title: Neonatal exposure to bisphenol A reduces the pool of primordial follicles in the rat ovary.
abstract: We evaluated whether exposure to bisphenol A (BPA) disrupts neonatal follicle development in rats. From postnatal day 1 (PND1) to PND7, pups received corn oil (control), diethylstilbestrol (DES20: 20 μg/kg-d, DES0.2: 0.2 μg/kg-d), or BPA (BPA20: 20mg/kg-d, BPA0.05: 0.05 mg/kg-d). We examined follicular dynamics, multioocyte follicles (MOFs) incidence, proliferation and apoptosis rates, expression of steroid receptors (ERα, ERβ, 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 ERβ and proliferation were both increased in recruited follicles. ERα 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.
authors.affiliation: Laboratorio de Endocrinología y Tumores Hormonodependientes, Ciudad Universitaria, Paraje El Pozo, Facultad de Bioquímica y Ciencias Biológicas, Universidad Nacional del Litoral, CP 3000 Santa Fe, Argentina.
authors.forename: Horacio A
authors.initials: HA
authors.lastname: Rodríguez
authors.forename: Noelia
authors.initials: N
authors.lastname: Santambrosio
authors.forename: Clarisa G
authors.initials: CG
authors.lastname: Santamaría
authors.forename: Mónica
authors.initials: M
authors.lastname: Muñoz-de-Toro
authors.forename: Enrique H
authors.initials: EH
authors.lastname: Luque
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis / Q000187:drug effects; D001559:Benzhydryl Compounds; D049109:Cell Proliferation / Q000187:drug effects; D002470:Cell Survival / Q000187:drug effects; D050760:Cyclin-Dependent Kinase Inhibitor p27 / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D052244:Endocrine Disruptors / Q000008:administration & dosage / Q000633:toxicity*; D004968:Estrogens, Non-Steroidal / Q000008:administration & dosage / Q000633:toxicity*; D005260:Female; D005854:Germ Cells / Q000187:drug effects* / Q000254:growth & development / Q000378:metabolism / Q000473:pathology; D009866:Oogenesis / Q000187:drug effects*; D006080:Ovarian Follicle / Q000187:drug effects* / Q000254:growth & development* / Q000378:metabolism / Q000473:pathology; D010636:Phenols / Q000008:administration & dosage / Q000633:toxicity*; D016649:Primary Ovarian Insufficiency / Q000139:chemically induced; D020033:Protein Isoforms / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D011944:Receptors, Androgen / Q000378:metabolism; D011960:Receptors, Estrogen / Q000378:metabolism; D011980:Receptors, Progesterone / Q000378:metabolism; D000098826:Bisphenol A Compounds
chemical_list: D001559:Benzhydryl Compounds; D050760:Cyclin-Dependent Kinase Inhibitor p27; D052244:Endocrine Disruptors; D004968:Estrogens, Non-Steroidal; D010636:Phenols; D020033:Protein Isoforms; D011944:Receptors, Androgen; D011960:Receptors, Estrogen; D011980:Receptors, Progesterone; C493962:Cdkn1b protein, rat; C006780:bisphenol A; D000098826:Bisphenol A Compounds