Cavaco J E, van Blijswijk B, Leatherland J F, Goos H J, Schulz R W
Research Group for Comparative Endocrinology, Faculty of Biology, Utrecht University, The Netherlands.
Cell Tissue Res. 1999 Aug;297(2):291-9. doi: 10.1007/s004410051357.
The present report focuses on the mechanism(s) involved in the steroid-induced decrease of androgen production in immature African catfish testes that was observed in previous studies. Juvenile animals were implanted with Silastic pellets containing different 11-oxygenated androgens (11-ketotestosterone, KT; 11 beta-hydroxyandrostenedione, OHA; 11-ketoandrostenedione, KA), testosterone (T) or estradiol-17 beta (E2). Control groups received steroid-free pellets. Two weeks later, testis tissue fragments were either incubated with increasing concentrations of catfish luteinizing hormone (LH), or incubated with [3H]-pregnenolone ([3H]-P5) or [3H]-androstenedione ([3H]-A). Tissue fragments were also prepared for the quantitative assessment of Leydig cell morphology. Most of the parameters studied were not affected significantly by implantation of E2. Implantation of all androgens inhibited both the basal and the LH-stimulated androgen secretory capacity in vitro. This was associated with a reduced size of the Leydig cells and loss of half of their mitochondria. The studies on the metabolism of tritiated steroid hormones indicated that steroidogenic steps prior to 11 beta-hydroxylation, probably C17-20 lyase activity, were affected by all androgens. Although the effects of 11-oxygenated androgens and T on Leydig cells were mostly similar, previous work showed that only the 11-oxygenated androgens stimulated spermatogenesis, suggesting that distinct mechanisms of action are used by 11-oxygenated androgens and T. These mechanisms, however, seem to merge on the same target(s) to impair Leydig cell androgen production. Such a negative feedback mechanism may be of relevance in the context of the decline in androgen secretion per milligram testis tissue that accompanies the first wave of spermatogenesis in pubertal African catfish.
本报告聚焦于先前研究中观察到的类固醇诱导未成熟非洲鲶鱼睾丸雄激素生成减少所涉及的机制。将幼龄动物植入含有不同11-氧化雄激素（11-酮睾酮，KT；11β-羟基雄烯二酮，OHA；11-酮雄烯二酮，KA）、睾酮（T）或雌二醇-17β（E2）的硅橡胶丸。对照组接受不含类固醇的丸剂。两周后，将睾丸组织碎片与浓度递增的鲶鱼促黄体生成素（LH）一起孵育，或与[3H]-孕烯醇酮（[3H]-P5）或[3H]-雄烯二酮（[3H]-A）一起孵育。还制备了组织碎片用于对睾丸间质细胞形态进行定量评估。大多数研究参数不受E2植入的显著影响。所有雄激素的植入均抑制了体外基础和LH刺激的雄激素分泌能力。这与睾丸间质细胞大小减小以及其一半线粒体的丧失有关。对氚标记类固醇激素代谢的研究表明，11β-羟基化之前的类固醇生成步骤，可能是C17-20裂解酶活性，受到所有雄激素的影响。尽管11-氧化雄激素和T对睾丸间质细胞的作用大多相似，但先前的研究表明只有11-氧化雄激素刺激精子发生，这表明11-氧化雄激素和T使用了不同的作用机制。然而，这些机制似乎在同一靶点上汇聚，从而损害睾丸间质细胞雄激素的产生。这种负反馈机制可能与青春期非洲鲶鱼首次精子发生波伴随的每毫克睾丸组织雄激素分泌下降有关。
