Primary Study Of The Mechanism In Compensatory Secretion Of Testosterone In Remaining Testis Induced By Hemicastration In Adult Mouse

Compensatory elevation of testosterone in remaining testis after hemicastration is well recognized phenomena. However, the mechanism is unknown for many years. Hemicastration of adult male animal can cause the double of concentration of testosterone in the testicular vein within few hours, often less than 36 hours, which makes the circular testosterone to recover to normal level. The mechanism is unclear for the compensatory increase of testosterone since it appears without any change in the level of serum LH and prolactin or theirs receptors. Although a significant elevation of systemic FSH was noted after hemicastration, it occurred later than the establishment of compensatory increase of testosterone. So FSH is not the trigger for the compensatory increase of testosterone. Investigations shows that nerve system take part in the regulation of basal testosterone secretion and the compensatory increase of testosterone in unilateral castration of adult male animals. But to its mechanism and the molecular metabolism of its reaction with gonoduct, no report was released yet. Nitric Oxide is recently recognized messenger which is synthesized by the Nitric oxide synthase (NOS) in the body of animals or human beings. NOS is found distributing in all level of reproduction systems from the brain, hypothalamus and to the gonad. And in the testis it is distributed in the leydig cell or others like vessel endothelium cells that are very near from them. Researches of last few years revealed that NO plays a crucial role in reproduction systems, and NO is involved in the regulation of testicular steroidogenesis. But as to whether the NO involves in the compensatory increase of testosterone, no report has been released yet. The present experiment was undertaken to explore the role of NO in the compensatory increase of gonadotropin in hemicastrated mouse. And the data show that there is a great decrease in the concentration of NO and in the activity of nitric oxide synthase, which catalyzed synthesis of NO in organs, in the remaining testis 4 to 36 hours after hemicastration. And meanwhile the serum testosterone shows a relative increase, which negatively correlated with the change of testis NOS activity. Intraperitoneal injection of NO donor SNP can suppress the compensatory increase of steroid, while NOS inhibitor can either promote the increase of testosterone or reverse the suppression effect of SNP. These results suggested that NO mediated the compensation increase of steroidogenesis after hemicastration. And then the changing of NO concentration in turn enhances the function of leydig cells by releasing theinhibition with lowering NO concentration. And finally exhibit resumption of serum steroid level. Further investigation was taken since there might be other unknown factors that also influence both the activity of NOS and the mechanism that NO act on the leydig cells. To investigate other possible factors involved in the compensatory steroidogenesis after unilateral castration, we use fluorescence different display reverse transcript PCR technology to seek the genes that differentially expressed in the groups with and without hemicastration. 43 genes were found and 5 of which were cloned to pGEM-T-Easy Vector and were sequenced. Newly expressed genes were found after hemicastration. This primary data provide very important information for further research in broad spectrum.