Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

A reciprocal type of the relationship between superoxide dismutase (SOD) and hepatic ceruloplasmin levels in the liver and plasma has been demonstrated. This acts as an integrating mechanism of antioxidant resistance in hepatobiliary diseases. The value of SOD/ceruloplasmin ratio is presented which was low in primary biliary cirrhosis and chronic cholestatic hepatitis. A statistical significance for the differences between biochemical indices of cholestasis (bilirubin, cholesterol, alkaline phosphatase) was less than for SOD/ceruloplasmin ratio. The latter proved more informative in the diagnosis of cholestasis.
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PMID:[A new approach to the diagnosis of cholestasis by the activity of copper-containing enzymes]. 913 6

Patients with acute viral hepatitis B were found to have an increase in the processes of peroxidization of lymphocyte membrane lipids and in the activity of superoxide dismutase, an antioxidant enzyme, depending on the period of the disease and its severity. Patients with a severe form of the disease were found to have specific features of the intracellular metabolism of lymphocytes in comparison with patients having moderate forms of the disease. To a lesser degree, the characteristics of lymphocytes in hepatitis cases depended of the etiology of the disease, caused by hepatitis virus B, C or the combination of both. The properties of lymphocytes were found to reflect the immune reactiveness of the body and could be used for evaluating the severity of the disease, prognostication and the achievement of convalescence.
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PMID:[Intensity of the peroxidation of membrane lipids and metabolism of lymphocytes in viral hepatitis patients]. 982 4

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

To examine the mechanism of the preventive effect of tannins on the progression of carbon tetrachloride (CCl4)-induced acute liver injury in rats, sumac gall (SG) extract and gallic acid (GA) were used as substitutes for crude tannins, because SG is a kind of Chinese traditional medicinal herb containing large amounts of various tannins, and GA is one of the major constituents of SG. The protective effect of oral (p.o.) and intraperitoneal (i.p.) administration of each substance on progression of CCl4-induced hepatitis was investigated in rats. Speculating that the superoxide dismutase (SOD)-like activities (O2 radical-scavenging activities) and/or protective effects of these substances on cell membranes might play a key role in the mechanism opposing the progression of CCl4-induced hepatitis, the O2 radical-scavenging activities in liver cells and serum in rats were monitored. Both substances significantly prevented the progression of acute liver injury with both p.o. and i.p. administration. These findings suggest that the mechanism for this prevention might be due mainly to the protective effect of these substances on cell membranes rather than O2 radical-scavenging activities.
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PMID:Mechanism of the protective effects of sumac gall extract and gallic acid on the progression of CCl4-induced acute liver injury in rats. 986 21

Biotechnological techniques of cross-linking and microencapsulation of hemoglobin result in blood substitutes that can replace red blood cells. Unlike red blood cells they can be sterilized by pasteurization, ultrafiltration and chemical means. This removes microorganisms responsible for AIDS, hepatitis, etc. Since they are free of red blood cell blood group antigens, there is no need for cross-matching or typing. This saves time and facilities and allows on-the-spot transfusion such as the infusion of salt solution. Furthermore, they can be stored for a long time. Hemoglobin for modification can be extracted from human red blood cells. Other sources of hemoglobin include bovine hemoglobin and recombinant human hemoglobin. Clinical trials are ongoing testing the possible uses of cross-linked hemoglobin in cardiac, orthopedic, trauma and other types of surgery. It is also being tested for the replacement of lost blood in severe bleeding due to trauma or other causes. Cross-linked hemoglobins are first generation blood substitutes that only fulfil some of the functions of red blood cells. New generations of more complete red blood cell substitutes are being developed. These include cross-linked hemoglobin-catalase-superoxide dismutase and microencapsulated hemoglobin-enzyme systems.
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PMID:Modified hemoglobin blood substitutes: present status and future perspectives. 989 Jan 39

A zinc (Zn)-binding protein that is present specifically in the livers of male adult rats was detected by HPLC with in-line detection by mass spectrometry (ICP MS). The Zn-binding protein was purified on Sephadex G-75 and G3000SW HPLC columns. and was identified as carbonic anhydrase III (CAIII) based on the amino acid sequence of a peptide obtained on lysyl endopeptidase digestion. CAIII is expressed as one of the major Zn-binding proteins in the livers of male rats in an age-dependent manner, a comparable amount of Zn to that of copper, Zn-superoxide dismutase (Cu,Zn-SOD) being bound to CAIII at 8 weeks of age. Castration at 4 or 8 weeks of age was shown to reduce Zn bound to CAIII to 47.5% of the sham-operated control level, suggesting that the sex-dependent expression of CAIII is partly regulated by a sex hormone, androgen. The concentration of CAIII in the livers of Long-Evans rats with a cinnamon-like coat color (LEC rats), an animal model of Wilson disease, was also estimated as Zn bound to CAIII and shown to be lower than that in Wistar rats before the onset of hepatitis. The concentration of CAIII was decreased specifically by repeated injections of cupric ions without the Cu,Zn-SOD concentration being affected.
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PMID:Identification of the zinc-binding protein specifically present in male rat liver as carbonic anhydrase III. 1068 38

In order to understand the impact of viral hepatitis on anti-oxidant defence system of the body, blood levels of superoxide dismutase (SOD), an enzymatic anti-oxidant, and total anti-oxidant (TAO) were evaluated and co-related to etiological viral hepatitis in various forms of liver diseases. A total number of 110 patients including 50 patients with acute viral hepatitis (AVH), 30 patients with chronic active hepatitis (CAH) and 30 patients with cirrhosis of liver were analysed for different hepatitis viral markers and the anti-oxidant levels in their blood. For comparison, blood from 100 healthy persons were also simultaneously tested for anti-oxidant levels. Analysis of results indicated that none of the patients belonging to these three liver diseases had hepatitis A viral (HAV) and hepatitis D viral (HDV) infections. AVH group had mainly hepatitis B viral (HBV), hepatitis C viral (HCV) and hepatitis E viral (HEV) infections, CAH group had B and C infections and cirrhosis group had B, C and E infections. A sizeable number of patients in each group had no markers and were labelled as non-BCE group. On co-relating anti-oxidant levels to viral etiology in these patients, it was observed that in comparison to healthy control group, SOD level was significantly reduced in all the patients irrespective of the viral etiology (P<0.05-0.001). The impact of different viruses on reduction in SOD level was recorded to be the same with no significant difference in SOD level between any two viral infections. On the contrary, TAO level in the majority of patients was found to be comparable with that observed in healthy persons. An appreciable change in SOD level but little impact on TAO level during viral hepatitis may be explained by the possible adaptive rise of some other anti-oxidant level in the blood of these patients.
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PMID:Superoxide dismutase and total anti-oxidant levels in various forms of liver diseases. 1207 13

Long-Evans Cinnamon (LEC) rats spontaneously develop fulminant hepatitis, associated with excess Cu accumulation in the liver: thus, they are considered an animal model of Wilson's disease. In the present study, we investigated the ability of excess dietary histidine to reduce the excess accumulation of liver Cu in LEC rats by comparing them with Fischer rats. The results clearly showed that the excess-histidine diet markedly stimulated the Cu excretion in urine, and significantly decreased the liver Cu content in LEC rats by 47.5%. The serum Cu content in LEC rats was not influenced by excess dietary histidine. We also compared the effects of excess dietary histidine on some liver antioxidant enzyme activities, liver and serum lipid levels and serum alanine aminotransferase activity of LEC and Fischer rats. Dietary histidine decreased the activities of total and Cu,Zn-superoxide dismutase in the liver of both strains. In LEC rats, the liver cholesterol content decreased, and serum cholesterol and phospholipids levels increased on feeding the excess-histidine diet. When fed on the basal diet, the serum alanine aminotransferase activity was higher in LEC rats than in Fischer rats, but a significant decrease in serum alanine aminotransferase activity of LEC rats was observed on feeding the excess-histidine diet. These results suggest that excess dietary histidine is effective in removing Cu ions from the liver of LEC rats. Thus, it may be of benefit in the prevention or treatment of liver injury in LEC rats and in patients with Wilson's disease.
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PMID:Excess dietary histidine decreases the liver copper level and serum alanine aminotransferase activity in Long-Evans Cinnamon rats. 1312 63

Copper is an essential trace element with various biological functions. Excess copper, however, is extremely toxic, leading to many pathological conditions that are consistent with oxidative damage to membranes and molecules. Exposure to high levels of copper results in various changes in the tissues. In liver, hypertrophy of hepatocytes, hepatitis, hepatocellular necrosis, and hepatocellular death are the results. Lipid peroxidation causes dysfunction in the cell membrane, decreased fluidity, inactivation of receptors and enzymes, and changes ion permeability. In this study, we aimed to determine the effect of copper on oxidative and antioxidative substances in plasma and liver tissue in a rat model. Sixteen male Sprague-Dawley rats were divided into two groups: Group 1 rats included control rats given tap water. Group 2 rats were given water containing copper in a dose of 100 microg/mL. All rats were sacrificed at 4 wk under ether anesthesia. Plasma and liver superoxide dismutase (SOD) activities, plasma and liver MDA (malondialdehyde) levels, and liver glutathione (GSH) levels were studied. Plasma and liver SOD activities were found to be higher in group 2 than those in group 1. Although plasma MDA levels were higher in group 2, MDA levels in liver tissues were comparable. Liver tissue glutathione levels were lower in group 2. It was concluded that although copper is needed in trace amounts, an excess amount is toxic for the organism. It increases lipid peroxidation and depletes GSH reserves, which makes the organism more vulnerable to other oxidative challenges.
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PMID:Copper-mediated oxidative stress in rat liver. 1471


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