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)

Copper (Cu), iron (Fe), zinc (Zn) and manganese (Mn) levels in organs of LEC rats (Long-Evans rats with a cinnamon-like coat color), which develop spontaneous jaundice with hereditary hepatitis, were determined by instrumental neutron activation analysis method. Unusual accumulations of Cu in the liver of LEC rats were found, depending on the age of the animals, the metal concentration being more than approximately 20-40 times those of normal LEA rats (Long-Evans rats with an agouti coat color). Fe and Zn were also accumulated, in addition to Cu, significantly in the LEC rats. The unusual Cu accumulations in the liver of LEC rats were associated with the induction of metallothionein, estimated by radioimmunoassay method, in the liver of LEC rats, rather than that of superoxide dismutase, estimated by electron spin resonance -spin trapping method. These findings suggest that the unusual Cu accumulation in LEC rats is involved in the development of jaundice, hepatic injury and hepatocellular carcinoma.
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PMID:Unusual accumulation of copper related to induction of metallothionein in the liver of LEC rats. 131 72

Pretreatment with the reactive oxygen species scavengers superoxide dismutase (SOD) and catalase or with the xanthine oxidase inhibitor allopurinol protected mice against hepatitis induced by the combined administration of lipopolysaccharide (endotoxin) and D-galactosamine. In the sera of protected animals no tumor necrosis factor (TNF alpha) was detectable in contrast to abundant amounts in the sera of injured control animals. A similar protection by the suppression of systemic TNF alpha was observed following the pretreatment of mice with polystyrene-coupled SOD prior to endotoxic challenge. Both pretreatments were ineffective when hepatitis was evoked by administration of the mediator TNF alpha instead of endotoxin. These findings indicate that the formation of extracellular reactive oxygen species is a condition needed to induce the release of TNF alpha and thus to mediate endotoxin-induced toxicity.
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PMID:A link between extracellular reactive oxygen and endotoxin-induced release of tumour necrosis factor alpha in vivo. 155 88

Seventy-seven blood samples from normal controls aged 0-8 years and 93 blood samples from children of similar ages with various viral hepatitis were investigated by measuring plasma superoxide dismutase (EC 1.15.1.1) using chemiluminescence immunoassay (CLIA). Total and Cu,Zn-SOD activities of normal controls of group 2 (1-8 years old) were significantly higher than that of normal controls of group 1 (0-1 year old) (P less than 0.01, P less than 0.01), while there were no differences of Mn-SOD activities between the two groups. Total, Cu,Zn- and Mn-SOD activities significantly increased in the acute phase (0-4 weeks after onset) and dropped to the normal levels in the restoration phase (4th week later) for 29 children with cytomegalovirus hepatitis (CMVH), in comparison with group 1. Only Mn-SOD activities were significantly increased in the acute phase (with increased ALT levels) and restoration phase (with normal ALT levels) for 18 children with hepatitis A (HA). Total and Cu,Zn-SOD activities significantly decreased and Mn-SOD activities significantly increased in both the active (with increased ALT levels) and the inactive phases (with normal ALT levels) for 36 children with chronic persistent hepatitis (CPH). Only Cu,Zn-SOD activities fell significantly in both active and inactive phases for 10 children with chronic active hepatitis (CAH).
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PMID:Plasma superoxide dismutase measurement in children with viral hepatitis. 164 17

The components of the blood antioxidant systems (superoxide dismutase, catalase, ceruloplasmin, glutathione system) take a direct part in the molecular mechanisms of the body adaptation under conditions of viral hepatitis infection. The peculiarity of the mechanisms by which lipid peroxidation is regulated in different grades of hepatitis is of a role in the disease pathogenesis and underlies the prediction of the course of hepatitis.
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PMID:[The importance of the antioxidant protection systems of the blood in adaptation to the infectious process in viral hepatitis B]. 181 63

HCV infections are diagnosed by determining the circulating antibodies to the C 100 recombinant viral antigen using the ELISA method. Cut-off analysis from normal subjects and well documented NANBH patients suggests that screening of a low risk group such as blood donors might yield a relatively high ratio of false positives. An immunoblot assay (Chiron RIBA) using 3 recombinant antigens, C 100, 5-1-1 and SOD has been developed for evaluating the ELISA reactives as an additional, more specific assay. In the RIBA testing 51.5% were reactive and 28.5% were indeterminate in ELISA positive donor specimens, and 79.5% were reactive and 8.0% were indeterminate in ELISA positive non-A, non-B hepatitis patients specimens. These findings coincide with the ratio of theoretically calculated true positive. In a study done by Ortho U.S.A. viral RNA were detected in 70% of RIBA reactive, 33% of indeterminate and 3.6% non-reactive specimens by polymerase chain reaction (PCR). Furthermore, an advanced system using another immunogenic region of viral polyprotein including c33c encoded in NS3 has been on trial to evaluate the possibility of confirming HCV infection and detecting seroconversion at an earlier stage.
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PMID:[Interpretation of Ortho HCV Ab ELISA test results by chiron HCV recombinant immunoblot assay]. 184 12

In unseparated human blood the reactivity of yeast copper (I)-thionein on TPA-activated polymorphonuclear leukocytes was evaluated and compared with low Mr copper chelates exerting Cu2Zn2 superoxide dismutase mimetic activity. Cu, 18 microM, in the form of Cu-thionein was sufficient to inhibit the superoxide production of activated human blood phagocytes by 50%. Furthermore, the scavenging of hydroxyl radicals and singlet oxygen by Cu(I)-thionein was determined, using the 2-deoxyribose fragmentation assay induced by decaying K3CrO8 and the NADPH oxidation caused by UVA illuminated psoralen, respectively. The inhibitory reactivity of Cu-thionein in both assays was compared with that of serum proteins including albumin, ceruloplasmin, transferrin, and ferritin. The galactosamine/endotoxin-induced hepatitis in male NMRI mice was used to evaluate the antiinflammatory reactivity of Cu-thionein in vivo. The serum copper, superoxide dismutase, and sorbitol dehydrogenase concentrations, as well as the activity of polymorphonuclear leukocytes in unseparated blood seemed most appropriate to quantify the protective capacity of Cu-thionein in the course of an oxidative stress-dependent liver injury. The intraperitoneal application of 32.5 mumols/kg thionein-Cu limited this damage to 45%.
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PMID:Antiinflammatory reactivity of copper(I)-thionein. 224 84

Intravenous injection of murine recombinant tumor necrosis factor alpha(TNF-alpha) to male NMRI albino mice in doses greater than 4 micrograms/kg (specific activity 4 x 10(7) U/mg) resulted in a fulminant hepatitis when animals had been sensitized 1 hr before by intraperitoneal administration of 700 mg/kg galactosamine. Liver injury was assessed by measurement of serum transaminases as well as sorbitol dehydrogenase activity 8 hr after administration of TNF-alpha. Pretreatment with either galactosamine or 40 micrograms/kg TNF-alpha alone did not cause hepatitis. Pretreatment of galactosamine/TNF-alpha-injured mice with 800 mg/kg uridine or with 6 mg/kg calmidazolium fully protected the animals, while administration of either verapamil or nifedipine (100 mg/kg, respectively) had no significant effect. The following inhibitors of generation or action of leukotriene D4, which were previously shown to block galactosamine/endotoxin-induced hepatitis in mice, failed to protect against galactosamine/TNF-alpha-induced intoxication: 200 micrograms/kg dexamethasone, 174 mg/kg BW 755 C or 13 x 10 mg/kg FPL 55712. In addition, unlike in the galactosamine/endotoxin model no prevention was achieved by pretreatment of galactosamine/TNF-alpha-injured animals with the following substances blocking the development of an ischemia/reperfusion syndrome: 2 x 100 mg/kg allopurinol, 3.3 x 10(4) U/kg superoxide dismutase, 10(6) U/kg catalase or 10 micrograms/kg iloprost. We conclude from our results that tumor necrosis factor alpha is likely to act as a final mediator of endotoxin action in a sequence of events which includes formation of leukotriene D4 and reactive oxygen species.
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PMID:Tumor necrosis factor is a terminal mediator in galactosamine/endotoxin-induced hepatitis in mice. 246 8

Furazolidone produces a dilative cardiomyopathy and hepatitis in turkeys exposed to this drug in their diets. The ability of furazolidone to enhance free radical reactions when incubated with turkey cardiac or hepatic membranes was determined to evaluate if free radical reactions might contribute to the pathology. Furazolidone (0.135 mM) incubated with NADPH and hepatic microsomes increased oxygen consumption 350% over control incubations. Superoxide dismutase and catalase attenuated the furazolidone-mediated stimulation of oxygen consumption, indicating that the drug promoted the formation of superoxide and hydrogen peroxide. Lipid peroxidation was also stimulated by furazolidone incubated with microsomes, NADPH, and ferric chloride. At concentrations as low as 0.017 mM, lipid peroxidation was more than doubled by furazolidone. Incubation of cardiac sarcosomes with NADPH and furazolidone (0.135 mM) increased oxygen consumption 72% the rate of cytochrome c reduction 72%, and epinephrine oxidation 238% over control. Epinephrine oxidation was enhanced by concentrations of furazolidone as low as 0.017 mM (69% increase over control). This effect of furazolidone was blocked by superoxide dismutase or incubation in an argon atmosphere. These data establish the potential for furazolidone to enhance free radical reactions in cardiac, as well as hepatic tissue. Free radical reactions are therefore potential determinants of furazolidone-mediated hepatic and cardiac toxicities.
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PMID:Furazolidone-enhanced production of free radicals by avian cardiac and hepatic microsomal membranes. 253 46

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

Amino sugars such as galactosamine are hepatotoxic. It has been verified that toxic hepatitis induced by galactosamine is similar to that of CCl4 poisoning, and that both were inhibited by O2* scavengers. Fructosamine results from the union of glucose with the epsilon-amine of lysine. A test for fructosamine quantification is based on nitroblue tetrazolium (NBT) reduction, in which O2- is involved, the reduction being inhibited in the presence of superoxide dismutase (SOD). Given these facts, we attempted to elucidate if galactosamine and glucosamine reduce NBT and if that reduction is inhibited by SOD. This was confirmed. Subsequently, we incubated aminoacids (glycine, lysine, alanine) with glucose and galactose for 7 days and studied the action of the incubation products on NBT, using amino acids and sugars as controls. We found that NBT reduction increases proportionally to the length of incubation time of glucose/galactose with lysine, but not with other amino acids. Reduction of NBT by the Amadori compounds formed is inhibited by SOD. We suggest that oxygen radical generation by Amadori compounds must be taken into consideration as one cause of damage in diabetes of long duration.
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PMID:Oxygen radical generation by Maillard compounds. 283 94


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