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Hepatic mitochondrial glutathione depletion and progression of experimental alcoholic liver disease in rats

✍ Scribed by Akeshi Hirano; Neil Kaplowitz; Hidekazu Tsukamoto; Seiichiro Kamimura; Jose C. Fernandez-Checa

Publisher: John Wiley and Sons
Year: 1992
Tongue: English
Weight: 487 KB
Volume: 16
Category: Article
ISSN: 0270-9139
DOI: 10.1002/hep.1840160619

No coin nor oath required. For personal study only.

✦ Synopsis

Long-term ethanol feeding has been shown to selectively reduce hepatic mitochondrial glutathione content by impairing mitochondrial uptake of this thiol. In this study, we assessed the role of this defect in evolution of alcoholic liver disease by examining the mitochondrial glutathione pool and lipid peroxidation during progression of experimental alcoholic liver disease to centrilobular liver necrosis and fibrosis. Male Wistar rats were intragastrically infused with a high-fat diet plus ethanol for 3,6 or 16 w k (the duration that resulted in induction of liver steatosis, necrosis and fibrosis, respectively). During this feeding period, the cytosolic pool of glutathione remained unchanged in the ethanol-fed animals compared with that in pair-fed controls. In contrast, the mitochondrial pool of glutathione selectively and progressively decreased in rats infused with ethanol for 3,6 or 16 wk, by 39%. 61% and 85%, respectively. Renal mitochondrial glu- tathione level remained unaffected throughout the experiment. Serum ALT levels increased significantly in the ethanol-fed rats at 6 wk and remained elevated at 16 wk. In the mitochondria with severely depleted glutathione levels at 16 wk, enhanced lipid peroxidation was evidenced by increased malondialdehyde levels. Thus a progressive and selective depletion of mitochondrial glutathione is demonstrated in the liver in this experimental model of alcoholic liver disease and aeeociated with mitochondrial lipid peroxidation and progression of liver damage. (HEPATOLOGY 1992;16: 1423-1427.) The pathophysiology of alcoholic liver disease (ALD) remains uncertain. Many theories with supporting data have been proposed. A variety of evidence suggests a role for lipid peroxidation in the pathogenesis of ALD in experimental models and in human beings ( 1 -3 ~. A

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