This study looked at the possible association between alcohol abuse and free radical mediated oxidative injury by examining the presence of oxidative damage, as monitored by erythrocyte malonildialdehyde and plasma lipid hydroperoxides, in patients with liver cirrhosis and different lifetime daily alcohol intake. All patients with an alcohol intake above 100 g/day (ALC) showed concentrations of malonildialdehyde and lipid hydroperoxide on average four to fivefold higher than cirrhotic patients with alcohol intake below 100 g/day (NAC) or healthy controls. Further subgrouping of ALC patients showed that those with alcohol intake ranging between 100 and 200 g/day (ALC1) had malonildialdehyde and lipid hydroperoxide concentrations significantly lower than those with an intake higher than 200 glday (ALC2). These differences were not related to the extent of liver injury or to the liver derangement as assessed by Child's classification. The increase in lipid peroxidation markers in ALC cirrhotic patients was associated with a decrease in, respectively, plasma a-tocopherol and erythrocyte glutathione concentrations. Significant differences were also seen between ALC1 and ALC2 groups in plasma ox-tocopherol, but not in erythrocyte glutathione concentrations. The concentrations of ot-tocopherol and glutathione in the blood of NAC patients were in contrast not substantially different from those of healthy controls. The close association between oxidative damage and alcohol abuse suggested that free radical intermediates produced during ethanol metabolism might be responsible for causing oxidative damage. (Gut 1994; 35: 1637-1643 In recent years the finding that reactive oxygen species and hydroxyethyl radicalsl-3 are produced during the hepatic metabolism of ethanol has given new emphasis to the possible participation of free radical mediated damage in the pathogenesis of tissue injury resulting from alcohol abuse. The presence of oxidative damage in relation to alcoholic intoxication has also been investigated in clinical studies performed on alcoholic patients. These studies, however, have given contradictory results. For instance, lipoperoxide concentrations, measured by the thiobarbituric acid method in liver and in serum were found to be higher in heavy drinkers than in non-drinkers.'0 A significant increase in the conjugated diene content has also been detected in the lipids extracted from hepatic biopsy specimens of alcoholic patients at different stages of liver disease. These patients also presented a decrease in the hepatic concentrations of glutathione and ox-tocopherol that was unrelated with their nutritional state.'"'-Other authors have raised doubts, however, about the specificity of the association between oxidative damage and ethanol intoxication, as an increase in liver or serum thiobarbituric acid reactive substances has been seen in patients suffering from alcoholic as well as non-alcoholic liver disease. '4 15 A further problem in the interpretation of these results is that subsequent stud...
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