EFFECT OF LONG-TERM DEPRIVATION OF LUTEINIZING-HORMONE ON LEYDIG-CELL VOLUME, LEYDIG-CELL NUMBER, AND STEROIDOGENIC CAPACITY OF THE RAT TESTIS
EFFECT OF LONG-TERM DEPRIVATION OF LUTEINIZING-HORMONE ON LEYDIG-CELL VOLUME, LEYDIG-CELL NUMBER, AND STEROIDOGENIC CAPACITY OF THE RAT TESTIS
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DOI：
10.1210/endo-123-6-2906
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发表时间：
1988-12-01
期刊：
影响因子：
4.8
通讯作者：
EWING, LL
中科院分区：
文献类型：
--
作者：
KEENEY, DS;MENDISHANDAGAMA, SMLC;EWING, LL
LH 剥夺后 1-2 周内，Leydig 细胞萎缩，失去细胞质体积和分泌睾酮的能力。我们研究了长期（0-16 周）LH 剥夺对平均间质细胞体积、每个睾丸间质细胞体积、每个睾丸间质细胞数量以及体外灌注睾丸睾酮分泌的影响。成年大鼠的内源性黄体生成素通过睾酮/雌二醇填充 (TE) 硅橡胶植入物受到抑制。通过以下方式验证睾丸中间质细胞的存在：1)使用光学和电子显微镜进行形态学检查，2)3.β.-羟基类固醇脱氢酶活性（3.β.HSD)的组织化学定位，和3)通过体外灌注睾丸将孕烯醇酮转化为黄体酮。对照组和治疗组大鼠间质细胞形态存在显着的数量差异。 TE植入后平均间质细胞的体积和每个睾丸间质细胞的总体积迅速且进行性地减少（P < 0.01）。第 16 周时，Leydig 细胞平均损失了 90% 的细胞质体积和 65% 的细胞核体积。方差分析未能检测到每个睾丸的 Leydig 细胞数量显着下降，尽管治疗 16 周的大鼠 (18.7 +-1.5 × 106) 中的值较对照大鼠 (22.2 + - 1.5 × 106) 减少了 16%。 TE植入后，体外灌注睾丸LH刺激的睾酮分泌在1周时迅速减少(P < 0.01)至对照值的5%，并在4-16周期间低于对照值的0.3%。相比之下，根据孕烯醇酮转化为黄体酮的比率，16 周时保留了 25% 的 3.β.HSD 活性（与对照相比，P < 0.01）。此外，当类固醇分泌率以间质细胞细胞质的单位体积表示时，治疗大鼠的睾丸分泌黄体酮的速度是对照组的两倍。 LH 撤除后睾丸睾酮分泌能力的丧失与 Leydig 细胞体积的减少有关，但与 Leydig 细胞数量的减少无关。因此，LH 需要维持 Leydig 细胞的分化结构和功能，但不需要维持成年大鼠睾丸中绝大多数 Leydig 细胞长达 16 周。此外，在长期 LH 剥夺后，Leydig 细胞保留了至少一种类固醇生成酶 3.β.HSD。
Leydig cells atrophy, losing cytoplasmic volume and the capacity for testosterone secretion, within 1-2 weeks of LH deprivation. We investigated the effects of long term (0-16 weeks) LH deprivation on the volume of an average Leydig cell, the volume of Leydig cells per testis, the number of Leydig cells per testis, and testosterone secretion by in vitro perfused testes. Endogenous LH was suppressed in adult rats by testosterone/estradiol-filled (TE) Silastic implants. The presence of Leydig cells in testes was verified by 1) morphological examination using light and electron microscopy, 2) histochemical localization of 3.beta.-hydroxysteroid dehydrogenase activity (3.beta.HSD), and 3) conversion of pregnenolone to progesterone by in vitro perfused testes. Marked quantitative differences existed in Leydig cell morphology among control and treated rats. The volume of an average Leydig cell and the total volume of Leydig cells per testis decreased (P < 0.01) rapidly and progressively after TE implantation. At 16 weeks, the average Leydig cell lost 90% of its cytoplasmic volume and 65% of its nuclear volume. Analysis of variance failed to detect a significant decline in Leydig cell number per testis, despite a 16% reduction from the value in control rats (22.2 .+-. 1.5 .times. 106) in rats treated for 16 weeks (18.7 .+-. 1.5 .times. 106). After TE implantation, LH-stimulated testosterone secretion by in vitro perfused testes diminished (P < 0.01) rapidly to 5% of the control values at 1 week and less than 0.3% of the control value from 4-16 weeks. In contrast, 25% of 3.beta.HSD activity was retained (P < 0.01 vs. controls) at 16 weeks, based on the rate of pregnenolone conversion to progesterone. Moreover, testes of treated rats secreted progesterone at a rate twice that of controls, when the steroid secretion rates were expressed per volume of Leydig cell cytoplasm. Loss of the testosterone-secreting capacity of testes after LH withdrawal was associated with a loss in the volume, but not a significant loss in the number, of Leydig cells. Thus, LH was required to maintain the differentiated structure and function of Leydig cells, but was not required to maintain the overwhelming majority of Leydig cells in the adult rat testis through 16 weeks. Moreover, at least one steroidogenic enzyme, 3.beta.HSD, was retained by Leydig cells after long term LH deprivation.