An ovary implanted into the spleen of an ovariectomized rat develops into a luteinized
tumor, growing in response to gonadotrophins. Previously, it was shown that in vivo
Buserelin, a gonadotrophin-releasing
hormone (
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 treatment with
buserelin did not modify
luteoma GnRH receptors. In organ incubations,
luteoma secreted significantly higher
estradiol and lower
progesterone than estrous ovaries; addition of
buserelin did not modify
steroid secretion. The same difference in basal
steroid secretion between
luteoma cells and luteal cells superovulated prepubertal ovaries was observed in cell cultures. Although
luteinizing-hormone (LH)-stimulated
progesterone in both kinds of cells,
buserelin significantly inhibited LH-stimulated
progesterone only in
luteoma cells. These results describe clear differences in basal
steroid secretion between tumoral and normal tissue. Furthermore, they show that
luteoma possess
GnRH receptors similar to those in normal ovarian tissue, and that
GnRH analogs have endocrine effects on these cells. Therefore, a direct effect of
buserelin on
luteoma cells can be postulated.