ELMSFORD, N.Y.)

PERGAMON-ELSEVIER SCIENCE LTD

Lugar: Amsterdam; Año: 2010 vol. 30 p. 550 - 557

0890-6238

We evaluated whether exposure to bisphenol A (BPA) disrupts neonatal follicle development in rats. Frompostnatal day 1 (PND1) to PND7, pups received corn oil (control), diethylstilbestrol (DES20: 20 g/kgd, DES0.2: 0.2 g/kg-d), or BPA (BPA20: 20 mg/kg-d, BPA0.05: 0.05 mg/kg-d). We examined folliculardynamics, multioocyte follicles (MOFs) incidence, proliferation and apoptosis rates, expression of steroidreceptors (ER, ER, PR, AR) and cyclin-dependent kinase inhibitor 1B (p27) in PND8 ovaries. DES20,DES0.2 and BPA20-ovaries showed fewer primordial follicles and increased growing follicles. DES20-ovaries exhibited increased incidence of MOFs. Oocyte survival, AR, PR and apoptosis were not changed.Primordial and recruited follicles from BPA20-ovaries showed higher p27, whereas ER and proliferationwere both increased in recruited follicles. ER positive primary follicles increased in BPA 20-ovaries.Results show that BPA reduces the primordial follicle pool by stimulating the neonatal initial recruitment,associated with an increased proliferation rate likely mediated by an estrogenic pathway