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成年食蟹猴睾酮诱导促性腺激素抑制后精原细胞发育和精子排放受损。

Impairment of spermatogonial development and spermiation after testosterone-induced gonadotropin suppression in adult monkeys (Macaca fascicularis).

作者信息

O'Donnell L, Narula A, Balourdos G, Gu Y Q, Wreford N G, Robertson D M, Bremner W J, McLachlan R I

机构信息

Prince Henry's Institute of Medical Research, Clayton, Victoria 3168, Australia.

出版信息

J Clin Endocrinol Metab. 2001 Apr;86(4):1814-22. doi: 10.1210/jcem.86.4.7400.

Abstract

Human male hormonal contraceptive regimens do not consistently induce azoospermia, and the basis of this variable response is unclear. This study used nine adult macaque monkeys (Macaca fascicularis) given testosterone (T) implants for 20 weeks to study changes in germ cell populations in relation to sperm output. Germ cell numbers were determined using the optical disector stereological method. Four animals achieved consistent azoospermia (azoo group), whereas five animals did not (nonazoo group). T-induced gonadotropin suppression in all animals decreased A pale (Ap) spermatogonia to 45% of baseline within 2 weeks, leading to decreased B spermatogonia (32--38%) and later germ cells (20--30%) after 14 and 20 weeks. Though the reduction in later germ cell types could be primarily attributed to the loss of spermatogonia, the data suggested that some cells were lost during the spermatocyte and spermatid phase of development. B spermatogonial number was more markedly suppressed in azoospermic animals, compared with the nonazoo group, as was the conversion ratio between Ap and B spermatogonia. Abnormal retention of elongated spermatids (failed spermiation) was also prominent in some animals after long-term T administration. We conclude that: 1) the variable suppression of sperm output is attributed to the degree of inhibition of germ cell development from type B spermatogonia onwards, and this is related to the degree of FSH suppression; and 2) inhibition of Ap and B spermatogonial development and of spermiation are the major defects caused by long-term T administration to monkeys.

摘要

人类男性激素避孕方案并不能持续诱导无精子症,这种可变反应的基础尚不清楚。本研究使用9只成年食蟹猴给予睾酮(T)植入物20周,以研究生殖细胞群体变化与精子输出的关系。使用光学分割体视学方法确定生殖细胞数量。4只动物实现了持续无精子症(无精子组),而5只动物未实现(非无精子组)。所有动物中T诱导的促性腺激素抑制在2周内使A型精原细胞(Ap)减少至基线的45%,导致14周和20周后B型精原细胞(减少32%-38%)和后期生殖细胞(减少20%-30%)减少。虽然后期生殖细胞类型的减少可能主要归因于精原细胞的损失,但数据表明在发育的精母细胞和精子细胞阶段有些细胞丢失了。与非无精子组相比,无精子症动物中B型精原细胞数量受到更明显的抑制,Ap和B型精原细胞之间的转化率也是如此。长期给予T后,一些动物中也出现了长形精子细胞异常滞留(精子形成失败)。我们得出结论:1)精子输出的可变抑制归因于从B型精原细胞开始的生殖细胞发育抑制程度,这与FSH抑制程度有关;2)Ap和B型精原细胞发育的抑制以及精子形成的抑制是长期给猴子施用T所导致的主要缺陷。

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