Kolasa Agnieszka, Marchlewicz Mariola, Kurzawa Rafał, Głabowski Wojciech, Trybek Grzegorz, Wenda-Rózewicka Lidia, Wiszniewska Barbara
Department of Histology and Embryology, Pomeranian Medical University, Powstanców Wlkp. 72, 70-111, Szczecin, Poland.
Cell Mol Biol Lett. 2009;14(3):511-27. doi: 10.2478/s11658-009-0019-z. Epub 2009 Apr 29.
In our previous studies, we showed that a finasteride-induced DHT deficiency may cause changes in the morphology of the seminiferous epithelium without any morphological alteration of the epididymis. In this study, we demonstrated the constitutive immunoexpression of inducible nitric oxide synthase (iNOS) in the testis and epididymis of Wistar rats treated with finasteride for 28 days (the duration of two cycles of the seminiferous epithelium) and 56 days (the duration of one spermatogenesis). We noted that a 56-day finasteride treatment mainly caused a decrease in the level of circulating DHT, as well as a statistically insignificant decrease in the level of T. The hormone deficiency also led to a change in the iNOS immnoexpression in the testis and epididymis of the finasteride-treated rats. In vitro, DHT did not modify NO production by the epithelial cells of the caput epididymis even when stimulated with LPS and IFNgamma, but it did give rise to an increase in NO production by the epithelial cells of the cauda epididymis without the stimulation. DHT did not have a statistically significant influence on estradiol production by cultured, LPS- and IFNgamma-stimulated epithelial cells from the caput and cauda epididymis. In conclusion, our data clearly indicates that a finasterideinduced DHT deficiency intensifies the constitutive expression of iNOS in most rat testicular and epididymal cells, so it can be expected that the expression of inducible nitric oxide synthase (iNOS) could be regulated by DHT. On the other hand, the profile of the circulating DHT and T levels strongly suggests that the regulation of constitutive iNOS expression is complex and needs more detailed study.
在我们之前的研究中，我们发现非那雄胺诱导的双氢睾酮（DHT）缺乏可能会导致生精上皮形态发生变化，而附睾却没有任何形态改变。在本研究中，我们展示了在接受非那雄胺治疗28天（生精上皮两个周期的时长）和56天（一个精子发生周期的时长）的Wistar大鼠的睾丸和附睾中，诱导型一氧化氮合酶（iNOS）的组成性免疫表达。我们注意到，56天的非那雄胺治疗主要导致循环DHT水平下降，以及睾酮（T）水平有统计学意义但不显著的下降。激素缺乏还导致了非那雄胺治疗大鼠的睾丸和附睾中iNOS免疫表达的变化。在体外，即使在用脂多糖（LPS）和γ干扰素（IFNγ）刺激时，DHT也不会改变附睾头上皮细胞的一氧化氮（NO）生成，但它确实在没有刺激的情况下使附睾尾上皮细胞的NO生成增加。DHT对来自附睾头和附睾尾的经LPS和IFNγ刺激的培养上皮细胞的雌二醇生成没有统计学意义上的显著影响。总之，我们的数据清楚地表明，非那雄胺诱导的DHT缺乏会增强大多数大鼠睾丸和附睾细胞中iNOS的组成性表达，因此可以预期诱导型一氧化氮合酶（iNOS）的表达可能受DHT调节。另一方面，循环DHT和T水平的情况强烈表明，组成性iNOS表达的调节是复杂的，需要更详细的研究。
