GNRH RECEPTORS AND GNRH ENDOCRINE EFFECTS ON LUTEOMA CELLS

An ovary implanted into the spleen of an ovariectomized rat develops i nto a luteinized tumor, growing in response to gonadotrophins. Previou sly, it was shown that in vivo Buserelin, a gonadotrophin-releasing ho rmone (GnRH) analog, inhibited tumor growth. To determine if GnRH had a direct effect on tumor cells, the presence of GnRH receptors as well as the endocrine effects of buserelin were studied on tumoral tissue. GnRH receptors were present in luteoma in similar concentrations and dissociation constant (Kd) to control estrous ovaries. In vivo treatme nt with buserelin did not modify luteoma GnRH receptors. In organ incu bations, luteoma secreted significantly higher estradiol and lower pro gesterone than estrous ovaries; addition of buserelin did not modify s teroid secretion. The same difference in basal steroid secretion betwe en luteoma cells and luteal cells superovulated prepubertal ovaries wa s observed in cell cultures. Although luteinizing-hormone (LH)-stimula ted progesterone in both kinds of cells, buserelin significantly inhib ited LH-stimulated progesterone only in luteoma cells, These results d escribe clear differences in basal steroid secretion between tumoral a nd normal tissue. Furthermore, they show that luteoma possess GnRH rec eptors similar to those in normal ovarian tissue, and that GnRH analog s have endocrine effects on these cells. Therefore, a direct effect of buserelin on luteoma cells can be postulated.