ETHANOL-INDUCED LIPID-PEROXIDATION - POTENTIATION BY LONG-TERM ALCOHOL FEEDING AND ATTENUATION BY METHIONINE

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  • 1 January 1981
    • journal article
    • research article
    • Vol. 98  (3) , 417-424
Abstract
Lipid peroxidation was incriminated in some types of drug-induced liver, but it was unclear whether it contributed to or was present in alcoholic liver injury. To study this question, hepatic lipid peroxidation (measured as formation of diene conjugates) and hepatic GSH [glutathione] were assessed in baboons and rats after short- and long-term ethanol administration. Compared to controls, baboons fed alcohol for 1-4 yr (chronic administration) had increased hepatic diene conjugates (16.9 .+-. 4.8 OD[optical density]/g liver) and depressed GSH (3.8 .+-. 0.6 vs. 6.3 .+-. 0.8 .mu.mol/g liver; P < 0.01) after an overnight withdrawal from ethanol. Administration of 1.6 g/kg ethanol over 6 h (acute administration) increased diene conjugates (17.6 .+-. 4.3) and decreased GSH (3.2 .+-. 0.5; P < 0.01) in control animals and had a greater effect in animals chronically fed alcohol (diene conjugates 48.5 .+-. 9.2; GSH 1.8 .+-. 0.3; P < 0.001). In 6 rats fed alcohol for 5-6 wk (chronic administration), an increase in diene conjugates was detected in microsomes (0.343 .+-. 0.210 OD/mg lipid) and mitochondria (0.143 .+-. 0.061), accompanied by decreases in arachidonic acid and C22 polyenes, after acute ethanol administration (3 g/kg orally) but no significant change in GSH. Simultaneous administration of methionine attenuated diene conjugate formation (0.107 .+-. 0.058 and 0.035 .+-. 0.020 OD/mg lipid, respectively) and fatty acid changes. Chronic alcohol feeding potentiated lipid peroxidation produced by an acute dose of ethanol; these changes were not dependent on GSH depression but may be potentiated by it.