Testosterone secretion by cultured arrhenoblastoma cells: suppression by a luteinizing hormone-releasing hormone agonist.
A patient with virilization was studied. The basal urinary excretion of 17-ketosteroids was at the upper limit of normal, but the plasma testosterone concentration was greatly elevated. Testosterone secretion could be stimulated by hCG, suppressed by dexamethasone, and was not affected by ACTH. At operation, an arrhenoblastoma of the left ovary was found. Isolated tumor cells in culture secreted testosterone. The addition of a LRH agonist (10 ng/ml) suppressed the secretion of testosterone by 50% (P less than 0.01). The inhibiting effect of a LRH agonist on steroidogenesis suggests that LRH receptors were present on this tumor and that treatment with LRH agonists might be beneficial in patients with metastatic steroid hormone-secreting ovarian and testicular tumors.
D015068:17-Ketosteroids / Q000652:urine; D000324:Adrenocorticotropic Hormone; D002478:Cells, Cultured; D006063:Chorionic Gonadotropin; D003907:Dexamethasone; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000031:analogs & derivatives* / Q000494:pharmacology; D017273:Goserelin; D006801:Humans; D008875:Middle Aged; D010051:Ovarian Neoplasms / Q000378:metabolism*; D018310:Sertoli-Leydig Cell Tumor / Q000378:metabolism*; D013739:Testosterone / Q000378:metabolism*
D015068:17-Ketosteroids; D006063:Chorionic Gonadotropin; D017273:Goserelin; D007987:Gonadotropin-Releasing Hormone; D013739:Testosterone; D003907:Dexamethasone; D000324:Adrenocorticotropic Hormone