Rai U, Haider S
Centre of Advanced Study in Zoology, Banaras Hindu University, India.
Eur J Morphol. 1995 Nov;33(5):443-55.
The effects of FSH, testosterone and either cyproterone acetate (CPA) alone or in combination with FSH or testosterone on testis and epididymis in male lizards were studied histologically and histochemically during recrudescent phase to find out whether the onset of spermatogenesis is androgen dependent or FSH dependent. The testes of control lizards consisted of mainly spermatogonia, a few primary spermatocytes and secondary spermatocytes rarely. The interstitial or Leydig cells were atrophied. FSH treatment induced spermatogenic activity substantially as indicated by increase in number of primary and secondary spermatocytes and transformation of secondary spermatocytes into spermatids and into spermatozoa in a few cases. Besides, steroidogenic activity was also remarkably stimulated as evidences by considerable depletion of sudanophilic lipid and an increase in Delta5-3beta-hydroxysteroid dehydrogenase enzyme activity in Leydig cells. However, testosterone treatment resulted in the inhibition of spermatogenesis. A significant inhibition of spermatogenesis was noted in lizards treated either with CPA alone or in combination with FSH. The inhibitory effect of CPA on spermatogenesis was increased when it was given in combination with testosterone. The results indicate that onset of spermatogenic activity is dependent on FSH (or FSH-like protein), but not on the androgen. The ductus epididymidis in control lizards was regressed with low cuboidal epithelium. The lumen of the tubules was totally devoid of secretory material and spermatozoa. FSH treatment induced a marked hypertrophy in epididymidis. The lumen became filled with secretory material mixed with spermatozoa. The hypertrophy in epididymidis was also recorded after the treatment with testosterone, but the degree of induction was not to that extent as noted in FSH treated ones. However, CPA injected either with FSH or with testosterone resulted in the profound atrophy in epididymidis.
在雄性蜥蜴的性腺再发育阶段,对促卵泡激素(FSH)、睾酮以及单独使用醋酸环丙孕酮(CPA)或其与FSH或睾酮联合使用对睾丸和附睾的影响进行了组织学和组织化学研究,以确定精子发生的起始是雄激素依赖性还是FSH依赖性。对照蜥蜴的睾丸主要由精原细胞组成,只有少数初级精母细胞,很少有次级精母细胞。间质细胞或莱迪希细胞萎缩。FSH处理显著诱导了生精活性,这表现为初级和次级精母细胞数量增加,少数情况下次级精母细胞转化为精子细胞并进而转化为精子。此外,类固醇生成活性也受到显著刺激,这可通过莱迪希细胞中嗜苏丹脂质的大量消耗以及Δ5-3β-羟基类固醇脱氢酶活性的增加得到证明。然而,睾酮处理导致精子发生受到抑制。单独使用CPA或其与FSH联合处理的蜥蜴中,精子发生受到显著抑制。当CPA与睾酮联合使用时,其对精子发生的抑制作用增强。结果表明,生精活性的起始依赖于FSH(或FSH样蛋白),而非雄激素。对照蜥蜴的附睾管退化,上皮为低立方上皮。小管腔完全没有分泌物质和精子。FSH处理诱导附睾显著肥大。管腔充满了与精子混合的分泌物质。睾酮处理后也记录到附睾肥大,但诱导程度不如FSH处理的蜥蜴。然而,注射CPA与FSH或睾酮均导致附睾严重萎缩。