Testicular maturation in the rat. In vivo effect of gonadotropins on steroidogenic enzymes in the hypophysectomized immature rat.

Testicular maturation in the rat. In vivo effect of gonadotropins on steroidogenic enzymes in the hypophysectomized immature rat.
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大鼠睾丸成熟。

DOI:
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发表时间:
1979
影响因子:
3.6
通讯作者:
Anita H. Payne
Anita H. Payne
中科院分区:
生物学2区
文献类型:
--
作者:
E. Murono;Anita H. Payne

文献摘要

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用LH或FSH处理垂体切除的未成熟大鼠,以评估这些激素在性成熟过程中对睾丸类固醇生成酶活性的作用。在第21天切除大鼠垂体,并在第27天开始激素治疗,持续5或10天。测定10,000 X g睾丸匀浆上清液的17 β 3-羟基类固醇脱氢酶、β-3 α-羟基类固醇脱氢酶异构酶、5 β s-还原酶和5 n-雄甾烷-3 α +3 β-羟基类固醇脱氢酶活性。垂体切除后,所有酶活性均下降。LH处理10天,5 n-还原酶活性提高6倍,β ′-3 β-羟基类固醇脱氢酶活性提高4倍,5 ′ s-雄甾烷-3o +3j 3-羟基类固醇脱氢酶活性提高2倍,17 ′ 1-羟基类固醇脱氢酶活性仅提高50%。FSH处理10天后,17 P-羟类固醇脱氢酶活性增加2倍以上。虽然FSH处理5天显著增加β-羟基类固醇脱氢酶异构酶活性(56%)和5 n-雄甾烷-3 n +3 f-羟基类固醇脱氢酶活性(30%),但这些增加在10天的处理期内没有维持。FSH处理既没有维持也没有刺激作用的Scs-还原酶活性。FSH处理增加1713-羟基类固醇脱氢酶活性的证明与我们先前的假设一致(Payne等人,1977),性成熟过程中17 F3-羟基类固醇脱氢酶活性的增加可能受FSH调节,这可能是FSH增加睾丸对LI-1反应性的一种机制。
Hypophysectomized immature rats were treated with LH or FSH to assess the role of these hormones on the activity of testicular steroidogenic enzymes during sexual maturation. Rats were hypophysectomized on Day 21 and hormone treatment was initiated on Day 27 and continued for 5 or 10 days. A 10,000 X g supernatant of testicular homogenates was assayed for 17j3-hydroxysteroid dehydrogenase, � -3a-hydroxysteroid dehydrogenase-isomerase, 5�s-reductase and 5 n-androstane-3a+3�-hydroxysteroid dehydrogenase activities. All enzyme activities decreased after hypophysectomy. Treatment with LH for 10 days stimulated 5n-reductase by 6-fold, �‘-3�-hydroxysteroid dehydrogenase by 4-fold, 5�s-androstane-3o+3j3-hydroxysteroid dehydrogenase by 2-fold and 17�1-hydroxysteroid dehydrogenase by only 50%. In constrast, treatment with FSH for 10 days stimulated 17P-hydroxysteroid dehydrogenase more than 2-fold. Although FSH treatment for 5 days significantly increased �-3#{216}-hydroxysteroid dehydrogenase-isomerase activity (56%) and 5n-androstane-3n+3f3-hydroxysteroid dehydrogenase activity (30%), these increases were not maintained for the 10 day treatment period. FSH treatment had neither a maintenance nor a stimulatory effect on Scs-reductase activity. The demonstration that FSH treatment increased 1 713-hydroxysteroid dehydrogenase activity is consistent with our previous hypothesis (Payne et al., 1977) that the increase in 17f3-hydroxysteroid dehydrogenase activity during sexual maturation may be regulated by FSH and that this may be one mechanism by which FSH increases testicular responsiveness to LI-I.