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雌二醇和孕酮对大鼠卵巢17-羟化酶及3β-羟类固醇脱氢酶活性的影响。

The effects of estradiol and progesterone on rat ovarian 17-hydroxylase and 3 beta-hydroxysteroid dehydrogenase activities.

作者信息

Munabi A K, Cassorla F G, Pfeiffer D G, Albertson B D, Loriaux D L

出版信息

Steroids. 1983 Jan;41(1):95-8. doi: 10.1016/0039-128x(83)90019-3.

Abstract

Testosterone biosynthesis by Leydig cells can be modulated by estradiol. This modulation appears to occur at the 17-hydroxylase and 17,20-desmolase stage. In this study we have examined the effects of estradiol and progesterone on the activities of the 17-hydroxylase (17-OH) and 3 beta-hydroxysteroid dehydrogenase (3 beta-HSD) in rat ovarian tissue, to examine the hypothesis that estradiol may regulate these enzymes in the ovary as well as in the testis. Estradiol capsule implants produced a decrease in 17-OH activity (0.5 +/- 0.05 vs. 2.1 +/- 0.1 nmol/mg protein/min, mean +/- SEM, p less than 0.001), and an increase in 3 beta-HSD activity (15.5 +/- 0.9 vs 9.7 +/- 0.7 nmol/mg protein/min p less than 0.001). Progesterone injections produced a decrease in both 17-OH (0.9 +/- 0.1 vs. 2.3 +/- 0.2 p less than 0.005) and 3 beta-HSD (2.5 +/- .4 vs. 8.6 +/- 0.5; p less than 0.005) activities. We conclude that estradiol decreases 17-OH activity in the ovary as it does in the testis. This, coupled with an increase in 3 beta-HSD may explain the pre-ovulatory increase in progesterone seen in many species. Progesterone seems to decrease the steroidogenic activity of the ovarian tissue, perhaps offering an explanation for the gonadotropin resistance seen in corpus luteus bearing ovaries.

摘要

睾丸间质细胞的睾酮生物合成可受到雌二醇的调节。这种调节似乎发生在17-羟化酶和17,20-裂解酶阶段。在本研究中,我们检测了雌二醇和孕酮对大鼠卵巢组织中17-羟化酶(17-OH)和3β-羟类固醇脱氢酶(3β-HSD)活性的影响,以验证雌二醇可能在卵巢和睾丸中调节这些酶的假说。植入雌二醇胶囊使17-OH活性降低(0.5±0.05对2.1±0.1 nmol/mg蛋白/分钟,均值±标准误,p<0.001),3β-HSD活性升高(15.5±0.9对9.7±0.7 nmol/mg蛋白/分钟,p<0.001)。注射孕酮使17-OH(0.9±0.1对2.3±0.2,p<0.005)和3β-HSD(2.5±0.4对8.6±0.5;p<0.005)活性均降低。我们得出结论,雌二醇在卵巢中与在睾丸中一样会降低17-OH活性。这一点,再加上3β-HSD活性的增加,可能解释了许多物种排卵前孕酮的增加。孕酮似乎会降低卵巢组织的类固醇生成活性,这或许可以解释黄体化卵巢中出现的促性腺激素抵抗现象。

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