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人睾丸中孕酮在不同年龄、病理生理状况下以及雌激素或促性腺激素治疗期间的体外转化。

In vitro conversion of progesterone in the human testis at different ages, pathophysiological conditions, and during treatment with estrogens or gonadotrophic hormones.

作者信息

Hammar M, Petersson F, Berg A A

出版信息

Arch Androl. 1985;14(2-3):143-9. doi: 10.3109/01485018508988290.

Abstract

The enzyme 17 alpha-hydroxylase catalyzes the conversion of progesterone to 17 alpha-hydroxyprogesterone in the testis and may be studied with the use of incubation of testicular tissue with [3H] progesterone in vitro. The enzyme 20 alpha-hydroxysteroid dehydrogenase catalyzes the conversion of progesterone to 20 alpha-dihydroprogesterone. These enzymes were studied in testicular tissue from 105 human males regarding the effects of aging, different pathophysiological conditions, and gonadotrophic or estrogenic treatment. 17 alpha-Hydroxylase activity was low in vitro in testicular tissue from prepubertal boys, adult men with pituitary tumors, and estrogen-treated elderly men. In nontreated elderly men and certain infertile adult men, 17 alpha-hydroxylase was more active than in the above-mentioned patient groups, albeit lower than in adolescent and adult men. Gonadotropic treatment increased the conversion mediated by 17 alpha-hydroxylase in prepubertal as well as adult testicular tissue. In conclusion, the activity of 17 alpha-hydroxylase may be influenced by gonadotrophic hormones and may be an indicator of the testicular endocrine state at the moment of biopsy. Testicular 20 alpha-hydroxysteroid dehydrogenase seems to be active during low gonadotrophic influence and might even be inhibited by gonadotrophic stimulation.

摘要

17α-羟化酶可催化睾丸中孕酮转化为17α-羟孕酮,可通过在体外将睾丸组织与[3H]孕酮孵育来研究该酶。20α-羟类固醇脱氢酶可催化孕酮转化为20α-二氢孕酮。针对衰老、不同病理生理状况以及促性腺激素或雌激素治疗的影响,对105名男性的睾丸组织中的这些酶进行了研究。青春期前男孩、患有垂体肿瘤的成年男性以及接受雌激素治疗的老年男性的睾丸组织在体外的17α-羟化酶活性较低。在未接受治疗的老年男性和某些不育成年男性中,17α-羟化酶的活性高于上述患者组,尽管低于青少年和成年男性。促性腺激素治疗可增加青春期前以及成年睾丸组织中由17α-羟化酶介导的转化。总之,17α-羟化酶的活性可能受促性腺激素影响,并且可能是活检时睾丸内分泌状态的一个指标。睾丸20α-羟类固醇脱氢酶在促性腺激素影响较低时似乎具有活性,甚至可能受到促性腺激素刺激的抑制。

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