Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.17.3.2 (xanthine oxidase)
8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The ability of Oxyphenbutazone (a non-steroidal antiinflammatory drug) to react with singlet oxygen and superoxide anions, possible mediators of the damage to the lipids of the cell membranes during inflammation was studied. Oxyphenbutazone inhibited the reduction of nitroblue tetrazolium in aerobic riboflavin-photosensitized oxidation of methionine, but did not influence the cytochrome C-reduction by superoxide-generating system xanthine-xanthine oxidase. Oxyphenbutazone was photooxidized in the presence of Rose Bengal, the latter being a photosensitizer. The increase of the reaction rate of Oxyphenbutazone-oxidation in D2O as compared to H2O, as well as the inhibition of oxidation by singlet oxygen-quencher sodium azide confirmed the participation of singlet oxygen in this process. It was found that Oxyphenbutazone reacted with singlet oxygen, but did not react with superoxide anions. This was supported by the observed protection of erythrocyte membranes from the hemolytic action of the singlet oxygen-generating system Rose Bengal + light.
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PMID:Reactions of oxyphenbutazone with active oxygen species. 282 29

The cardioprotective agents troxerutin and methionine are radical scavengers and compete with the DMPO adduct formation of .OH generated by the Fenton reaction. The concentration of trapped .O2- generated by the xanthine oxidase/hypoxanthine reaction is lowered in the presence of troxerutin. The decay of DMPO-OH is decreased by troxerutin compared to the control. In the presence of methionine a carbon-centered radical is produced. The investigations support the opinion that the scavenging of oxygen derived free radicals is of importance for the cardioprotective action of these agents.
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PMID:Effect of troxerutin and methionine on spin trapping of free oxy-radicals. 290 55

The effects on neutrophil function of the new immunomodulatory agent fanetizole mesylate were studied. Fanetizole did not affect random or stimulated migration, phagocytosis, or degranulation by normal human neutrophils. Production of superoxide in response to the chemotactic factor formyl-methionyl-leucyl-phenylalanine (f-Met-Leu-Phe) was markedly inhibited (41.3 +/- 3.9%) by 250 microM fanetizole. This inhibition was not due to scavenging of superoxide by fanetizole, as there was no impairment of superoxide detection in a cell-free xanthine-xanthine oxidase system. Inhibition was dose dependent (no effect seen with 1 or 10 microM fanetizole) and stimulus specific (no impairment of superoxide production in response to phorbol myristate acetate). Washing the cells after fanetizole treatment partially restored their superoxide response to f-Met-Leu-Phe. Suppression of neutrophil production of toxic oxygen metabolites may partially explain the antiarthritic effect of fanetizole, and study of such selective inhibitors may be useful in probing the contribution of neutrophils to inflammatory tissue damage.
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PMID:Inhibition of neutrophil superoxide production by fanetizole. 299 53

We have assessed whether oxygen-derived free radicals produced by xanthine oxidase may be an important trigger mechanism in the genesis of reperfusion-induced arrhythmias. We have examined (i) the effects of inhibition of xanthine oxidase by both folic acid solution and amflutizole; (ii) the effects of the inhibitor of xanthine dehydrogenase to xanthine oxidase conversion, soybean trypsin inhibitor; (iii) the effects of administration of superoxide dismutase and catalase, both singly and in combination and (iv) in an isolated rat heart preparation we have investigated the ability of free radical scavengers to reduce reperfusion arrhythmias caused by the infusion of xanthine oxidase and hypoxanthine. The prior administration of folic acid solution, amflutizole, superoxide dismutase, catalase, and superoxide dismutase plus catalase all reduced the incidence of reperfusion-induced arrhythmias and resultant mortality, caused by reperfusion after a transient period of coronary artery occlusion in the anaesthetised rat. Prior administration of soybean trypsin inhibitor significantly reduced mortality. In an isolated, perfused rat heart preparation with temporary coronary artery occlusion, addition of xanthine oxidase-hypoxanthine to the perfusion medium increased the incidence of reperfusion arrhythmias and decreased the total duration of sinus rhythm during reperfusion. Further addition of superoxide dismutase or L-methionine increased significantly the total duration of sinus rhythm. These results suggest that in the rat heart xanthine oxidase may be involved in the genesis of reperfusion-induced arrhythmias.
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PMID:Reperfusion-induced arrhythmias: a study of the role of xanthine oxidase-derived free radicals in the rat heart. 336 77

To investigate the mechanism for changes in xanthine oxidase activity in response to dietary protein and iron, we fed rats diets containing 50, 20 or 5% casein with either normal iron (35 mg Fe/kg diet) or low iron (5 mg Fe/kg diet). Xanthine oxidase activity changed in liver and intestinal mucosa in response to protein and iron, but immunologically detectable xanthine oxidase protein did not change. When total liver RNA isolated from these rats was translated by a rabbit reticulocyte lysate, we found no difference in the amount of xanthine oxidase that was translated. These results demonstrated that the changes in xanthine oxidase activity were not accompanied by changes in the amount of protein. Since xanthine oxidase can exist in an inactive desulfo form, we asked if xanthine oxidase activity was changed by the content of sulfur-containing amino acids in the diet. Xanthine oxidase activity in intestinal mucosa of the rats fed the 5% casein + methionine diet was significantly greater than that of the rats fed the 5% casein diet alone. These findings suggest that xanthine oxidase activity may be regulated by interconversion of active and inactive desulfo enzyme.
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PMID:Regulation of xanthine oxidase activity and immunologically detectable protein in rats in response to dietary protein and iron. 366 83

The potential protective effect of N-acetylcysteine against various types of oxidative stress (exposure to hyperoxia, treatment with paraquat, incubation in the presence of the hypoxanthine-xanthine oxidase system) was tested in primary cultures of porcine aortic endothelial cells. It was compared to that of selenomethionine (Se-Met), known to increase glutathione peroxidase activity, when given either alone or in combination with N-acetylcysteine. LDH release, 3H-thymidine (TdR) incorporation into DNA and DNA content were measured to assess the cytotoxic effect of the conditions tested. Total and oxidized glutathione content was also determined. Whereas Se-Met had a partial protective effect on all the conditions but paraquat treatment, N-acetylcysteine administration had no effect on the hyperoxia induced changes and significantly worsened the cytotoxic action of paraquat. On the other hand, LDH release following an incubation in the presence of the hypoxanthine-xanthine oxidase was significantly reduced after N-acetylcysteine treatment. No major change in total nor in oxidized glutathione followed N-acetylcysteine treatment in control and experimental conditions. A dose-dependent protective effect of N-acetylcysteine was obtained when this agent was given concomitantly with the xanthine oxidase system. These data suggest that in cultured endothelial cells a N-acetylcysteine-related protective effect, if present, is most likely to result from the direct scavenging action of N-acetylcysteine.
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PMID:Comparative study on the selenium- and N-acetylcysteine-related effects on the toxic action of hyperoxia, paraquat and the enzyme reaction hypoxanthine-xanthine oxidase in cultured endothelial cells. 368 96

The aim of this study was to characterize granulocyte behaviour, in venules, after enzymatic generation of free radicals on the surface of the hamster cheek pouch and to elucidate the role of superoxide anion radical (O2-), H2O2 and hydroxyl radical in these changes. A decrease in granulocyte velocity, which was dissociated from a concomitant increase in red cell velocity, was found while granulocyte rolling frequency and granulocyte adhesion increased in the venules studied. These alterations in granulocyte behaviour could be completely inhibited by superoxide dismutase, an enzymatic scavenger of O2-, but not by catalase, which decomposes H2O2 or by L-methionine which may scavenge OH. and quench singlet O2. Our results are consistent with the concept than an O2-dependent lipid hydroperoxide generated on the hamster cheek pouch by the xanthine oxidase system markedly alters granulocyte behaviour in vivo.
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PMID:Evidence for the participation of superoxide anion radical in altering the adhesive interaction between granulocytes and endothelium, in vivo. 608 11

Polymorphonuclear leukocytes undergo the respiratory burst when exposed to a variety of stimuli. This is associated with the production of superoxide anion radical (O-2). Dismutation of O-2 can occur spontaneously to produce hydrogen peroxide (H2O2) and in the presence of metal catalysts O-2 and H2O2 can react to form hydroxyl radical (OH.). Some of these reactive species are released into the interstitium and may cause lipid peroxidation and depolymerization of macromolecules. We have studied the effect of free radicals on vascular permeability. Hypoxanthine and xanthine oxidase were applied topically on the hamster cheek pouch microcirculation model, injected intravenously with FITC-dextran 150 (Mw 150,000) to visualize permeability changes. This caused a flux of O-2 and a significant increase in macromolecular leakage. An attempt was made to elucidate the roles of different radicals by addition of superoxide dismutase (SOD), catalase (CAT), dimethyl sulfoxide (DMSO) and L-methionine to the reaction mixture. A significant decrease in leakage was found with all these substances, indicating OH. or possibly singlet oxygen damage. These results indicate that a free radical flux can cause permeability changes, and we suggest that part of the permeability change seen during inflammation may be related to free radical flux produced by activated leukocytes.
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PMID:Evidence for participation of hydroxyl radical in increased microvascular permeability. 616 80

Purified ferredoxin-(cytochrome c)-NADP+ oxidoreductase and xanthine oxidase were found to catalyse the reduction of nitrofurantoin to the free radical. Under aerobic conditions, the nitrofurantoin radical underwent autoxidation to regenerate the parent compound with the concomitant production of superoxide and eventually hydrogen peroxide. The nitrofurantoin radical was also shown to react with hydrogen peroxide to generate a highly reactive species which was capable of oxidising methionine to ethylene. This active oxygen radical appeared to be identical with the crypto-OH . radical, previously proposed as being formed from the analogous reaction of the methyl viologen radical with hydrogen peroxide [R.J. Youngman and E.F. Elstner, FEBS Lett. 129, 265 (1981)]. Catalase inhibited nitrofurantoin-dependent ethylene formation in both enzyme systems, whereas superoxide dismutase was only inhibitory in the xanthine oxidase mediated reaction. Although the primary function of the respective enzyme systems is to generate the nitrofurantoin radical, the xanthine oxidase reaction is markedly more complex than that of ferredoxin-(cytochrome c)-NADP+ oxidoreductase. The differences between the two enzyme reactions appear to be due to the endogenous autoxidation of xanthine oxidase. The aerobic activation of nitrofurantoin by xanthine oxidase involved the superoxide anion as an intermediate, whereas the nitrofuran was directly reduced by ferredoxin-(cytochrome c)-NADP+ oxidoreductase without a requirement for active oxygen species.
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PMID:Mechanisms of oxygen activation by nitrofurantoin and relevance to its toxicity. 629 96

Guinea-pig mammary tissue was perfused in vitro, radiolabelled with [35S]methionine and intracellular protein precursors of the milk-fat-globule membrane (FGM) recovered by immunoabsorption techniques. Labelled xanthine oxidase was solely detected in post-microsomal supernatants and butyrophilin in carbonate-washed membranes. A major glycoprotein (Gp 55), was initially present in a membrane-bound form, but after longer perfusion times a fraction of this protein was recovered in the post-microsomal supernatant. These results are discussed with reference to formation of the apically-derived FGM.
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PMID:Protein synthesis in lactating guinea-pig mammary tissue perfused in vitro. II. Biogenesis of milk-fat-globule membrane proteins. 653 41


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