Meachem Sarah J, Robertson David M, Wreford Nigel G, McLachlan Robert I, Stanton Peter G
Prince Henry's Institute of Medical Research Block E, Level 4, Monash Medical Centre, 246 Clayton Road, Clayton, Victoria 3168, Australia.
J Endocrinol. 2005 Jun;185(3):529-38. doi: 10.1677/joe.1.05970.
Oestrogen is a metabolite of testosterone, but its role in spermatogenesis is ill-defined. Oestrogen may exert its effects on spermatogenesis, as oestrogen receptor (ER)-beta has been localised to both germ and somatic cells. This study sought to establish whether the restoration of early germ cell numbers in spermatogenesis by high-dose exogenous testosterone was influenced by its metabolite, oestrogen. The ER antagonist (ICI 182780) was administered, at a dose known to impair oestrogen action in the male reproductive tract, during testosterone treatment of gonadotrophin-releasing hormone (GnRH)-immunised rats, and germ cell numbers were determined. GnRH-immunised adult Sprague-Dawley rats (n=7-8 per group) received two doses of testosterone, either as a Silastic implant (24 cm (T24 cm)) or an injectable ester for 10 days alone or in combination with ICI 182780 (2 mg/kg, s.c. injection daily). Control rats received vehicle alone. Testes were perfusion-fixed and germ cells were quantified by the optical disector technique. GnRH-immunisation reduced (P<0.001) both type A/ intermediate spermatogonial and type B spermatogonial/ preleptotene spermatocyte number (56% of control) and leptotene/zygotene spermatocyte number (63% of control). Pachytene spermatocyte and round spermatids were reduced to 12% and l% (P<0.01) of control respectively. Testosterone treatment did not increase type A/intermediate spermatogonial number compared with GnRH-immunised controls over the 10-day study period. Treatment with testosterone-esters increased type B spermatogonial/preleptotene spermatocytes and leptotene/zygotene spermatocyte numbers (both being 83% of control, P<0.05), while T24 cm treatment did not significantly increase their numbers (73% of control) compared with GnRH-immunised controls. Both treatments increased pachytene spermatocyte and round spermatid numbers to 55% and 8% of control respectively. Co-administration of ICI 182780 had no effect on any of these germ cell numbers. We conclude that oestrogen action plays no role in the short-term restoration of spermatogenesis by testosterone in the GnRH-immunised rat.
雌激素是睾酮的一种代谢产物,但其在精子发生中的作用尚不明确。雌激素可能对精子发生产生影响,因为雌激素受体(ER)-β已定位在生殖细胞和体细胞中。本研究旨在确定高剂量外源性睾酮恢复精子发生早期生殖细胞数量的过程是否受其代谢产物雌激素的影响。在对促性腺激素释放激素(GnRH)免疫的大鼠进行睾酮治疗期间,给予已知会损害雄性生殖道中雌激素作用剂量的ER拮抗剂(ICI 182780),并测定生殖细胞数量。GnRH免疫的成年Sprague-Dawley大鼠(每组n = 7 - 8只)接受两剂睾酮,要么通过硅橡胶植入物(24 cm(T24 cm)),要么通过注射酯,单独给药10天或与ICI 182780(2 mg/kg,皮下每日注射)联合给药。对照大鼠仅接受赋形剂。对睾丸进行灌注固定,并通过光学分割技术对生殖细胞进行定量。GnRH免疫降低了(P<0.001)A型/中间型精原细胞和B型精原细胞/前细线期精母细胞数量(为对照的56%)以及细线期/偶线期精母细胞数量(为对照的63%)。粗线期精母细胞和圆形精子细胞分别降至对照的12%和1%(P<0.01)。在为期10天的研究期间,与GnRH免疫的对照相比,睾酮治疗并未增加A型/中间型精原细胞数量。睾酮酯治疗增加了B型精原细胞/前细线期精母细胞和细线期/偶线期精母细胞数量(两者均约为对照的83%,P<0.05),而与GnRH免疫的对照相比,T24 cm治疗并未显著增加它们的数量(约为对照的73%)。两种治疗均将粗线期精母细胞和圆形精子细胞数量分别增加至对照的55%和8%。同时给予ICI 182780对这些生殖细胞数量均无影响。我们得出结论,在GnRH免疫的大鼠中,雌激素作用在睾酮对精子发生的短期恢复中不起作用。