ACETALDEHYDE INDUCES MYOCARDIAL IRON DELOCALIZATION AND LIPID-PEROXIDATION - POSSIBLE MECHANISM IN ALCOHOLIC CARDIOMYOPATHY - ACETALDEHYDE INDUCES IRON DELOCALIZATION

The purpose of this study was to investigate a proposed mechanism of i njury in alcoholic cardiomyopathy. We tested the hypothesis that aceta ldehyde enhances myocardial lipid peroxidation. The effect of free rad ical scavengers and iron chelators on acetaldehyde-induced myocardial lipid peroxidation was also determined. Turkey and rat left ventricula r homogenates with and without free radical scavengers (superoxide dis mutase, catalase, mannitol and histidine) and iron chelator deferoxami ne were incubated with acetaldehyde for 60 minutes, The extent of myoc ardial lipid peroxidation and the amount of low molecular weight chela ted (LMWC) iron were determined using malondialdehyde and lipid hydrop eroxide production and by measuring LMWC iron levels in these myocardi al homogenates. Acetaldehyde increased myocardial lipid peroxidation i n a dose-dependent manner as reflected by an increase in both malondia ldehyde and lipid hydroperoxide levels. Acetaldehyde released LMWC iro n from myocardial cells; the iron chelator deferoxamine was effective in reducing the acetaldehyde-induced increase in lipid peroxidation. T hese in vitro results suggest that a possible mechanism for alcoholic cardiomyopathy is acetaldehyde-induced release of LMWC iron with subse quent initiation of lipid peroxidation and myocardial injury. Should a similar effect occur in vivo, these results would enhance our underst anding of acetaldehyde and ethanol induced myocardial injury and sugge st a role for iron chelators in possible treatment and prevention of a lcohol induced heart muscle disease.