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)

We tested the preventive effects of catalase, an enzymatic scavenger of hydrogen peroxide, or dimethyl sulfoxide (DMSO), a hydroxyl radical scavenger, on intravenous alloxan-induced lung edema in four groups of pentobarbital sodium-anesthetized, ventilated dogs for 3 h: saline (20 ml.kg-1.h-1) infusion alone (n = 5), alloxan (75 mg/kg) + saline infusion (n = 5), catalase (150,000 U/kg) + alloxan + saline infusion (n = 5), or DMSO (4 mg/kg) + alloxan + saline infusion (n = 5). Catalase or DMSO significantly prevented the increase in plasma thromboxane B2 and 6-keto-prostaglandin F1 alpha over 3 h after alloxan and the accumulation of extravascular lung water after 3 h [3.95 +/- 0.52 (SE) g/g with catalase, 3.06 +/- 0.42 g/g with DMSO] but not early pulmonary arterial pressor response. An electron microscopic study indicated that catalase or DMSO significantly reduced the endothelial cellular damages after alloxan. These findings strongly suggest that hydrogen peroxide and hydroxyl radical are major mediators responsible for intravenous alloxan-induced edematous lung injury in anesthetized ventilated dogs.
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PMID:Pretreatment with catalase or dimethyl sulfoxide protects alloxan-induced acute lung edema in dogs. 144 76

Pyrimidine base-derived radical spin adducts were detected in reaction mixtures containing pyrimidine bases, glutathione, and alloxan by the ESR spin trapping technique with a spin trap, alpha-phenyl-N-tert-butyl nitrone (PBN). Pyrimidine nucleoside- and nucleotide-, and ribose- and deoxyribose-derived radical spin adducts of PBN were also observed. However, purine base- and nucleoside-derived radical spin adducts of PBN were not detected. A cytosine-derived radical spin adduct of PBN was not generated under anaerobic conditions. Catalase and mannitol inhibited the formation of the cytosine-derived radical spin adduct of PBN but superoxide dismutase (SOD) did not. EDTA stimulated it and desferrioxamine suppressed it nearly completely. From these results it is presumed that the hydroxyl radical is involved in the formation of the cytosine-derived radical spin adduct of PBN generated by alloxan.
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PMID:Detection of nucleic acid-derived radicals formed by alloxan. 285 9

The direct in vitro effects of alloxan on the Ca2+ handling by microsomal membranes isolated from dog mesenteric arteries were investigated. Preincubation of the vascular muscle microsomal membranes with alloxan showed a suppressive effect on both binding of Ca2+ (in the absence of ATP) and ATP-driven Ca2+ transport. Such an inhibition was time dependent, dose dependent, and temperature dependent. ATP-driven Ca2+ transport was much more susceptible to the inhibitory action of alloxan than Ca2+ binding under all experimental conditions examined. Alloxan inhibited ATP-driven Ca2+ transport at a comparable level over the entire period of Ca2+ uptake, but had no significant effect on the efflux of Ca2+ from preloaded microsomal membranes. This suggests that alloxan exerts its inhibitory effect on the ATP-driven Ca2+ transport via its action on the Ca-pump protein rather than the membrane permeability to Ca2+. Catalase and mannitol but not superoxide dismutase partially protected against such as inhibition by alloxan. The possible involvement of H2O2 mediating the inhibitory action of alloxan was further supported by the finding of a similar in vitro inhibitory effect of H2O2 on the ATP-driven Ca2+ transport by the vascular smooth muscle microsomes.
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PMID:Mechanism of inhibition by alloxan of ATP-driven calcium transport by vascular smooth muscle microsomes. 297 55

The incubation of lambda DNA in the reaction system of alloxan plus NADPH-cytochrome P450 reductase (fp2) in the presence of ferritin caused strand breaks after a lag time of about 5 min. Addition of ferritin to the reaction system at concentrations below 50 micrograms/ml caused the strand breaks of DNA in a concentration-dependent fashion. Catalase, scavengers of hydroxyl radicals (HO.) and iron-chelators almost completely inhibited the DNA strand breaks, but superoxide dismutase (SOD) did not, suggesting that the strand breaks are induced by the generation of HO. via the reaction of H2O2 and Fe(II), namely, the Fenton reaction. When the ferritin was incubated in the reaction system of alloxan plus fp2, the iron release from ferritin increased with incubation time depending on the amount of fp2. The addition of increasing concentrations of ferritin to the reaction system resulted in progressive increase in the iron release and a decrease in the electron spin resonance signal intensity of alloxan radical (HA.), the one electron reduced form of alloxan, suggesting that HA. generated in the reaction system is capable of releasing iron from ferritin. These results support the possibility that the iron released from ferritin may be involved in the diabetogenic action of alloxan.
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PMID:Effect of ferritin on lambda DNA strand breaks in the reaction system of alloxan plus NADPH-cytochrome P450 reductase: ferritin's role in diabetogenic action of alloxan. 774 95

lambda DNA strand breaks were easily induced in a reaction system involving alloxan with reduced glutathione (GSH) in the presence of FeCl3 in a HEPES-NaOH buffer, pH 7.4. Increasing concentrations of FeCl3 in the reaction system caused DNA strand breaks in a concentration-dependent fashion, suggesting that iron is required to induce the DNA strand breaks. Catalase, scavengers of hydroxyl radicals (HO.) and iron-chelators almost completely inhibited the DNA strand breaks, but superoxide dismutase (SOD) did not do so, suggesting that the HO., formed by a Fenton-type reaction, was the species responsible for the DNA strand breaks. The addition of FeCl3 to the solution containing DNA caused the formation of a DNA-Fe(III) complex, in which Fe(III) was reduced by an alloxan radical (HA.) but not by a superoxide radical. Only when apotransferrin was added to the reaction mixtures before the addition of FeCl3, were both the DNA strand breaks and the reduction of Fe(III) strongly inhibited. These results suggest that the Fe(III) bound to DNA catalyzes the DNA strand breaks which may be caused by the generation of site-specific HO. via an HA.-dependent Fenton-type reaction.
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PMID:A role of iron in lambda DNA strand breaks in the reaction system of alloxan with reduced glutathione: iron(III) binding to the DNA. 820 21

Alloxan-induced diabetic rats were treated with insulin (i.p.) or with Capparis decidua powder as a hypoglycaemic agent mixed with diet. The effect was assessed on lipid peroxidation (LPO) and the antioxidant defense system in rat tissues. The increased levels of blood glucose in diabetes produce superoxide anions and hydroxyl radicals in the presence of transition metal ions which cause oxidative damage to cell membranes. The heart tissue showed an increased lipid peroxidation (LPO) in diabetic rats while no significant change was observed in the liver and kidney. The treatment with C. decidua lowered LPO in these tissues even more effectively than insulin-treated rats. The superoxide dismutase (SOD) activity increased in the heart and kidneys in the diabetic group of rats probably to increase dismutation of superoxide anions. However, treatment with C. decidua decreased SOD activity in the liver and kidney and was comparable to control rats. Catalase (CAT) activity was not significantly affected in any of the tissues in diabetic and insulin-treated animals, however, CAT activity markedly increased in tissues with C. decidua treatment. Total and Se-dependent glutathione peroxidase (GSH-Px) in the heart was markedly lowered in diabetic rats which recovered with insulin as well as with C. decidua treatment. The increase in GSH-Px and CAT activity with C. decidua treatment may lower H2O2 toxicity and reduce oxidative stress in diabetes. However, glutathione (GSH) content in the heart and kidney and glutathione reductase (GSH-R) activity in all the tissues studied increased in diabetic rats while treatment with insulin lowered GSH content and GSH-R activity in these tissues. The treatment with C. decidua also decreased GSH-R activity in the kidney and heart which resulted in the decrease in GSH content in these tissues. The changes such as the increase in kidney and heart SOD may be an adaptive response in order to neutralize superoxide anions. The increase in GSH content and GSH-R activity in the tissue are in response to neutralize superoxide anions and to counteract oxidative stress in diabetes. Glutathione S-transferase (GST) was not significantly affected in diabetic rat tissue, however, heart GST increased with antidiabetic treatments. The increase in glucose-6-phosphate dehydrogenase (G6PDH) in the kidney and heart of diabetic rats subsequently decreased with C. decidua treatment. The increase in G6PDH in tissues may increase NADPH generation required for GSH-R activity and GSH production. It is suggested that these changes initially counteract the oxidative stress in diabetes, however, a gradual decrease in the antioxidative process may be one of the factors which results in chronic diabetes. The data indicate that C. decidua may have potential use as an antidiabetic agent and in lowering oxidative stress in diabetes.
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PMID:Action of capparis decidua against alloxan-induced oxidative stress and diabetes in rat tissues. 936 67

Alloxan is known to induce diabetes in experimental animals through destruction of insulin-producing 3-cells of pancreas. The mechanism of DNA damage induced by alloxan was investigated using 32P-labeled human DNA fragments. Cu(II)-dependent DNA damage increased with the concentration of alloxan and NADH. Alloxan induced DNA cleavage frequently at thymine and cytosine residues in the presence of NADH and Cu(II). Catalase and bathocuproine, a Cu(I)-specific chelator, almost completely inhibited DNA damage, suggesting the involvement of H2O2 and Cu(I). Alloxan induced Cu(II)-dependent production of 8-oxodG in calf thymus DNA in the presence of NADH. UV-visible and electron spin resonance (ESR) spectroscopic studies showed that superoxide anion radical and alloxan radical were generated by the reduction of alloxan by NADH, and also by the autoxidation of dialuric acid, the reduced form of alloxan. These results suggest that the copper-oxygen complex derived from the reaction of H2O2 with Cu(I) participates in Cu(II)-dependent DNA damage by alloxan plus NADH and dialuric acid. The mechanism of DNA damage is discussed in relation to diabetogenic action of alloxan.
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PMID:Metal-mediated DNA damage induced by diabetogenic alloxan in the presence of NADH. 974 96

The present study was designed to evaluate the oxidative stress-related parameters in alloxan-induced diabetes in rabbits. After 3, 6, 12 and 24 weeks of hyperglycaemia the enzymatic and non-enzymatic factors were measured in heart tissue of diabetic and control groups. Superoxide dismutase and glutathione peroxidase activities and the contents of total sulfhydryl compounds significantly increased at all time intervals. Catalase activity increased initially (after 3 and 6 weeks), decreased after 12 weeks and increased again at the 24th week of the experiment. Glutathione reductase activity increased initially (at 3rd week), decreased below control level after 6 and 12 weeks, then increased again. Ascorbic acid concentration decreased after 3 and 6 weeks, and increased at the 12th and 24th weeks. The level of lipid peroxidation products was reduced after 3, 6 and 12 weeks of the experiment. After 24 weeks it was significantly elevated. These data suggest that hyperglycaemia induces oxidative stress in the heart but the defense mechanisms in the heart tissue are fairly efficacious against oxidative injury.
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PMID:Changes in antioxidant status of heart muscle tissue in experimental diabetes in rabbits. 1236 95

Oxidative stress induced by alloxan has been shown to damage pancreatic beta-cell and produce hyperglycemia in rats. Aegle marmelos leaf extract is being used in Ayurveda as a medicine for diabetes. The present study examined the action of Aegle marmelos against experimental diabetes as well as the antioxidant potential of the drug. A methanolic extract of Aegle marmelos was found to reduce blood sugar in alloxan diabetic rats. Reduction in blood sugar could be seen from 6th day after continuous administration of the extract and on 12th day sugar levels were found to be reduced by 54%. Oxidative stress produced by alloxan was found to be significantly lowered by the administration of Aegle marmelos extract. This was evident from a significant decrease in lipid peroxidation, conjugated diene and hydroperoxide levels in serum as well as in liver induced by alloxan. Catalase and glutathione peroxidase activity in blood and liver were found to be increased from 9th day onwards after drug administration. Superoxide dismutase and glutathione levels were found to be increased only on 12th day. These results indicate that Aegle marmelos extract effectively reduced the oxidative stress induced by alloxan and produced a reduction in blood sugar.
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PMID:Antidiabetic activity of Aegle marmelos and its relationship with its antioxidant properties. 1527 Mar 73

The aim of this study was to analyse the effect of the new oral antidiabetic drug repaglinide on antioxidant factors and lipid peroxidation in tissues of alloxan-induced diabetic rabbits after 4 and 8 weeks treatment. The activity of superoxide dismutase (diabetic vs. control values, mean+/-S.E.M., p<0.05) in diabetic kidney was diminished (1.5+/-0.2 vs. 2.8+/-0.3 and 1.8+/-0.1 vs. 2.9+/-0.3 U/mg protein) and significantly increased after 8 weeks of repaglinide treatment (2.4+/-0.2 U/mg protein). Catalase activity was significantly increased in diabetic liver (67.5+/-3.6 vs. 39.7+/-5.6 and 62.3+/-2.7 vs. 52.6+/-5.3 micromol H(2)O(2)/min/mg protein) and normalised by repaglinide (49.2+/-4.0 and 41.2+/-3.8 micromol H(2)O(2)/min/mg protein). In diabetic kidney the level of ascorbic acid was diminished after 4 weeks (1.5+/-0.1 vs. 3.0+/-0.1 micromol/g tissue) and increased after the drug treatment (2.0+/-0.2 micromol/g tissue). In diabetic kidney the level of lipid peroxidation products was elevated (33.3+/-2.4 vs. 23.7+/-2.4 and 29.5+/-3.1 vs. 18.2+/-0.8 nmol/g tissue) and diminished by repaglinide (10.3+/-1.4 and 13.3+/-3.0 nmol/g tissue). This study shows that oxidative stress in diabetic tissues is partly corrected by repaglinide. The drug does not affect glucose concentration and its antioxidative effect is not secondary to its action on hyperglycaemia. This study suggests an additional advantage of repaglinide which contributes to its effectiveness in therapy.
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PMID:Oxidative stress in kidney and liver of alloxan-induced diabetic rabbits: effect of repaglinide. 1594 40


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