Lack of evidence for increased lipid peroxidation in ethanol‐induced centrilobular necrosis of rat liver

Wiley - Tập 7 Số 4 - Trang 233-239 - 1987
Tomoo INOMATA1,2, G. Ananda Rao3, Hidekazu Tsukamoto1,2
1Department of Internal Medicine, University of California Davis, School of Medicine, Davis, California, USA
2Hepatopancreatic, VA Medical Center, Martinez, California, USA
3Alcohol Research Laboratories, VA Medical Center, Martinez, California, USA

Tóm tắt

ABSTRACT— The pathogenetic role of lipid peroxidation in ethanol‐induced liver injury was previously supported by demonstration of increased formation of diene conjugates and decreased hepatic levels of reduced glutathione in ethanol‐fed animals and alcoholic patients with liver injury. The present study was carried out to investigate whether these findings can be extended to a rat model that was shown to produce a spontaneous ethanol‐induced liver injury progressing from steatosis to necrosis and fibrosis (Hepatology 6: 814, 1986). Despite the histological evidence of progression from hepatic steatosis to centrilobular necrosis in these animals, diene conjugate formation in mitochondrial and microsomal lipids was not enhanced when compared to pair‐fed controls. In addition, hepatic levels of neither methionine nor glutathione were decreased in the ethanol‐fed animals. The fatty acid composition of mitochondrial phospholipids from these animals was similar to that in the controls. However, in the microsomal phospholipids, the level of arachidonate (20:4) was depressed by about 50% as compared to the controls. These results demonstrate the lack of evidence for a pathogenetic relationship between lipid peroxidation and ethanol‐induced liver injury progressing to centrilobular necrosis. They further suggest that the decreased levels of 20:4 commonly seen after chronic ethanol intake may not be due to a peroxidative loss.

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Tài liệu tham khảo

10.1126/science.152.3727.1390-a

Shaw S., 1981, Ethanol‐induced lipid peroxidation: potentiation by long‐term alcohol feeding and attenuation by methionine, J Lab Clin Med, 98, 417

10.1016/0024-3205(82)90743-3

10.1042/bj2120625

10.1007/BF01299917

10.1016/0014-4800(68)90018-X

10.1079/BJN19690038

10.1016/S0041-008X(77)80031-8

10.1002/path.1711260103

Speisky H., 1985, Lack of changes in diene conjugate levels following ethanol induced glutathione depletion of hepatic necrosis, Res Commun Chem Pathol Pharmacol, 48, 77

10.1016/0005-2760(85)90156-0

Lieber C S, 1976, Animal models of ethanol dependence and liver injury in rats and baboons, Fed Proc, 35, 1232

10.1002/hep.1840060503

Tsukamoto H., 1984, Long‐term cannulation model for blood sampling and intragastric infusion in the rat, Am J Physiol, 247, R595

10.1002/hep.1840050212

10.1139/y59-099

10.1007/BF02533548

10.1016/0003-2697(76)90326-2

10.1016/0014-4800(70)90064-X

10.1016/0006-2952(85)90057-7

Lieber C S., 1982, Medical disorders of alcoholism. Pathogenesis and treatment, 259

10.1016/0003-9861(83)90606-9

10.1016/0041-008X(83)90181-3

French S W, 1971, The effect of ethanol on the fatty acid composition of hepatic microsomes and inner and outer mitochondria membranes, Res Commun Chem Pathol Pharmacol, 2, 567

10.1016/0163-7827(79)90007-9

10.1111/j.1530-0277.1983.tb05445.x

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Wiley

Tập 7 Số 4

233-239

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