Estrogens exert a variety of regulatory functions on growth development and differentiation in both the female and male. The estrogen actions are mediated by the estrogen receptors(ERs), members of the nuclear receptor (NR) superfamily, whichare encoded by two distinct genes, ERa and ERb. Recently, it has been suggest that estrogens, acting through the ERa, have been shown to repress expression of the gene encoding insulin-like 3, a small peptide produced by testicular Leydig cells that is essential for normal testis descent and that ERa is required for male fertility. In this study we investigated the effects of triptorelin (the long-actinggonadotropin releasing hormon analog able to induce hypogonadism) and/or testosterone treatement on the expression of ERa and aromatase in Leydig cells of adult male rats. In addition, levels of testosterone and estradiol produced by Leydig cells from control and treated rats were followed. The results of real time PCR analysis showed that triptorelin treatement dramaticaly decreased the expression of both, aromatase and ERa. Moreover, testosterone treatment of triptorelin-induced hypogonadal rats was not able to recover decreased aromatase and ERa expression, while testosterone alone induced the same inhibitory effect as triptorelin. In the same cells, production of both, aromatase substrate testosterone, as well as estradiol was significantly decreased in all treated groups. Collectively, these results sugest that triptorelin and testosterone treatement, alone or in commbination, strongly inhibited the estrogenic mashinery in Leydig cells and that model of hypogonadal rats maybe the good model to extend knowledge on the role ERa in male reproductive functions.

This work was supported by the Serbian Ministry of Science (Grant No. 143055) and Autonomic Province of Vojvodina (Grant No. 0667).