[Experimental and clinical studies on enzymes of mitochondria in various liver diseases; with special reference to alcoholic liver disease (author's transl)].
Mitochondrial enzymes in rat livers or intestines were investigated in experimental models with ethanol- or other hepatotoxic agent-induced liver injuries and extrahepatic cholestasis. In clinical experiment, activities of mitochondrial GOT (mGOT) and ornithine carbasmyl transferase (OCT) were examined in alcoholisms and patients with other various liver diseases. Results obtained are as follows; 1) The activities of OCT and mGOT were increased particularly at onset of acute hepatitis, in chronic active hepatitis and intrahepatic cholestasis, showing that mitochondria were injured strikingly in these diseases. The activities in alcoholics were not so great, however mGOT/total-GOT ratio was increased in level than in other diseases. 2) Changes in mitochondrial enzymes of rat liver treated with ethanol were too varied to catch the actual tendency in this pathologic state. 3) Administration of galactosamine, carbon tetrachloride, or alpha-naphthyl isothiocyanate (ANIT) caused a significant fall in activities of succinate cytochrome C reductase and OCT, along with increase in serum activity of OCT, indicating severe mitochondrial injury with these drugs. Extrahepatic cholestasis following bile duct ligation showed the same changes of mitochondrial enzymes in liver tissue and serum. 4) These data indicate that observation of activities of serum OCT, mGOT, along with mGOT/total-GOT ratio are useful for estimation of mitochondrial damage in extra- and intra-hepatic cholestasis, and acute or chronic active hepatitis. The changes in alcoholic fatty liver was not so subtle as compared with other liver diseases. 5) It is surmized that smooth endoplasmic reticulum was increased in content and pentose phosphate shunt was inhibited by chronic ethanol treatment, estimating from increased activities of NADH-ferricyanide reductase and gamma-glutamyl transpeptidase, and decreased activity of glucose-6-phosphate dehydrogenase. 6) The changes in hepatic enzymes with ethanol treatment were paralleled with those of intestinal ones, indicating that metabolic changes in intestine contribute someway in the formation of alcoholic fatty liver. 7) Chronic ethanol treatment induced lowered active transport in intestinal mucosa, which indicates inhibition in absorption of various nutrients by ethanol.
D015058:1-Naphthylisothiocyanate; D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002251:Carbon Tetrachloride; D056486:Chemical and Drug Induced Liver Injury; D005688:Galactosamine; D005952:Glucose-6-Phosphatase / Q000378:metabolism; D005954:Glucosephosphate Dehydrogenase / Q000378:metabolism; D006801:Humans; D008108:Liver Diseases, Alcoholic / Q000201:enzymology*; D008297:Male; D008930:Mitochondria, Liver / Q000201:enzymology*; D006899:Mixed Function Oxygenases / Q000378:metabolism; D009251:NADPH-Ferrihemoprotein Reductase / Q000378:metabolism; D009954:Ornithine Carbamoyltransferase / Q000378:metabolism; D051381:Rats; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism; D013384:Succinate Cytochrome c Oxidoreductase / Q000378:metabolism
D015058:1-Naphthylisothiocyanate; D005688:Galactosamine; D002251:Carbon Tetrachloride; D006899:Mixed Function Oxygenases; D013384:Succinate Cytochrome c Oxidoreductase; D005954:Glucosephosphate Dehydrogenase; D009251:NADPH-Ferrihemoprotein Reductase; D009954:Ornithine Carbamoyltransferase; D001219:Aspartate Aminotransferases; D005952:Glucose-6-Phosphatase; D000254:Sodium-Potassium-Exchanging ATPase