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Purified cholera enterotoxin was as effective as adrenocorticotropin (ACTH) in stimulating steroidogenesis in adrenal tumor cells in tissue culture. In contrast to the rapid response to ACTH, there was a 60-min lag before increased steroidogenesis could be detected. Ten minutes of exposure to cholera toxin followed by removal of toxin resulted in maximal stimulation of steroidogenesis after incubation for 2 hr. Equine antiserum to choleragenoid or mixed gangliosides effectively blocked cholera toxin-induced steroidogenesis. Further studies suggested that cholera enterotoxin induced steroidogenesis in adrenal tumor cells by interacting with a membrane receptor distinctive from the ACTH receptor. Half maximal doses of cholera enterotoxin and ACTH produced an additive effect on steroidogenesis. There was no calcium requirement for cholera enterotoxin-induced steroidogenesis as opposed to stimulation by ACTH. A mutant cell line unresponsive to ACTH was stimulated by cholera enterotoxin.
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Wishnow et al. (1974) studied this question.