Studies on the mechanism of the antifertility activity of human chorionic gonadotropin in rodents.
Administration of 2.0 IU (3300 IU/mg) Human Chorionic Gonadotropin (hCG) to rats on days 7 to 13 or pregnancy induced complete embryonic resorption. This commercial preparation was also active in the mouse and hamster at 20 and 50 IUs per animal per day, respectively. It was inactive in the rat when administered after day 13 of pregnancy. Studies to determine how hCG could exert this effect resulted in the following findings: Concomitant administration of progesterone (8 mg/rat) to ovariectomized pregnant rats reduced the antifertility activity of hCG. Little or no estrogen could be identified by radioimmunoassay in the hCG preparations which had antifertility activity. The antifertility activity was, however, found associated with a molecular fraction which could be destroyed by both boiling and treatment with pronase, and which cross-reacted with anti-hCG. The antifertility activity of hCG was abolished by anti-hCG. Finally, serum estrogen levels in pregnant rats were found to be elevated by treatment with hCG.
D000818:Animals; D006063:Chorionic Gonadotropin / Q000032:analysis / Q000037:antagonists & inhibitors / Q000494:pharmacology*; D006224:Cricetinae; D020964:Embryo Loss / Q000139:chemically induced*; D004967:Estrogens / Q000097:blood; D005260:Female; D005313:Fetal Death / Q000139:chemically induced*; D051379:Mice; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000187:drug effects*; D011374:Progesterone / Q000097:blood; D051381:Rats; D013045:Species Specificity
D006063:Chorionic Gonadotropin; D004967:Estrogens; D011374:Progesterone