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十一酸睾酮注射诱导大鼠不完全生精抑制的定量(体视学)研究

Quantitative (stereological) study of incomplete spermatogenic suppression induced by testosterone undecanoate injection in rats.

作者信息

Yang Zheng-Wei, Guo Yang, Lin Li, Wang Xing-Hai, Tong Jian-Sun, Zhang Gui-Yuan

机构信息

Morphometric Research Laboratory, North Sichuan Medical College, Nanchong, Sichuan 637007.

出版信息

Asian J Androl. 2004 Dec;6(4):291-7.

PMID:15546019
Abstract

AIM

To evaluate the key lesions in spermatogenesis suppressed partially by testosterone undecanoate (TU) treatment.

METHODS

Adult male SD rats were treated with vehicle or TU (19 mg/kg) injection (i.m.) every 15 days for 130 days. The numbers of all types of cells (nuclei) in the seminiferous tubules and the interstitial tissue were estimated using a contemporary stereological tool, the optical disector.

RESULTS

In response to TU treatment, the numbers of non-type B spermatogonia, type B spermatogonia and late elongated spermatids per testis were reduced to 51 %, 66 % and 14 % of the controls, respectively. The conversion ratios from type B spermatogonia to early spermatocytes and pachytene spermatocytes were not significantly affected and the ratios to the later germ cell types fell to 51 % - 65 % of the controls. Less than 1.0 % of immature round spermatids were seen sloughing into the tubule lumen, 4.0 % of elongated spermatids retained in the seminiferous epithelium, and about half of the elongated spermatid nuclei appreciably malformed. Leydig cells were atrophied but their number and the peritubular myoid cell number per testis were unchanged.

CONCLUSION

Double inhibition of spermatogenesis (i.e. inhibition at spermiation and spermatogonial conversion to type B spermatogonia), a scenario seen in the monkey and human following gonadotrophin withdrawal, was not sufficiently effective for a complete spermatogenic suppression in the rat after TU treatment, probably due to ineffective inhibition of the Leydig cell population and therefore the intra-testicular testosterone levels.

摘要

目的

评估十一酸睾酮(TU)治疗部分抑制精子发生过程中的关键损伤。

方法

成年雄性SD大鼠每隔15天接受一次溶剂或TU(19mg/kg)注射(肌肉注射),共持续130天。使用现代体视学工具光学分割器估计生精小管和间质组织中各类细胞(细胞核)的数量。

结果

接受TU治疗后,每只睾丸中非B型精原细胞、B型精原细胞和晚期延长型精子细胞的数量分别降至对照组的51%、66%和14%。B型精原细胞向早期精母细胞和粗线期精母细胞的转化率未受到显著影响,而向后期生殖细胞类型的转化率降至对照组的51%-65%。不到1.0%的未成熟圆形精子细胞脱落至小管腔中,4.0%的延长型精子细胞滞留在生精上皮中,约一半的延长型精子细胞核明显畸形。睾丸间质细胞萎缩,但每只睾丸中其数量和睾丸周肌样细胞数量未发生变化。

结论

精子发生的双重抑制(即射精抑制和精原细胞向B型精原细胞转化的抑制),这在猴子和人类促性腺激素撤药后可见,在TU治疗后的大鼠中对完全抑制精子发生的效果不充分,可能是由于对睾丸间质细胞群体以及因此对睾丸内睾酮水平的抑制无效。

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