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Abstract
Cholera enterotoxin caused a delayed accumulation of adenosine 3′,5′-monophosphate (cyclic AMP) in human leukocytes, associated with an increase in leukocyte adenyl cyclase activity. The action of cholera enterotoxin contrasted with that of other agents which stimulate adenyl cyclase: (a) the effects of the toxin were delayed in onset, while prostaglandin-E1 (PGE1) and isoproterenol acted rapidly; (b) removal of the soluble toxin from the extracellular medium did not abolish its effects on cyclic AMP and inhibition of antigenic histamine release, while removal of PGE1 did prevent its effects; (c) PGE1, but not cholera enterotoxin, stimulated adenyl cyclase activity when added directly to broken cell preparations. Binding of the toxin to leukocytes was rapid and irreversible, and was followed by a gradual increase in cyclic AMP which was not prevented by cycloheximide.
Authors
Henry R. Bourne, Robert I. Lehrer, Lawrence M. Lichtenstein, Gerald Weissmann, Robert Zurier
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