Bartlett J M, Weinbauer G F, Nieschlag E
Max Planck Clinical Research Unit for Reproductive Medicine, The University Münster, Federal Republic of Germany.
Biol Reprod. 1990 Apr;42(4):603-12. doi: 10.1095/biolreprod42.4.603.
Studies of synchronization of spermatogenesis following vitamin A deficiency have suggested that this may provide an in vivo model for the study of stage-dependent changes in hormonal action and protein secretion within the seminiferous epithelium. However, until now, no information on the stability or durability of this condition has been available. In this study, 200 seminiferous tubules from each of 40 rats (including controls) were classified according to their spermatogenic stage after withdrawal and replenishment of vitamin A. Following 15 wk withdrawal and subsequent replenishment of vitamin A, spermatogenesis was initiated in a synchronous fashion. This synchrony remained stable for more than 10 cycles of the seminiferous epithelium (2.5 spermatogenic cycles). In association with the extended period of vitamin A deficiency, a proportion of tubules (30%) showed morphological characteristics of either Sertoli cells only or Sertoli cells plus spermatogonia with occasional pachytene spermatocytes. During the 11-wk period of observation in this study, no significant change in proportions of damaged tubules were observed. Testicular testosterone concentrations, although elevated with respect to controls, showed no correlation with the stage of the cycle of the seminiferous epithelium observed, whereas pituitary and serum follicle-stimulating hormone levels were elevated, probably due to the number of damaged tubules observed. The persistence of synchrony in spermatogenesis following vitamin A treatment suggests that this model is applicable for studies of paracrine actions within the testis. However, the decreased ratio of synchrony observed with time may provide evidence that duration of the individual stages of the cycle of the seminiferous epithelium might be subject to temporal variation, leading to a progressive desynchronization of spermatogenesis in this model system.
维生素A缺乏后精子发生同步化的研究表明,这可能为研究生精上皮内激素作用和蛋白质分泌的阶段依赖性变化提供一个体内模型。然而,到目前为止,尚无关于这种情况的稳定性或持久性的信息。在本研究中,对40只大鼠(包括对照组)中每只大鼠的200条生精小管在维生素A撤除和补充后根据其精子发生阶段进行分类。在15周的维生素A撤除及随后补充后,精子发生以同步方式启动。这种同步性在生精上皮的10多个周期(2.5个精子发生周期)内保持稳定。与维生素A缺乏的延长时期相关,一部分小管(30%)表现出仅支持细胞或支持细胞加精原细胞并偶尔伴有粗线期精母细胞的形态学特征。在本研究的11周观察期内,未观察到受损小管比例的显著变化。睾丸睾酮浓度虽然相对于对照组有所升高,但与观察到的生精上皮周期阶段无相关性,而垂体和血清促卵泡激素水平升高,可能是由于观察到的受损小管数量所致。维生素A处理后精子发生同步性的持续存在表明该模型适用于睾丸旁分泌作用的研究。然而,随时间观察到的同步性比例下降可能提供证据,表明生精上皮周期各阶段的持续时间可能会随时间变化,导致该模型系统中精子发生逐渐失同步。