Mechanism by which 17 beta-estradiol inhibits ovarian androgen production in the rat.
Mechanism by which 17 beta-estradiol inhibits ovarian androgen production in the rat.
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发表时间：
1981
期刊：
影响因子：
4.8
通讯作者：
D. Magoffin;G. Erickson
中科院分区：
文献类型：
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作者：
D. Magoffin;G. Erickson
探讨了17β-雌二醇抑制卵巢雄激素生物合成的机制。未成熟的25日龄大鼠用雌二醇处理2d后，将整个卵巢分散，检测促性腺激素结合和cAMP及类固醇激素的产生。当未处理的对照卵巢分散细胞与hCG(100 ng/ml)孵育时，类固醇的产生显著增加(10倍)，主要类固醇是孕酮和雄烯二酮。HCG对类固醇合成的刺激作用呈剂量依赖性(ED50=100pg/mlhCG)。雌二醇处理2天后，卵巢细胞对雄烯二酮、睾酮、17α-羟孕烯醇酮和17α-羟孕酮的最大hCG刺激作用被抑制了90%，孕烯醇酮的产生没有变化，而孕酮的产生增加了30%。时程研究表明，雌二醇作用12h后，hCG对雄激素产生的刺激作用被最大限度地抑制(90%)。单侧卵巢囊下植入迷你雌二醇胶囊后，hCG对雌二醇处理细胞产生雄激素的刺激作用降低了77%，而孕酮的产生无明显变化。HCG刺激的对侧卵巢类固醇激素合成未见改变。雌二醇处理不影响卵巢的结合能力、hCG对cAMP产生的刺激或卵巢中产生类固醇的细胞数量。实验结果表明，外源性雌二醇通过快速抑制17α-羟化作用，直接作用于大鼠卵巢，消除hCG对雄激素产生的刺激作用。
The mechanism by which 17 beta-estradiol inhibits ovarian androgen biosynthesis was investigated. Immature 25-day-old rats were treated for 2 days with estradiol, after which whole ovaries were dispersed, and gonadotropin binding and cAMP and steroid hormone production were examined. When dispersed cells from untreated control ovaries were incubated with hCG (100 ng/ml), there were marked increases (10-fold) in steroid production, with the major steroids being progesterone and androstenedione. The stimulation of steroidogenesis by hCG was dose-related (ED50 = 100 pg/ml hCG). After 2 days of estradiol treatment, the maximum hCG stimulation of androstenedione, testosterone, 17 alpha-hydroxypregnenolone, and 17 alpha-hydroxyprogesterone production by ovarian cells was inhibited by 90%; pregnenolone production was unchanged, while progesterone production was increased by 30%. Time course studies showed that the stimulatory effect of hCG on androgen production was maximally inhibited (90%) after 12 h of estradiol treatment. Implanting miniestradiol capsules unilaterally under the ovarian bursa caused a 77% decrease in the hCG stimulation of androgen production by the estradiol-treated cells, while progesterone production was unchanged. hCG-stimulated steroidogenesis in the contralateral ovary was not altered. Estradiol treatment did not affect the binding capacity, the hCG stimulation of cAMP production, or the number of steroid-producing cells in the ovaries. It is concluded from these experiments that exogenous estradiol acts directly on the rat ovary to abolish the hCG stimulation of androgen production by rapidly inhibiting 17 alpha-hydroxylation.