Characterization of the desensitized state of Leydig tumor cells.
A perifusion system has been used to study the in vitro desensitization of isolated Leydig tumor cells. It was observed that the cells become refractory, as measured by decreased rates of steroidogenesis, during continuous perifusions with saturating concentrations of either human choriogonadotropin (CG), cholera toxin, or 8-bromo-cyclic AMP. Furthermore, an initial perifusion of the cells with either human CG, cholera toxin, or 8-bromo-cyclic AMP causes subsequent desensitization towards all three stimuli. Thus, each of these stimuli is equally effective in inducing a state of desensitization in these cells that is manifested by a steroidogenic lesion(s) distal to cyclic AMP formation. It was found that the post-cyclic AMP lesion(s) in the desensitized state occurs prior to the formation of pregnenolone. However, the decreased rates of steroidogenesis do not seem to arise from a depletion of intracellular cholesterol.
D015124:8-Bromo Cyclic Adenosine Monophosphate; D000616:Aminoglutethimide / Q000494:pharmacology; D000818:Animals; D002460:Cell Line; D002772:Cholera Toxin / Q000494:pharmacology*; D002784:Cholesterol / Q000378:metabolism; D002788:Cholesterol Esters / Q000378:metabolism; D006063:Chorionic Gonadotropin / Q000494:pharmacology*; D000242:Cyclic AMP / Q000031:analogs & derivatives* / Q000096:biosynthesis / Q000494:pharmacology; D007984:Leydig Cell Tumor / Q000378:metabolism; D051379:Mice; D011284:Pregnenolone / Q000096:biosynthesis; D013256:Steroids / Q000096:biosynthesis*
D002788:Cholesterol Esters; D006063:Chorionic Gonadotropin; D013256:Steroids; D000616:Aminoglutethimide; D015124:8-Bromo Cyclic Adenosine Monophosphate; D011284:Pregnenolone; D002772:Cholera Toxin; D002784:Cholesterol; D000242:Cyclic AMP