Impaired ovarian response to exogenous gonadotropins in female rat offspring born to mothers perinatally exposed to Bisphenol A

The ovary is sensitive to disruption by the environmental estrogen Bisphenol A (BPA). Our aim was to investigate whether perinatal exposure to BPA (50 μg/kg day), orally administered, affects ovarian response to exogenous gonadotrophins (PMSG or PMSG + hCG) in prepubertal female offspring. An altere...

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Detalles Bibliográficos
Autores: Santamaría, Clarisa Guillermina, Rodriguez, Horacio Adolfo, Abud, Julián Elías, Rivera, Oscar Edgardo, Muñoz de Toro, Monica Milagros, Luque, Enrique Hugo
Tipo de recurso: artículo
Estado:Versión publicada
Fecha de publicación:2017
País:Argentina
Institución:Consejo Nacional de Investigaciones Científicas y Técnicas
Repositorio:CONICET Digital (CONICET)
Idioma:inglés
OAI Identifier:oai:ri.conicet.gov.ar:11336/56123
Acceso en línea:http://hdl.handle.net/11336/56123
Access Level:acceso abierto
Palabra clave:Bisphenol A
Folliculogenesis
Ovarian Toxicology
https://purl.org/becyt/ford/3.1
https://purl.org/becyt/ford/3
Descripción
Sumario:The ovary is sensitive to disruption by the environmental estrogen Bisphenol A (BPA). Our aim was to investigate whether perinatal exposure to BPA (50 μg/kg day), orally administered, affects ovarian response to exogenous gonadotrophins (PMSG or PMSG + hCG) in prepubertal female offspring. An altered response to gonadotrophins was observed in BPA-exposed rats. Increased proportion of antral follicles, altered levels of ovarian steroidogenic enzymes, gonadotropin receptors, AR and ERβ were observed in PMSG group. Besides that, in response to PMSG + hCG, a persistent high Fshr mRNA expression and a decreased number of follicles with high expression of PR before ovulation were observed. After ovulation, there was an increase in antral atretic follicles, reduced Lhcgr mRNA expression and high serum levels of E2. Therefore, an early exposure to a low dose of BPA during perinatal period induces ovarian changes leading to an altered response to exogenous gonadotropin treatment later in life.