The stimulation of Leydig cells by the administration of a single injection of 100 IU human CG (hCG) to adult male rats caused a significant biphasic stimulation of serum testosterone levels at 2 h and 3 days after injection. Serum immunoreactive (IR)-inhibin levels were elevated by 6 h and peaked at 24 h after hCG, then progressively declined thereafter. The removal of Leydig cells in vivo by the injection of the cytotoxic drug ethane dimethane sulfonate (EDS) causes a significant decrease in serum testosterone levels within 4 days, which is sustained 1 and 2 weeks after EDS. Serum IR-inhibin levels, however, rise significantly 2 and 4 weeks after injection of EDS. An injection of 100 IU hCG, 4 days after EDS (when no Leydig cells were present in vivo), failed to provoke an elevation of either testosterone or IR-inhibin levels in serum. But 2 or 4 weeks after administration of EDS, as a new population of Leydig cells develops in the interstitium, an injection of 100 IU hCG provokes a significant increase in serum testosterone and IR-inhibin levels. The possibility that the failure of IR-inhibin levels to rise after EDS and hCG treatment could be due to changes in the seminiferous epithelium, caused by testosterone deprivation induced by Leydig cell destruction after EDS, was examined by administering high doses of testosterone known to maintain spermatogenesis. Under such conditions, hCG failed to induce a rise of IR-inhibin after EDS treatment had destroyed the Leydig cells. These data strongly support the concept that the Leydig cells are involved in the regulation of IR-inhibin secretion in vivo through factors other than testosterone.
|Number of pages||6|
|Publication status||Published - 1989|