| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 2594171 | Reproductive Toxicology | 2012 | 9 Pages |
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.
► We analyzed the kinetic changes of acetaldehyde level in ovary during follicular development. ► The level was transiently increased as a byproduct in a steroidogenic pathway. ► However, the level was decreased in an ALDH dependent manner. ► The reduction of acetaldehyde level was required for granulosa cell differentiation during follicular development.
