The effect of lipid peroxidation on transport function in human erythrocytes.
We have reported that the generation of oxygen free radicals within human red cells resulting from treatment with phenazine methosulfate (PMS) induces several toxic effects in membranes; lipid peroxidation, a binding of methemoglobin and a loss of intracellular K+. The specific K+ carriers are only slightly inhibited (Na+, K+ pump; Na+, K+ cotransport) and the K+ loss is mainly due to an increase in the passive K+ permeability. This could result from a toxic effect on the membrane such as lipid peroxidation or methemoglobin binding. The use of "oxygen free radical scavenger" molecules and pro-oxidative molecules showed that the PMS-dependent increase in passive K+ permeability is consequent to lipid peroxidation rather than to methemoglobin binding.
D001692:Biological Transport / Q000187:drug effects; D004050:Ditiocarb / Q000494:pharmacology; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D007700:Kinetics; D008054:Lipid Peroxides / Q000097:blood*; D008315:Malondialdehyde / Q000097:blood; D008706:Methemoglobin / Q000378:metabolism; D008773:Methylphenazonium Methosulfate / Q000494:pharmacology; D013481:Superoxides / Q000097:blood*
D008054:Lipid Peroxides; D013481:Superoxides; D008773:Methylphenazonium Methosulfate; D008315:Malondialdehyde; D008706:Methemoglobin; D004050:Ditiocarb