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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Changes in the antioxidant system of red blood cells may be recorded in chronic liver diseases (persistent and active hepatitis, liver cirrhosis): activation of superoxide dismutase and glutathione reductase, diminution of the activity of total and membrane-bound catalase, of the content of reduced glutathione. In liver cirrhosis, the activity of glutathione peroxidase decreases. The changes in the antioxidant system are accompanied by the reduction of the content of total and membrane-bound protein sulfhydryl groups.
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PMID:[The erythrocyte antioxidant system in chronic liver diseases]. 259 69

Thirty-six wild-caught woodchucks (Marmota monax) were characterized according to sex, weight, trapping locality, liver pathology, and serum or hepatic markers of woodchuck hepatitis virus. Liver subcellular fractions were assayed for microsomal cytochromes P-450, aryl hydrocarbon hydroxylase, glutathione, cytosolic enzymes involved in its metabolism (glutathione S-transferase, glutathione peroxidase, and glutathione reductase), in the hexose monophosphate shunt (glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase), NADH- and NADPH-dependent diaphorases, and DT diaphorase. Moreover, liver postmitochondrial fractions were assayed for their ability to activate procarcinogens [i.e., a tryptophan pyrolysate product, aflatoxin B1, 2-aminofluorene, and trans-7,8-dihydrobenzo(a)pyrene] to mutagenic metabolites in the Ames reversion test and to decrease the activity of direct-acting mutagens [i.e., 4-nitroquinoline N-oxide, 2-methoxy-6-chloro-9-[3-(2-chloroethyl)aminopropylamino]acridine X 2HCl, and sodium dichromate]. A considerable interindividual variability in metabolism was observed among the examined woodchucks. Some of the investigated parameters were more elevated in virus carriers, especially in those suffering from chronic active hepatitis, but only a few of the recorded differences (i.e., oxidized glutathione reductase and NADPH-dependent diaphorase) were statistically significant. The comparison of the monitored activities in woodchucks and in other rodent species (rat and mouse) led to the conclusion that the liver metabolism of mutagens and carcinogens in woodchucks is more oriented in the sense of activation, while detoxification mechanisms are more efficient in rats and mice.
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PMID:Metabolism of mutagens and carcinogens in woodchuck liver and its relationship with hepatitis virus infection. 360 50

As free radicals and lipid peroxidation are involved in the pathogenesis of different inflammatory diseases of the liver, the blood malondialdehyde content, the activity or quantity of free radical eliminating enzymes and the natural antioxidant, vitamin E serum level has been studied in ten patients with chronic active hepatitis and in six subjects with alcoholic liver disease. Thirty healthy volunteers served as controls. The serum malondialdehyde/thiobarbituric acid reactive substance and its concentrations increased significantly in both hepatitis groups. The superoxide dismutase content was also raised in the patients' sera. The serum glutathione peroxidase (GSH-Px) activity was decreased in both groups, while the red blood cell GSH-Px showed a significantly lower activity in the alcoholic hepatitis patients. Serum catalase activity and vitamin E levels in both types of chronic hepatitis were not significantly different from the healthy controls.
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PMID:Studies of the blood lipid peroxide status and vitamin E levels in patients with chronic active hepatitis and alcoholic liver disease. 375 86

The Long-Evans Cinnamon rat is a mutant strain that contracts hereditary hepatitis and, eventually, spontaneous hepatoma. Recently, abnormal copper accumulations in Long-Evans Cinnamon rat livers were shown to be genetically linked to the development of hepatitis. Because reduced glutathione and glutathione-related enzymes are known to play important roles in cellular resistance to transition metal toxicity, we determined the levels of reduced glutathione and glutathione-related enzymes in seven different tissues of Long-Evans Cinnamon and control Long-Evans Agouti rats. Of the enzymes examined, only hepatic glutathione peroxidase was markedly decreased in Long-Evans Cinnamon rats. Glutathione peroxidase content in the liver of Long-Evans Cinnamon rats was 39%, 53% and 58% of the control values at 9 (normal stage), 19 (acute hepatitis stage) and 27 (chronic hepatitis stage) wk of age, respectively. Northern-blot analysis revealed that messenger RNA levels of glutathione peroxidase in the livers of Long-Evans Cinnamon rats were about 40% of the control levels. The activity of glutathione S-transferase was slightly decreased in the livers of Long-Evans Cinnamon rats. These data suggest that the liver of the Long-Evans Cinnamon rat is poorly protected against active oxygen species, the production of which is enhanced in the presence of excess copper. Glutathione-reductase activity in the livers of Long-Evans Cinnamon rats increased to 166% and 148% of the control levels at 19 and 27 wk of age, respectively. No significant changes were observed in the activity of gamma-glutamylcysteine synthetase or in the content of total reduced glutathione in the liver of the Long-Evans Cinnamon rat.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Decreased expression of liver glutathione peroxidase in Long-Evans cinnamon mutant rats predisposed to hepatitis and hepatoma. 811 95

We report changes in free radical-metabolizing enzymes and the increased generation of lipid peroxides associated with extreme metal accumulation in the liver of the Long-Evans with cinnamon-like coat color (LEC) rat, a new mutant strain displaying hereditary hepatitis and subsequent hepatocellular carcinoma. The activity of free radical-metabolizing enzymes and lipid peroxides, and the concentration of metal in the liver were determined sequentially after birth. Mn-superoxide dismutase activity significantly increased immediately after the onset of hepatitis in LEC rats, whereas no remarkable change was observed in control rats. Cu, Zn-superoxide dismutase activity in LEC rats was similar to that in control rats. Glutathione reductase activity increased, while glutathione peroxidase activity was lower in LEC rats than in control rats throughout the observation periods. Lipid peroxides, estimated by thiobarbituric acid reaction, also increased 4- to 5-fold immediately after the onset of hepatitis in LEC rats. Copper concentration was 30- to 50-fold higher in the liver of LEC rats than in control rats, and the iron content also increased significantly before and after the onset of hepatitis. These findings suggested that an oxidant injury generated by toxic metals could be one of the factors responsible for hepatocellular damage in this unique hereditary hepatitis.
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PMID:Changes in free radical-metabolizing enzymes and lipid peroxides in the liver of Long-Evans with cinnamon-like coat color rats. 857 34

Galactosamine model of toxic hepatitis in rats which, as to its morphobiochemical picture, is considered adequate to human hepatitis was used to study the role of disturbances of the functional state of antioxidant and monooxygenase systems as well as humoral area of the systems of immune protection in pathogenesis of the given disease. It is shown that most components of enzymatic and nonenzymatic antioxidant system (superoxide dismutase, catalase, glutathione peroxidase, restored glutathione, phospholipids) are considerably inhibited by the toxin effect. At the same time content of ceruloplasmin is increased in the blood plasma. Considerable disturbances are also observed in the humoral chain of the immune system (content of immunoglobulins and circulating immune complexes varies) and in the processes of microsomal oxidation.
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PMID:[Status of the antioxidant, monooxygenase and humoral immune system of the body in d-galactosamine hepatitis]. 875 5

The liver is especially susceptible to the toxic effects of methionine due to its role in sulfur amino acid metabolism. Therefore, the excessive amounts of this amino acid may induce liver damage. To test the mechanisms of methionine-related hepatotoxicity, liver thiobarbituric acid reactive substances (TBARS), and activities of superoxide dismutase, catalase and selenium-dependent glutathione peroxidase were measured in rabbits fed a methionine-enriched diet for 6 or 9 mo. Morphological studies of livers were also made. Feeding rabbits the methionine-enriched diet for 9 mo resulted in a significant increase in liver TBARS levels and antioxidant enzyme activities. Moreover, an inflammatory infiltration of portal triads in the treated rabbits were observed. These results indicate that methionine may induce hepatitis by increasing free radical processes.
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PMID:Increased lipid peroxidation and antioxidant activity in methionine-induced hepatitis in rabbits. 887 49

Reactive oxygen species (ROS) are cytotoxic, causing inflammatory disease, including tissue necrosis, organ failure, atherosclerosis, infertility, birth defects, premature aging, mutations and malignancy. ROS are produced in the metabolism of drugs and industrial chemicals by (i) one-electron peroxidase oxidations to form cation radicals, (ii) cytochrome P450 metabolism to free radical products, (iii) stabilisation of the ROS-generator, CYP2E1, and (iv) futile cycling of other cytochromes P450. ROS production initiates inflammation which unless quenched may result in chronic inflammatory disease states, e.g. hepatitis, nephritis, myositis, scleroderma, lupus erythematosus, multiple system organ failure. Quenching of ROS is affected by the redox buffer, glutathione (GSH), and the antioxidants, ascorbic acid, tocopherols, retinoids, in conjunction with the redox enzymes, GSH reductase, GSH peroxidase, catalase and superoxide dismutase. Many industrial workers with symptoms of systemic inflammation, resulting from exposure to toxic chemicals, are diagnosed as having rheumatoid arthritis, virus infections, or other microbial lesions, largely because many physicians are unaware that exposure to certain chemicals can initiate inflammatory disease states.
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PMID:Chemical toxicity and reactive oxygen species. 911 92

The hepatic concentrations of copper, zinc, magnesium, calcium, and selenium were measured in LEC rats, which develop a spontaneous form of hepatitis at 3-4 months of age, and compared to trace metal concentrations in the LEA rat, its asymptomatic congenic strain. Consistent with results found by other groups, copper was found to accumulate within the liver of LEC rats to levels more than 50 times those measured in LEA rats. In addition, liver selenium concentration in LEC rats was found to be around 50% of that in LEA rats. The enzyme activity, and RNA for the selenium dependent enzyme, glutathione peroxidase, was also found to be reduced in LEC rat liver. These results indicate that hepatic selenium in the LEC rat is depleted and that, as a result of this, the capacity to protect cells from copper-induced free-radical damage is reduced.
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PMID:The LEC rat possesses reduced hepatic selenium, contributing to the severity of spontaneous hepatitis and sensitivity to carcinogenesis. 951 49

Antioxidant properties of cresacin were studied on the model of galactosamine hepatitis and on the isolated liver cells of white male rats. It has been shown, that cresacin in a dose of 20 mg/kg effectively inhibits the processes of lipid peroxidation induced by hepatotoxin. Cresacin also normalized some components of fermentative and non-enzymatic antioxidant system. In particular the indexes of the activity of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and the level of reduced glutathione, total phospholipids and ascorbic acid was increased for certain. In vitro, on the isolated hepatocytes, cresacin showed the dose-dependent antioxidant effect. This fact is confirmed by its property to inhibit the speed of formation of the malonic dialdehyde in the incubation medium.
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PMID:[Protective effect of cresacin in D-galactosamine-induced acute experimental hepatitis]. 984 42


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