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 superoxide radical O2.-, whether produced by the xanthine/xanthine oxidase reaction or infused as KO2, solubilized by a crown ether in dry dimethyl sulphoxide, initiated a free-radical chain oxidation of anionic 2-nitropropane. Superoxide dismutase, but not catalase, inhibited oxidation of the nitroalkane. Xanthine oxidase suffered a syncatalytic inactivation, during the co-oxidation of 2-nitropropane, which was reversed by dialysis. Cyanide exacerbated this syncatalytic inactivation and rendered it irreversible. The frequently observed oxidations of nitroalkanes by flavoenzymes now need to be re-examined to clarify the extent to which O2.--initiated free-radical chain oxidation contributed to the overall nitroalkane oxidation.
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PMID:Free-radical chain oxidation of 2-nitropropane initiated and propagated by superoxide. 302 20

Polymorphonuclear leukocytes (PMN) accumulating at inflammatory sites have the potential to degrade collagen by releasing the metalloproteinase collagenase (EC 3.4.24.7), which is stored within the specific granules of these cells in a latent, inactive, form. In order to elucidate the activation mechanism the latent enzyme (molecular weight 91,000) was purified from human PMN and incubated with the oxygen radical-generating system of xanthine oxidase (EC 1.1.3.22) and hypoxanthine. This coincubation resulted in the activation of the latent enzyme as assessed by the collagenolytic attack on human and bovine cartilaginous tissue. Two parameters for collagenolysis were used: loss of hydroxyproline-containing fragments, and mechanical measurements reflecting the stability of tissue specimens. Superoxide dismutase (EC 1.15.1.1) as well as catalase (EC 1.11.1.6) were capable of inhibiting the activation of latent PMN collagenase by the oxygen radical-generating system. The results indicate the hydroxyl radical to be the final oxidant responsible for the activation of latent PMN collagenase. Thus a new activation mechanism of latent collagenase is presented in this paper and discussed together with the potential relevance in pathophysiologic states of acute and chronic inflammation.
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PMID:Activation of latent collagenase from polymorphonuclear leukocytes by oxygen radicals. 303 4

Pyrazole, an effective inhibitor of alcohol dehydrogenase, was previously shown to be a scavenger of the hydroxyl radical. 4-Hydroxypyrazole is a major metabolite in the urine of animals administered pyrazole in vivo. Experiments were conducted to show that 4-hydroxypyrazole was a product of the interaction of pyrazole with hydroxyl radical generated from three different systems. The systems utilized were the iron-catalyzed oxidation of ascorbate, the coupled oxidation of hypoxanthine by xanthine oxidase, and NADPH-dependent microsomal electron transfer. Ferric-EDTA was added to all the systems to catalyze the production of hydroxyl radicals. A HPLC procedure employing either uv detection or electrochemical detection was utilized to assay for the production of 4-hydroxypyrazole. The three systems all supported the oxidation of pyrazole to 4-hydroxypyrazole by a reaction which was sensitive to inhibition by competitive hydroxyl radical scavengers such as ethanol, mannitol, or dimethyl sulfoxide and to catalase. The sensitivity to catalase implicates H2O2 as the precursor of the hydroxyl radical by all three systems. Superoxide dismutase inhibited production of 4-hydroxypyrazole only in the xanthine oxidase reaction system. In the absence of ferric-EDTA (and azide), microsomes catalyzed the oxidation of pyrazole to 4-hydroxypyrazole by a cytochrome P-450-dependent reaction which was independent of hydroxyl radicals. This latter pathway may be primarily responsible for the in vivo metabolism of pyrazole to 4-hydroxypyrazole. The production of 4-hydroxypyrazole from the interaction of pyrazole with hydroxyl radicals may be a sensitive, rapid technique for the detection of these radicals in certain tissues or under certain conditions, e.g., increasing oxidative stress.
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PMID:Production of 4-hydroxypyrazole from the interaction of the alcohol dehydrogenase inhibitor pyrazole with hydroxyl radical. 303 2

The effect of scavengers of oxygen radicals on canine cardiac sarcoplasmic reticulum (SR) Ca2+ uptake velocity was investigated at pH 6.4, the intracellular pH of the ischemic myocardium. With the generation of oxygen radicals from a xanthine-xanthine oxidase reaction, there was a significant depression of SR Ca2+ uptake velocity. Xanthine alone or xanthine plus denatured xanthine oxidase had no effect on this system. Superoxide dismutase (SOD), a scavenger of .O2-, or denatured SOD had no effect on the depression of Ca2+ uptake velocity induced by the xanthine-xanthine oxidase reaction. However, catalase, which can impair hydroxyl radical (.OH) formation by destroying the precursor H2O2, significantly inhibited the effect of the xanthine-xanthine oxidase reaction. This effect of catalase was enhanced by SOD, but not by denatured SOD. Dimethyl sulfoxide (Me2SO), a known .OH scavenger, completely inhibited the effect of the xanthine-xanthine oxidase reaction. The observed effect of oxygen radicals and radical scavengers was not seen in the calmodulin-depleted SR vesicles. Addition of exogenous calmodulin, however, reproduced the effect of oxygen radicals and the scavengers. The effect of oxygen radicals was enhanced by the calmodulin antagonists (compounds 48/80 and W-7) at concentrations which showed no effect alone on Ca2+ uptake velocity. Taken together, these findings strongly suggest that .OH, but not .O2-, is involved in a mechanism that may cause SR dysfunction, and that the effect of oxygen radicals is calmodulin dependent.
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PMID:Calmodulin participation in oxygen radical-induced cardiac sarcoplasmic reticulum calcium uptake reduction. 303 9

Reactive oxygen species have been found to be responsible for the tissue injury caused in experimental pyelonephritis in mice. The extent of lipid peroxidation (as assayed by malondialdehyde formation) was found to be increased significantly (p less than .001) in the infected group as compared to the normal mice. Superoxide dismutase and catalase (oxygen free radical scavengers) showed a significant decrease (p less than .001) in the extent of lipid peroxidation even in the presence of infection. Dimethyl sulfoxide, a hydroxyl ion scavenger, was however found to be effective only at 4 and 7 days postinfection (p less than .001). Allopurinol, an inhibitor of xanthine oxidase, did not significantly (p greater than .05) inhibit the formation of lipid peroxides, even upto 7 days postinfection. There was a significant decrease (p less than .05) in the activities of renal brush border membrane enzymes used as markers of renal tissue damage (i.e. alkaline phosphatase, leucine amino-peptidase and gamma-glutamyl transpeptidase) in the infected group as compared to the normal group. In the presence of superoxide dismutase, dimethylsulfoxide and catalase except allopurinol, the activities of all the enzymes but maltase were found to be increased significantly (p less than .05) as compared to the infected group. There was a significant increase (p less than .01) in the bacterial count in the presence of superoxide dismutase and DMSO in infected mice as compared to the infected control mice. However, no significant difference was observed in the catalase and allopurinol treated groups.
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PMID:Effect of various oxygen free radical scavengers in preventing tissue injury caused by Escherichia coli in pyelonephritic mice. 305 56

Haemocuprein was discovered fifty years ago by T. Mann and D. Keilin as a copper protein of red blood cells, later named erythrocuprein. Superoxide dismutase was discovered twenty years ago by J.M. McCord and I. Fridovich as an enzymatic activity in preparations of carbonic anhydrase or myoglobin that inhibited the aerobic reduction of cytochrome c by xanthine oxidase. Astonishingly the superoxide dismutase proved to be haemocuprein. Around this time zinc was found in haemocuprein, in equimolar amount to the copper. Haemocuprein thus became copper-zinc superoxide dismutase after thirty years as an obscure cuproprotein of red blood cells. This historical article is a tribute to the achievement of J.M. McCord and I. Fridovich. Their discovery of superoxide dismutase revolutionized the study of oxygen free-radicals in biochemistry.
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PMID:From haemocuprein to copper-zinc superoxide dismutase: a history on the fiftieth anniversary of the discovery of haemocuprein and the twentieth anniversary of the discovery of superoxide dismutase. 306 13

Experiments were designed to determine the role of oxygen-derived free radicals in modulating contractions of vascular smooth muscle and endothelium-mediated relaxations to acetylcholine. The effects of generating or scavenging these radicals were studied in rings of canine coronary arteries suspended for isometric tension recording. Xanthine oxidase plus xanthine caused relaxations, which were greater in rings with endothelium than in rings without endothelium; the relaxations were not affected by superoxide dismutase or mannitol, but could be prevented by catalase. Xanthine oxidase plus xanthine depressed endothelium-mediated relaxations to acetylcholine; this effect was prevented by superoxide dismutase, but was not affected by catalase or mannitol. Exogenous hydrogen peroxide induced catalase-sensitive relaxations, which were depressed by the removal of the endothelium. Superoxide dismutase evoked catalase-sensitive relaxations only in rings with endothelium. Endothelium-mediated relaxations to acetylcholine were slightly depressed by superoxide dismutase or catalase alone; the combination of the two enzymes or mannitol caused a major shift to the right of the concentration-response curve to acetylcholine. In rings without endothelium, relaxations caused by sodium nitroprusside were not affected by the scavengers (alone or in combination) but were augmented by xanthine oxidase plus xanthine. These data suggest that the endothelium-derived relaxing factor released by acetylcholine is not likely to be an oxygen-derived free radical; hydrogen peroxide has a direct inhibitory action on coronary arterial smooth muscle and triggers endothelium-dependent relaxations; and superoxide anions depress and hydroxyl radicals facilitate endothelium-dependent relaxations caused by activation of muscarinic receptors.
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PMID:Oxygen-derived free radicals, endothelium, and responsiveness of vascular smooth muscle. 308 20

Reactive oxygen metabolites have been reported to be responsible for the pathogenesis of ischemia-induced gastric mucosal lesions. We have investigated the possible protective effect of specific enzymes and oxygen radical scavenging agents on oxygen metabolite-induced injury to cultured gastric mucosal cells. Oxygen-reactive metabolites were generated by 1 mM xanthine and 10-100 mU/ml xanthine oxidase. Cytotoxicity was quantified by measuring 51Cr release from prelabeled cells. Xanthine oxidase caused a dose-dependent increase of 51Cr release in the presence of 1 mM xanthine. Catalase (an enzyme that reduces hydrogen peroxide) diminished xanthine-xanthine oxidase-induced 51Cr release in a dose-dependent manner. Superoxide dismutase (a scavenger of superoxide radical) failed to affect the amounts of 51Cr release induced by xanthine plus xanthine oxidase. Pretreatment with diethyl maleate, which depletes intracellular glutathione, potentiated oxygen radical-mediated 51Cr release dose dependently. The presence of ferrous ion or ethylenediaminetetraacetic acid-chelated iron, which promote the formation of hydroxyl radical, did not alter xanthine-xanthine oxidase-induced cellular injury. Furthermore, agents that inactivate hydroxyl radical also failed to protect the cells from oxygen metabolite-induced injury. We conclude that in vitro oxygen metabolites, extracellularly generated, have a direct toxic effect on gastric mucosal cells; hydrogen peroxide is a major mediator of oxygen metabolite-induced gastric cell injury; the oxygen-derived superoxide and hydroxyl radicals are less toxic to gastric mucosal cells than hydrogen peroxide; and intracellular glutathione, which detoxifies hydrogen peroxide, may be involved in antioxidant defense mechanisms.
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PMID:Oxygen metabolite-induced cytotoxicity to cultured rat gastric mucosal cells. 311 Dec 74

Administration of physiological saline or drugs together with saline into the airways is becoming common clinical practice. However, there are few studies on possible side effects. We have studied the effects of saline, saline plus xanthine oxidase, and saline plus xanthine oxidase plus superoxidase dismutase on lung-thorax compliance and on arterial blood gases in anesthetized, paralyzed guinea pigs, ventilated for 2.5 h. Saline bolus (2-3 ml isotonic saline/kg body weight) into the airways reduced the compliance within 20 min to a mean of 39% of the pretreatment levels, and necessitated as increase in the respirator pressure. Saline plus xanthine oxidase decreased the compliance to 16% of the pretreatment levels. The xanthine oxidase-induced (but not saline-induced) decrease in lung compliance was relieved by superoxide dismutase. According to the present results xanthine oxidase induces a lung injury possible by production of free oxygen radicals. Superoxide dismutase can be valuable in prevention of free oxygen radical-mediated lung damage. Saline alone can be harmful when applied to the airways. This should be considered in clinical trials and in clinical practice.
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PMID:Respiratory failure caused by intratracheal saline: additive effect of xanthine oxidase. 316 34

The mechanism of tissue and cell injury in ischaemic bowel necrosis is unclear. The present study investigated the role of oxygen derived free radicals in the development of bowel necrosis using injections of platelet activating factor (PAF) into the mesenteric vasculature. Animals were pretreated with allopurinol or superoxide dismutase together with catalase, before administration of PAF. Superoxide dismutase/catalase markedly improved the PAF-induced lesions, indicating that most of the intestinal damage after PAF injection is because of the release of oxygen radicals. The major source of oxygen radicals is xanthine oxidase, as allopurinol ameliorated small bowel lesions. Pretreatment with allopurinol produced a significant (p less than 0.01) preventive effect on PAF induced hypotension. In contrast, superoxide dismutase/catalase did not alter PAF induced hypotension. Superoxide dismutase/catalase pretreatment improved PAF induced haemoconcentration and leucopenia, while allopurinol showed no effect.
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PMID:Role of oxygen derived free radicals in platelet activating factor induced bowel necrosis. 319 95


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