Erythrocyte membrane fluidity, lipid peroxidation and lysis in alcoholic liver disease.

The still unexplained occurrence of hemolytic anemia in cases of alcoholic liver disease prompted us to study the toxic effect of ethanol on the membrane and metabolic properties of erythrocytes (RBC) in chronic alcoholics (n = 7). Raised susceptibility of RBC to hydrogen peroxide with significantly increased fluidity of membrane lipids were obtained signaling an oxidative metabolic stress. A twofold reduction of ATP and GSH initiated an oxidation of cellular sulfhydryl groups thus impairing enzyme kinetics of pyruvate kinase (PK). Yet heat stability of PK was markedly reduced only in those fractions containing older RBC. Further results indicate that ethanol-induced acquired PK instability may be triggered by a dialyzable and hence non-protein-bound compound, not detectable by experimental procedures owing to its low molecular weight. Thus it is conceivable that the hemolytic implication of ethanol in alcoholic liver disease may be due to abnormal membrane fluidity and metabolic disorder finally involving PK-control mechanism.