Stimulation of mammalian erythropoiesis by 5beta-H steroid metabolites.
The effects of a number of steroid compounds on erythropoiesis in normal and polycythemic mice were examined. Of the steroids that stimulated erythropoiesis, the hormone testosterone and certain 5beta-H C(19) and C(21) nonhormonal metabolites were the most effective. Anti-erythropoietin abolished the erythropoiesis-stimulating effects of testosterone but not those exerted by the 5beta-H steroid, 11-ketopregnanolone. Similarly, testosterone but not 11-ketopregnanolone evoked the production of erythropoiesis-stimulating factor in rats. It is concluded that two mechanisms underlie the stimulating actions of steroids on erythropoiesis; one through the production of erythropoietin and the second involving a more direct influence on the blood-forming tissues. The 5beta-H steroid metabolites are postulated to act on erythropoiesis via the latter mechanism.
D000818:Animals; D013196:Dihydrotestosterone / Q000494:pharmacology*; D004912:Erythrocytes / Q000378:metabolism; D004920:Erythropoiesis / Q000187:drug effects*; D004958:Estradiol / Q000494:pharmacology*; D005043:Etiocholanolone / Q000494:pharmacology*; D005260:Female; D006854:Hydrocortisone / Q000494:pharmacology*; D007501:Iron / Q000378:metabolism; D007503:Iron Isotopes; D007659:Ketones / Q000494:pharmacology*; D051379:Mice; D011086:Polycythemia / Q000503:physiopathology; D011278:Pregnanes / Q000494:pharmacology*; D011409:Propylene Glycols / Q000494:pharmacology; D013268:Stimulation, Chemical
D007503:Iron Isotopes; D007659:Ketones; D011278:Pregnanes; D011409:Propylene Glycols; D013196:Dihydrotestosterone; D004958:Estradiol; D005043:Etiocholanolone; D007501:Iron; D006854:Hydrocortisone