The question of whether or not ethanol-induced liver injury is related to or accompanied by lipid peroxidation has been a subject of controversy. Short-term ethanol administration was shown by some to produce hepatic lipid peroxidation in rats,
but
very
large doses of ethaol had to be used. Furthermore, some investigators failed to confirm these effects of ethanol. Fewer studies have explored the relationship between alcohol consumption and lipid peroxidation. In order to study this question and
clarify the role of oxygen derived free radicals and lipid peroxidation of the RBC in inducing the alcoholic live diseases, we measured the thiobarbituric acid reactivities in normal controls and patients with alcoholic liver disease. The
subjects
were
divided into three groups according to the liver function tests and the amounts of alcohol drinking; group I-normal controls, group II-cases showing normal liver function test in spite of frequent alcohol drinking over 3 days per week and 45 g
alcohol
per one time, group III-patients with alcoholic liver disaesae, drinking alcohol over 4 times per week. The thiobarbituric acid reactive substances were measured as a marker of lipid peroxidation by the method of Uchiyama and Mihara. The
colorimetric
method was used by a measurment of malonyldialdehyde [MDA, nmold/ml (packed cells)] concentration. The results were as follows;
-Ki Baik Hahm, et al : Role of Lipid Peroxidation in Pathogenesis of Alcoholic liver Diseases-
The mean MDA concentrations of group III was 1.67±1.01 nmol/ml (packed cells), which was significantly higher than those of group I [0.73±0.01 nmol/ml (packed cells)] and group II(1.01±0.39 nmol/ml (packed cells)). the MDA concentrations was
significantly correlated with total protein (r=0.47, p<0.05), total cholesterol.(r=0.49, p<0.05), and frequency of alcohol drinking (r=0.49, p<0.05) in group III. There was a significant difference in mean MDA concentration between the cases with
normal
serum albumin and cases with hypoalbuminemia in patients with alcoholic liver cirrhosis. These data suggest that lipid peroxidation might play a contributing role in the pathogenesis of alcoholic liver disease.
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