Volume 6, Issue 4 (December 2004) 6, 291–297;
Quantitative (stereological) study of incomplete spermatogenic suppression induced by testosterone undecanoate injection in rats
Z.W. Yang, Y. Guo, L. Lin, X.H. Wang, J.S. Tong, G.Y. Zhang
1.Morphometric Research Laboratory, North Sichuan Medical College, Nanchong 637007, China 2.Photography Studio, Nanchong Medical School, Nanchong 637000, China 3.Jiangsu Family Planning Institute, Nanjing 210029, China 4.National Research Institute for Family Planning, Beijing 100081, China
Advance online publication 1 December 2004
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.
Full Text |
|
|
Browse: 2312 |
|