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分离的成年小鼠睾丸间质细胞的类固醇生成能力不会随年龄增长而下降。

Steroidogenic capacity of isolated adult mouse Leydig cells does not decrease with age.

作者信息

Schäfer G, Holstein A F, Hilz H

出版信息

Endocrinology. 1982 Apr;110(4):1362-6. doi: 10.1210/endo-110-4-1362.

Abstract

Leydig cells were isolated from the testes of adult young (5--7 months), old (21 months), and senile (27 months) mice using a highly preservative Percoll procedure. The yield in Leydig cells per testis from young animals was slightly lower than from the old age groups. hCG-induced testosterone synthesis proceeded in a linear fashion for at least 5 h in all three groups. The maximal steroidogenic capacity of cells from old animals was identical to that from young adults. There was no significant difference between Leydig cells from young and old mice with respect to hCG-induced cAMP accumulation and protein kinase activation. Determination of hCG concentrations required for half-maximal stimulation of testosterone synthesis and cAMP accumulation showed identical, or even lower, values in the old age groups. The phenomenon may be connected with the significant augmentation with age of the DNA content per cell (polyploidization), possibly acting as a compensatory mechanism of age-induced deficiencies. Detailed kinetic studies of cAMP accumulation, protein kinase activation, protein kinase activation, and steroidogenesis as well as ultrastructural analyses support the findings of unimpaired or increased capacities of the testosterone-forming cells in old animals. Thus, the aging of Leydig cells appears to differ from that of other tissues of the mouse (e.g. skeletal muscle), which exhibit decreasing abilities to respond to stimuli.

摘要

采用高度防腐的 Percoll 程序,从成年幼龄(5 - 7 个月)、老龄(21 个月)和老年(27 个月)小鼠的睾丸中分离出 Leydig 细胞。幼龄动物每个睾丸中 Leydig 细胞的产量略低于老龄组。在所有三个组中,hCG 诱导的睾酮合成至少在 5 小时内呈线性进行。老龄动物细胞的最大类固醇生成能力与年轻成年动物的相同。在 hCG 诱导的 cAMP 积累和蛋白激酶激活方面,幼龄和老龄小鼠的 Leydig 细胞之间没有显著差异。测定睾酮合成和 cAMP 积累半最大刺激所需的 hCG 浓度,老龄组的值相同,甚至更低。这种现象可能与细胞 DNA 含量随年龄显著增加(多倍体化)有关,这可能是一种年龄诱导缺陷的补偿机制。对 cAMP 积累、蛋白激酶激活、蛋白激酶激活和类固醇生成的详细动力学研究以及超微结构分析支持了老龄动物中睾酮生成细胞能力未受损或增强的发现。因此,Leydig 细胞的衰老似乎与小鼠的其他组织(如骨骼肌)不同,后者对刺激的反应能力呈下降趋势。

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