HOMOCYSTEINE-INDUCED OXIDATIVE DAMAGE - MECHANISMS AND POSSIBLE ROLESIN NEURODEGENERATIVE AND ATHEROGENIC PROCESSES

Increased blood plasma concentrations of the sulphur amino acid homocy steine (''homocysteinemia'') have been brought into context with neuro degenerative and arteriosclerotic symptoms and diseases. We recently r eported on biochemical model reactions on the prooxidative activity of homocysteine including the desactivation of Na+/K+-ATPases and hemoly sis of erythrocytes (Preibisch et al., 1993). In this communication we extend our model reactions including the oxidation of methionine, met abolization of pyridoxalphosphate and dihydroxyphenylalanine, desactiv ations of transaminases and peroxidation of low density lipoprotein.