Title

Adenosine triphosphate inhibits LH stimulated testosterone accumulation by isolated rabbit ovarian follicles

Document Type

Article

Department

Paediatrics and Child Health (East Africa)

Abstract

Testosterone is a major secretory product of the rabbit follicle. Work from our laboratory also suggests that the steroidogenic responses of the follicles to LH and cAMP are different in that the LH effects were more long lasting whereas the response to cAMP could be evoked at will. Cyclic AMP is accepted as the second messenger which mediates the steroidogenic response to LH. It was therefore of interest to determine whether different responses could be elicited when LH and nucleotides were added together to isolated rabbit follicles. Unless otherwise stated procedures used were similar to those previously described. It was not determined whether ATP inhibited the binding of LH to the follicular cells. This possibility must be considered since the binding of HCG to bovine corpora lutea membranes can be inhibited by nucleotides. Although ATP could have inhibited LH binding it is apparent that this inhibition is not complete since testosterone production could be observed after the ATP was removed (panel e, final 2 h of incubation). The resumption of steroidogenesis after the removal of ATP is similar to data obtained with inhibitors of protein synthesis and lends further support to our contention that LH binding to follicular cells initiates an irreversible series of events which can be delayed at sites beyond gonadotropin binding, by various inhibitors.

Testosterone is a major secretory product of the rabbit follicle. Work from our laboratory also suggests that the steroidogenic responses of the follicles to LH and cAMP are different in that the LH effects were more long lasting whereas the response to cAMP could be evoked at will. Cyclic AMP is accepted as the second messenger which mediates the steroidogenic response to LH. It was therefore of interest to determine whether different responses could be elicited when LH and nucleotides were added together to isolated rabbit follicles. Unless otherwise stated procedures used were similar to those previously described. It was not determined whether ATP inhibited the binding of LH to the follicular cells. This possibility must be considered since the binding of HCG to bovine corpora lutea membranes can be inhibited by nucleotides. Although ATP could have inhibited LH binding it is apparent that this inhibition is not complete since testosterone production could be observed after the ATP was removed (panel e, final 2 h of incubation). The resumption of steroidogenesis after the removal of ATP is similar to data obtained with inhibitors of protein synthesis and lends further support to our contention that LH binding to follicular cells initiates an irreversible series of events which can be delayed at sites beyond gonadotropin binding, by various inhibitors

Publication

IRCS Medical Science

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