Iodoacetic acid inhibition of calcium-dependent potassium efflux in red blood cells.
The metabolic inhibitor, iodoacetic acid (IAA), has commonly been used to increase Ca-dependent K efflux in red blood cells. It is thought that this effect of IAA involves the irreversible inhibition of glyceraldehyde-phosphate dehydrogenase (EC 1.2.1.12), resulting in the energy depletion of the cell. Without energy, active transport stops, and the K loss is enhanced both by increasing cellular Ca and by preventing K reuptake. The present study shows that in addition to this metabolic effect, which increases Ca-dependent K efflux, IAA also inhibits this efflux. This inhibition is irreversible and is not related to the ATP or Ca concentrations of the cells. The carboxymethylation of a specific protein band correlates with IAA inhibition of K efflux.
D002104:Cadmium / Q000494:pharmacology; D002118:Calcium / Q000494:pharmacology*; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000097:blood; D006801:Humans; D007460:Iodoacetamide / Q000494:pharmacology; D007461:Iodoacetates / Q000494:pharmacology*; D019807:Iodoacetic Acid; D008970:Molecular Weight; D011188:Potassium / Q000097:blood*
D007461:Iodoacetates; D002104:Cadmium; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D011188:Potassium; D002118:Calcium; D019807:Iodoacetic Acid; D007460:Iodoacetamide