Experimental heart muscle damage in alcohol feeding is associated with increased amounts of reduced- and unreduced-acetaldehyde and malondialdehyde-acetaldehyde protein adducts

Chronic and excessive alcohol consumption induces defined myocardial lesion s characterized by impaired structural, mechanical and biochemical features . The pathogenic mechanisms are unknown, although it is possible that prote in adduct formation by reactive metabolites of ethanol may be a contributor y process. Hither to, this has only been tested with respect to antibodies against reduced-acetaldehyde protein adducts in clinical studies, despite t he fact that during alcohol toxicity the formation of reduced-acetaldehyde, unreduced-acetaldehyde, malondialdehyde, malondialdehyde-acetaldehyde and hydroxyethyl protein adducts have been reported in non-cardiac tissues. It was our hypothesis that the heart is particular ly sensitive to the formati on of protein adducts in alcohol toxicity. To test this hypothesis, we anal ysed hearts from rats fed nutritionally complete liquid diets containing et hanol as 35% of total calor ies for 6 weeks, using the Lieber-DeCarli pair- feeding protocol. Control rats were treated identically and fed the same di et in which ethanol was replaced by isocaloric glucose. At the end of the f eeding period, the hearts were dissected and ventricular muscle analysed. A fter 6 weeks' ethanol feeding, ELISA analysis showed increased amounts of r educed-acetaldehyde protein adducts (p < 0.01) unreduced-acetaldehyde (p < 0.01) and malondialdehyde-acetaldehyde (p = 0.01) protein adducts. However, malondialdehyde and alpha-hydroxyethyl-protein adducts were not significan tly increased in hearts of ethanol-fed rats compared to pair-fed control (p > 0.1 in both instances). This is the first report of acetaldehyde adduct formation in alcoholic cardiomyopathy. This suggests that either immune pro cess may develop or functional impairment of affected proteins may occur.