The Effect of Cholera Enterotoxin on Steroidogenesis in Cultured Adrenal Tumor Cells

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 choler...

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Bibliographic Details
Published in:The Journal of infectious diseases 1974-06, Vol.129 (6), p.690-695
Main Authors: Wishnow, Rodney M., Feist, Patty
Format: Article
Language:English
Subjects:
Adipocytes
Adrenal Cortex Hormones - biosynthesis
Adrenal Gland Neoplasms - metabolism
Adrenal Gland Neoplasms - pathology
Adrenocorticotropic Hormone - administration & dosage
Adrenocorticotropic Hormone - pharmacology
Animals
Antitoxins - pharmacology
Calcium - metabolism
Cattle
Cell Line
Cell lines
Cell Membrane - drug effects
Cholera
Culture Techniques
Cyclic AMP - pharmacology
Dose-Response Relationship, Drug
Drug Synergism
Enterotoxins
Enterotoxins - administration & dosage
Enterotoxins - isolation & purification
Enterotoxins - pharmacology
Gangliosides - pharmacology
Horses - immunology
Immune Sera - pharmacology
Major Articles
Mice
Mice, Inbred Strains
Mutation - drug effects
Neoplasms, Experimental - metabolism
Receptors
Receptors, Drug - drug effects
Steroidogenesis
Steroids
Time Factors
Toxins
Tumor cell line
Tumors
Vibrio
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Summary: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.
ISSN:0022-1899
1537-6613
DOI:10.1093/infdis/129.6.690