在小鼠卵巢窦卵泡发育过程中内源性乙醛毒性。
Endogenous acetaldehyde toxicity during antral follicular development in the mouse ovary.
机构信息
Graduate School of Biosphere Science, Hiroshima University, Higashi-Hiroshima, Hiroshima 739-8528, Japan.
出版信息
Reprod Toxicol. 2012 Jun;33(3):322-30. doi: 10.1016/j.reprotox.2012.01.001. Epub 2012 Jan 18.
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.
摘要
雄激素的生物合成需要多个步骤，在这个过程中，CYP17a1 将孕烯醇酮转化为 17α-羟孕烯醇酮和脱氢表雄酮 (DHEA)。在窦卵泡发育过程中，颗粒细胞中可能会潜在地形成乙醛作为副产物。在这项研究中，eCG 刺激后乙醛水平显著增加，在 eCG 后 36 小时达到最高水平。到 48 小时时，乙醛水平下降，同时诱导醛脱氢酶 (ALDH) 家族成员 1 型。当不成熟的小鼠同时注射 ALDH 抑制剂氰氨和 eCG 时，参与颗粒细胞分化的基因表达受到抑制，排卵的卵母细胞数量减少。体外研究表明，ALDH 抑制剂可阻止 FSH 诱导的颗粒细胞分化。这些结果表明，乙醛是类固醇生成过程中的副产物，可产生毒性作用，损害颗粒细胞的分化，减少排卵并降低卵母细胞质量。
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