Demonstration of a direct effect of inhibitors of the degradation of receptor-bound human choriogonadotropin on the steroidogenic pathway.
Results presented in the previous paper (Ascoli, M., and Puett, D. (1978) J. Biol. Chem. 253, 7832--7838) show that the degradation of receptor-bound 125I-labeled human choriogonadotropin can be inhibited by chloroquine, protease inhibitors, and metabolic inhibitors. These compounds were also shown to inhibit gonadotropin-stimulated steroidogenesis. It is reported herein that these inhibitors also block the stimulation of steroidogenesis by both cholera toxin and 8-Br-adenosine 3':5'-monophosphate, thus showing that they are not specific for the hormonal stimuli. These results, taken together with previous observations that show that NH2Cl can block hormone degradation without inhibiting hormone-stimulated steroidogenesis, strongly suggest that the degradation of choriogonadotropin is not required for its stimulatory action on progesterone production.
D000643:Ammonium Chloride / Q000494:pharmacology*; D000818:Animals; D002738:Chloroquine / Q000494:pharmacology*; D006063:Chorionic Gonadotropin / Q000378:metabolism*; D003486:Cyanides / Q000494:pharmacology*; D003837:Deoxy Sugars / Q000494:pharmacology*; D003847:Deoxyglucose / Q000494:pharmacology*; D007700:Kinetics; D007984:Leydig Cell Tumor / Q000378:metabolism; D008297:Male; D051379:Mice; D011480:Protease Inhibitors / Q000494:pharmacology*; D011956:Receptors, Cell Surface / Q000187:drug effects / Q000378:metabolism*; D013256:Steroids / Q000096:biosynthesis*
D006063:Chorionic Gonadotropin; D003486:Cyanides; D003837:Deoxy Sugars; D011480:Protease Inhibitors; D011956:Receptors, Cell Surface; D013256:Steroids; D000643:Ammonium Chloride; D002738:Chloroquine; D003847:Deoxyglucose