Leydig cell aging and the mechanisms of reduced testosterone synthesis

被引:165
作者
Midzak, Andrew S. [1 ]
Chen, Haolin [1 ]
Papadopoulos, Vassilios [2 ]
Zirkin, Barry R. [1 ]
机构
[1] Johns Hopkins Bloomberg Sch Publ Hlth, Div Reprod Biol, Dept Biochem & Mol Biol, Baltimore, MD 21205 USA
[2] McGill Univ, McGill Univ Hlth Ctr, Res Inst, Montreal, PQ H3H 2R9, Canada
关键词
Leydig cell; Testosterone; Luteinizing hormone; Steroidogenesis; ACUTE REGULATORY PROTEIN; LUTEINIZING-HORMONE RECEPTORS; BROWN-NORWAY RAT; MITOCHONDRIAL CHOLESTEROL TRANSPORT; NICOTINAMIDE-ADENINE DINUCLEOTIDE; AGE-RELATED DECLINE; BENZODIAZEPINE-RECEPTOR; ARACHIDONIC-ACID; STEROIDOGENIC ENZYMES; LIPID-PEROXIDATION;
D O I
10.1016/j.mce.2008.07.016
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
In mates, serum testosterone levels decline with advancing age. Though part of a complex process, this age-related decline in testosterone appears to occur, in part, due to a significant decline in the ability of aged Leydig cells to produce testosterone maximally in response to luteinizing hormone (LH). The structure of the molecular machinery responsible for the synthesis of testosterone is described, and placed in the context of Leydig cell biology. Multiple parameters related to the synthesis of testosterone by the Leydig cell have been observed to change with age. Relationships among these changes are reviewed. A discussion of potential causes of the age-related decline in Leydig cell steroidogenic capacity presents a model in which the inability of aged cells to adequately respond to hormonal stimulation results in cellular regression with concomitant decline in maximal testosterone output. (C) 2008 Published by Elsevier Ireland Ltd.
引用
收藏
页码:23 / 31
页数:9
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