Mechanisms of action of cholera and Escherichia coli enterotoxins.
Current information is reviewed on the mechanism of secretion in small intestine, including how it is altered by cyclic 3',5'-adenosine monophosphate and on the structures and properties of cholera and both heat-labile and heat-stable Escherichia coli enterotoxins. Two separate active ion transport processes are altered by cyclic 3',5'-adenosine monophosphate: 1) coupled absorption of NaCl is inhibited in villus cells and 2) active anion secretion is stimulated, probably in crypt cells. Cholera and heat-labile E. coli toxins exert their secretory effect by stimulating intestinal mucosal adenylate cyclase. This stimulation results from the A1 subunit catalyzed transfer of adenosine diphosphate ribose from NAD to a membrane-bound guanosine triphosphatase, thereby inhibiting the enzyme, which normally represses adenylate cyclase. Heat-stable E. coli enterotoxin stimulates intestinal mucosal guanylate cyclase, which appears to be the basis for its enterotoxicity.
D000818:Animals; D001681:Biological Assay; D001692:Biological Transport; D002772:Cholera Toxin / Q000302:isolation & purification / Q000502:physiology*; D004355:Drug Stability; D004768:Enterotoxins / Q000494:pharmacology*; D004848:Epithelium / Q000502:physiology; D004926:Escherichia coli / Q000502:physiology; D020558:GTP Phosphohydrolases / Q000378:metabolism; D006162:Guanylate Cyclase / Q000378:metabolism; D006358:Hot Temperature; D006801:Humans; D007413:Intestinal Mucosa / Q000187:drug effects / Q000502:physiology; D007421:Intestine, Small / Q000382:microbiology*; D007477:Ions; D046911:Macromolecular Substances; D008564:Membrane Potentials; D009712:Nucleotides, Cyclic / Q000378:metabolism; D014734:Vibrio cholerae / Q000502:physiology
D004768:Enterotoxins; D007477:Ions; D046911:Macromolecular Substances; D009712:Nucleotides, Cyclic; D002772:Cholera Toxin; D020558:GTP Phosphohydrolases; D006162:Guanylate Cyclase