Age-related decreased Leydig cell testosterone production in the brown Norway rat.
Age-related decreased Leydig cell testosterone production in the brown Norway rat.
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DOI：
10.1002/j.1939-4640.1994.tb00498.x
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发表时间：
1994-11
影响因子：
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通讯作者：
Haolin Chen;Matthew P. Hardy;Ilpo T. Huhtaniemi;B. Zirkin
中科院分区：
文献类型：
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作者：
Haolin Chen;Matthew P. Hardy;Ilpo T. Huhtaniemi;B. Zirkin
先前的研究表明，在布朗挪威大鼠中，睾丸间质细胞睾酮的产生随着年龄的增长而减少。本文所述研究的目的是检验年龄相关的类固醇生成下降的以下可能解释：（1）间质细胞数量下降;（2）促黄体激素（LH）刺激不足;（3）单个间质细胞产生睾酮的能力降低;（4）生殖细胞损失的影响。用离心淘洗法和Percoll密度梯度离心法从青年和老年大鼠睾丸中分离出的间质细胞，在最大程度地用LH或二丁酰环腺苷酸（dbcAMP）刺激时，检测其产生睾酮的能力。用体视学方法原位检测睾丸间质细胞的数量和体积。血清LH水平采用高灵敏度免疫荧光测定法测定。平均Leydig细胞体积随年龄的增长而下降，并与此观察一致，从老龄大鼠分离的单个Leydig细胞产生的睾酮显着低于年轻大鼠的细胞是否在体外培养的最大刺激LH或与dbcAMP。与年龄相关的睾酮产生减少不能用间质细胞数量、血清LH水平、间质细胞对LH的反应性或睾丸生殖细胞含量的变化来解释。综合这些结果，表明老年大鼠睾酮生成减少与LH受体-cAMP级联反应以外的类固醇生成途径缺陷有关。导致类固醇生成减少的初始年龄相关变化的性质尚不清楚，因此不知道这些变化是Leydig细胞内在的还是外在的。
Previous studies have demonstrated that Leydig cell testosterone production diminishes with age in Brown Norway rats. The objective of the studies presented herein was to test the following possible explanations for age-related decline in steroidogenesis: (1) decline in Leydig cell number; (2) understimulation by luteinizing hormone (LH); (3) reduced ability of individual Leydig cells to produce testosterone; and (4) influence of loss of germ cells. Leydig cells isolated from the testes of young and aged rats by centrifugal elutriation and Percoll density gradient centrifugation were examined for their ability to produce testosterone when stimulated maximally with LH or with dibutyryl cyclic AMP (dbcAMP). Leydig cell number and volume were examined in situ using stereological methods. Serum LH levels were measured using a highly sensitive immunofluorometric assay. Average Leydig cell volume decreased with age, and consistent with this observation, individual Leydig cells isolated from aging rats produced significantly less testosterone than those from young rats whether the cells were cultured in vitro with maximally stimulating LH or with dbcAMP. The age-associated diminished testosterone production could not be explained by changes in Leydig cell number, serum LH levels, Leydig cell responsiveness to LH, or testicular germ cell content. These results, taken together, suggest that the reduced testosterone production seen in aged rats is related to defects in the steroidogenic pathway beyond the LH receptor-cAMP cascade. The nature of the initial age-related changes that cause reduced steroidogenesis is not known, and therefore it is not known whether such changes are intrinsic or extrinsic to the Leydig cells.