Endogenous acetaldehyde toxicity during antral follicular development in the mouse ovary.
Reprod Toxicol
; 33(3): 322-30, 2012 Jun.
Article
en En
| MEDLINE
| ID: mdl-22285649
ABSTRACT
The biosynthesis of androgens requires multiple steps and during the conversion of pregnenolone to 17α-hydroxypregnenolone and dehydroepiandrosterone (DHEA) by CYP17a1. Acetaldehyde is potentially formed as a by-product in theca cells during antral follicular development. In this study, acetaldehyde level was significantly increased after eCG stimulation and reached a maximum level at 36-h post-eCG. By 48 h, the level of acetaldehyde decreased in association with the induction of aldehyde dehydrogenase (ALDH) type 1 family members. When immature mice were co-injected with the ALDH inhibitor, cyanamide, and eCG, the expression of genes involved in the differentiations of granulosa cells was suppressed and the number of ovulated oocytes was reduced. The in vitro studies showed that ALDH inhibitors prevented FSH-induced granulosa cell differentiation. These results indicate that acetaldehyde is generated as a by-product during steroidogenesis and can exert toxic effects to impair the differentiation of granulosa cells, reduce ovulation and decrease oocyte quality.
Texto completo:
1
Base de datos:
MEDLINE
Asunto principal:
Aldehído Deshidrogenasa
/
Folículo Ovárico
/
Acetaldehído
Idioma:
En
Revista:
Reprod Toxicol
Asunto de la revista:
EMBRIOLOGIA
/
MEDICINA REPRODUTIVA
/
TOXICOLOGIA
Año:
2012
Tipo del documento:
Article