Cholera toxin B-subunit protects mammalian cells from ricin and abrin toxicity.
The glycoproteins ricin and abrin intoxicate cells by inhibiting protein synthesis. Pretreatment of HeLa cells with cholera toxin partially protects them from ricin and abrin activity. The involvement in this phenomenon of the various effects of cholera toxin, namely, redistribution of membrane receptors elicited from protomer B and increasing cyclic AMP concentrations induced by protomer A, were studied. Substances able to enhance cyclic AMP concentrations do not affect ricin and abrin activity, while protomer B alone protects cells. In addition, the effects of several lectins on ricin or abrin toxicity were examined. Almost complete prevention of ricin or abrin activity was obtained using concanavalin A (Con A) and wheat germ agglutinin (WGA). Conversely, neither succinyl Con A nor Ulex europeus agglutinin (UEA) affected the cellular response. Both protomer B of cholera toxin and Con A did not alter the binding of ricin or abrin; they seem to protect cells by altering membrane structure.
D000036:Abrin / Q000037:antagonists & inhibitors*; D002772:Cholera Toxin / Q000494:pharmacology*; D003208:Concanavalin A / Q000494:pharmacology; D000242:Cyclic AMP / Q000096:biosynthesis; D006367:HeLa Cells; D006801:Humans; D037102:Lectins / Q000494:pharmacology; D010940:Plant Proteins / Q000037:antagonists & inhibitors*; D014176:Protein Biosynthesis; D011952:Receptors, Concanavalin A / Q000187:drug effects; D012276:Ricin / Q000037:antagonists & inhibitors*
D037102:Lectins; D010940:Plant Proteins; D011952:Receptors, Concanavalin A; D003208:Concanavalin A; D000036:Abrin; D012276:Ricin; D002772:Cholera Toxin; D000242:Cyclic AMP