Homocysteine-Induced Oxidative Damage: Mechanisms and Possible Roles in Neurodegenerative and Atherogenic Processes

Abstract

Increased blood plasma concentrations of the sulphur amino acid homocysteine ("homocysteinemia") have been brought into context with neurodegenerative and arteriosclerotic symptoms and diseases. We recently reported on biochemical model reactions on the prooxidative activity of homocysteine including the desactivation of Na+/K(+)-ATPases and hemolysis of erythrocytes (Preibisch et al., 1993). In this communication we extend our model reactions including the oxidation of methionine, metabolization of pyridoxalphosphate and dihydroxyphenylalanine, desactivations of transaminases and peroxidation of low density lipoprotein.