McLachlan R I, Wreford N G, Meachem S J, De Kretser D M, Robertson D M
Prince Henry's Institute of Medical Research, Monash Medical Centre, Clayton, Victoria, Australia.
Biol Reprod. 1994 Nov;51(5):945-55. doi: 10.1095/biolreprod51.5.945.
The aim of this study was to investigate the progression of germ cell populations through the rat spermatogenic cycle when spermatogenesis was suppressed by LH withdrawal through the use of a combination of testosterone (T) and estradiol (E) and then reinitiated by the administration of high doses of T. Adult Sprague-Dawley rats received 3-cm T and 0.4-cm E silastic implants for 6, 8, or 12 wk to suppress spermatogenesis followed by high-dose T (24-cm implants) for up to 12 wk to reinitiate spermatogenesis. The number of spermatogonia, primary spermatocytes, and round spermatids per testis was established by stereological techniques, and the elongated spermatid number was determined by the testicular content of nuclei resistant to homogenization in Triton X-100. Suppression for 6-12 wk resulted in moderate and significant (p < 0.05) reductions in the numbers of type A and type B spermatogonia (to 44-59% of control levels), preleptotene (68-72% of control), and leptotene/zygotene spermatocytes (62-79% of control) as well as in the numbers of stage I-VII (56-69% of control) and stage VIII-XIV (35-43% of control) pachytene spermatocytes. Round spermatids were suppressed to 29-45% of control levels (p < 0.05) while elongated spermatids were undetectable. The hourly production rates of germ cells (calculated using published time divisors) were used to study the cellular conversions through spermatogenesis (based on the ratios of the hourly production rates) and revealed that T withdrawal consistently abolished the conversion of round to elongated spermatids. The duration of suppression (6, 8, or 12 wk) had no effect on the degree to which germ cell populations or conversions were reduced. In response to high-dose T administration, spermatogonial and spermatocyte numbers and production rates (up to stage I-VII pachytene) remained suppressed, while stage VIII-XIV pachytene spermatocytes showed an increase of borderline significance. On the other hand, round and elongated spermatid numbers and production rates increased significantly (to 81% and 78% of control, respectively) and their conversion was normalized, i.e., the spermiogenic process was restored to a level consistent with the numbers of earlier germ cells proceeding through the cycle. These data suggest that, in the presence of low T levels, spermatogenesis proceeds at approximately 65% of normal levels between the spermatogonial and round spermatid stages, irrespective of the duration of T-induced suppression. This is followed by a precipitous decline in elongated spermatid number that is attributed to the disappearance of round spermatids.(ABSTRACT TRUNCATED AT 400 WORDS)
本研究的目的是，当通过联合使用睾酮（T）和雌二醇（E）撤去促黄体生成素（LH）抑制大鼠精子发生，随后给予高剂量T重新启动精子发生时，研究生殖细胞群体在大鼠精子发生周期中的进展情况。成年Sprague-Dawley大鼠接受3厘米的T和0.4厘米的E硅橡胶植入物6、8或12周以抑制精子发生，随后给予高剂量T（24厘米植入物）长达12周以重新启动精子发生。通过体视学技术确定每个睾丸中的精原细胞、初级精母细胞和圆形精子细胞的数量，并通过在Triton X-100中抗匀浆的细胞核的睾丸含量来确定长形精子细胞的数量。抑制6至12周导致A型和B型精原细胞数量（降至对照水平的44 - 59%）、前细线期细胞（降至对照的68 - 72%）、细线期/偶线期精母细胞（降至对照的62 - 79%）以及I - VII期（降至对照的56 - 69%）和VIII - XIV期（降至对照的35 - 43%）粗线期精母细胞数量出现中度且显著（p < 0.05）减少。圆形精子细胞被抑制至对照水平的29 - 45%（p < 0.05），而未检测到长形精子细胞。生殖细胞的每小时产生率（使用已发表的时间除数计算）用于研究精子发生过程中的细胞转化（基于每小时产生率的比率），结果显示撤去T始终消除了圆形精子细胞向长形精子细胞的转化。抑制持续时间（6、8或12周）对生殖细胞群体减少程度或转化减少程度没有影响。给予高剂量T后，精原细胞和精母细胞数量及产生率（直至I - VII期粗线期）仍受到抑制，而VIII - XIV期粗线期精母细胞显示出临界显著性增加。另一方面，圆形和长形精子细胞数量及产生率显著增加（分别达到对照的81%和78%），并且它们的转化恢复正常，即精子形成过程恢复到与早期生殖细胞通过周期的数量一致的水平。这些数据表明，在低T水平存在的情况下，精子发生在精原细胞和圆形精子细胞阶段之间以正常水平的约65%进行，与T诱导抑制的持续时间无关。随后长形精子细胞数量急剧下降，这归因于圆形精子细胞的消失。（摘要截断于400字）
