Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hyperplastic nodular cirrhosis was induced in rats by long-term (6 month) i.p. administration of thioacetamide at doses of 2.66 mmol/kg body wt, three times per week. The survival rate of animals at the end of the treatment was 90%. To follow the temporal changes samples at 0, 7, 15, 30, 45, 60, 90, 150 and 180 days from rats during thioacetamide intoxication and from chronological controls were obtained. The cirrhogenic ability of this treatment was assessed on the basis of morphological changes: the development of macronodular cirrhosis and the appearance of fibrous septa of collagen through portal spaces. Parameters of liver injury and cholestasis were obtained by assaying the serum activities of isocitrate dehydrogenase and gamma-glutamyltransferase. Enzymes and metabolites related to glutathione redox systems, as well as other antioxidant enzymes, were tested. Catalase and glutathione peroxidase, the two enzymes involved in the elimination of peroxides, and glutathione reductase decreased significantly at the end of the 6 months of intoxication, while Cu-Zn and Mn superoxide dismutases increased progressively during the long-term thioacetamide treatment. Protein thiol levels profile showed a biphasic change increasing from the 7th day and were insensitive to the 30% depletion of intracellular glutathione (GSH). To study the relationship of the intracellular thiols on the mechanisms of cell proliferation and differentiation during the cirrhogenic process, DNA content was assayed by flow cytometry in isolated hepatocytes, and DNA ploidy and distribution between G0-G1, S and G2 + M phases were determined. Remarkable changes in relation to a sharp increase in diploid population from 7 to 180 days (24.5%-->85.5%), a pronounced decrease in polyploid populations (tetraploid+octoploid) in the same period (73.7%-->12.3%), and elevations in the populations in S phase (S1 + S2) were observed in thioacetamide-treated rats. The results obtained indicate that hepatocytes isolated from thioacetamide-treated rats showed a marked tendency to diploidy, an enhancement in DNA replication parallel to the hepatic content of protein sulphydryl groups and a significant decline in antioxidant enzyme activities. The increase in protein thiols was independent of GSH level and of the thiol redox state.
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PMID:Relationship between antioxidant systems, intracellular thiols and DNA ploidy in liver of rats during experimental cirrhogenesis. 761 93

The activity of antioxidant defense enzymes and lipid peroxidation (LPO) was studied in the liver and blood of 126 patients with hepatobiliary diseases. The activity of superoxide dismutase (SOD) and catalase in the liver appeared inhibited and relevant interactions impaired. Catalase/peroxidase value in hepatic cirrhosis proved minimal. In response to hepatotropic drugs red cell SOD decreased, while glutathione and ceruloplasmin levels became elevated. Blood LPO values were adequate indicators of the disease progression. It is shown that deficient antioxidant defense of the liver in chronic affections contributes to oxygen radical formation which promotes pathological processes in the liver.
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PMID:[The clinical significance of the enzymatic system utilizing active forms of oxygen in chronic liver diseases]. 801 35

Selenium is an essential trace element and has been shown to protect the rats against dietary liver necrosis. This study was designed to evaluate the effects of selenium supplementation on different biochemical parameters in thioacetamide induced cirrhotic rats. For this purpose 24 male Albino wistar rats were divided into four groups (n=6). Group I, remained healthy control rats, Group II, received thioacetamide (at a dose of 200mg/kg b.w, i.p, for 12 weeks, twice a week) in first phase and saline in second phase, Group III, received thioacetamide (200mg/kg b.w, i.p for 12 weeks, twice a week) in first phase and sodium selenite ((1mg/kg b.w, i.p. for 12 weeks, three times a week ) in second phase and Group IV, received sodium selenite (1mg/kg b.w, i.p. for 12 weeks, three times a week) in first phase and saline in second phase. Biochemical analysis was evaluated by total and direct bilirubin, liver specific enzymes, and antioxidant enzymes. Marked increase in total and direct bilirubin and ALT activity was the indicative markers of liver cirrhosis while reduced antioxidant activity (SOD and GSH) and increased MDA and Catalase levels were observed in cirrhotic group. Sodium selenite supplementation markedly reduced total bilirubin and ALT activity and restored the antioxidant enzymes (SOD and GSH) and MDA and catalase activity. These results indicate that sodium selenite successively attenuates the thioacetamide induced liver cirrhosis.
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PMID:Role of selenium in protection of liver cirrhosis. 2419 12

This study was designed to evaluate the effects of sylimarin supplementation on different biochemical parameters in thioacetamide induced cirrhotic rats. For this purpose 24 male Albino wistar rats were divided into four groups (n=6). Group I, remained healthy control rats, Group II, received thioacetamide (at a dose of 200mg/kg b.w, i.p, for 12 weeks, twice a week) in first phase and saline in second phase, Group III, received thioacetamide (200mg/kg b.w, i.p for 12 weeks, twice a week) in first phase and silymarin (orally at a dosage of 200mg/kg b.w, twice a week, for 8 weeks) in second phase and Group IV, received silymarin (orally at a dosage of 200mg/kg b.w, twice a week, for 8 weeks) in first phase and saline in second phase. Biochemical analysis was evaluated by total and direct bilirubin (Retiman and Franhel, 1957, Sherlock, 1951), liver specific enzymes, antioxidant enzymes [SOD (Kono et al., 1978), Catalase (Sinha et al., 1979), Glutathione reductase (Calberg and Mannervik, 1985) and MDA (Okhawa et al., 1979)] and plasma and intraerythrocyte sodium and potassium (Tabssum et al., 1996). Marked increase in total and direct bilirubin and ALT activity was the indicative markers of liver cirrhosis while reduced antioxidant activity (SOD and GSH) and increased MDA and Catalase levels and disturbed electrolyte homeostasis were observed in cirrhotic group. Silymarin supplementation markedly reduced total bilirubin and ALT activity and restored the antioxidant enzymes (SOD and GSH), MDA and catalase activity and electrolyte homeostasis. These results indicate that silymarin successively attenuates the thioacetamide induced liver cirrhosis.
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PMID:Prevention of liver cirrhosis by Silymarin. 2903 15