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 effect of superoxide radical on the azide-insensitive ATP-dependent Ca2+-transport by a plasma membrane (PM)-enriched fraction (F2) and an endoplasmic reticulum (ER)-enriched fraction (F3) isolated from pig coronary artery was examined using xanthine oxidase plus xanthine to generate superoxide ions. A preincubation with xanthine oxidase plus xanthine at 37 degrees C preferentially inactivated the oxalate-stimulated Ca2+ uptake by the F3 fraction rather than the phosphate-stimulated uptake by the F2 fraction, indicating that the Ca2+ pump in the ER was more susceptible to this free radical. The inactivation of the Ca2+ uptake depended on the concentrations of xanthine oxidase and xanthine in the preincubation mixture as well as on the preincubation time. Furthermore, the inclusion of superoxide dismutase in the preincubation mixture prevented the inactivation. Thus the inactivation was caused by superoxide radical. Preincubation with xanthine oxidase plus xanthine, however, altered the half-life of efflux of Ca2+ from these vesicles only marginally. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the F3 fraction showed formation of a Ca2+-dependent acid stable phosphoenzyme at 0 degree C predominantly at a protein band corresponding to 100 kDa. The level of the 100-kDa acylphosphate intermediate was inhibited in parallel with the inhibition of the Ca2+ uptake by preincubation with xanthine oxidase plus xanthine. We conclude that superoxide radical inactivates the ER Ca2+ transport by lowering the level of the phosphoenzyme.
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PMID:Effect of superoxide radical on Ca2+ pumps of coronary artery. 284 93

This paper summarizes current knowledge on the biochemistry of oxygen toxicity in general and the ischemia-reoxygenation tissue injury in particular. The superoxide radical, hydrogen peroxide, and the hydroxyl radical in cells can be formed enzymically or nonenzymically. Primary effects of oxygen radicals result in lipid peroxidation, which is believed to be initiated by a perferryl radical. Secondary effects are believed to be due to a disturbance in cellular calcium homeostasis. Reactions and treatment potentials are highly complex and their effects on cells, tissues, and organism are difficult to predict. Treatment potentials include superoxide dismutase, catalase, calcium entry blockers, iron chelators, xanthine oxidase inhibitors, and agents to prevent leukocyte adhesion. Reoxygenation injury mechanisms during resuscitation from clinical death can be studied in animals by evaluating the effects of antireoxygenation injury therapies and by monitoring free radical reactions.
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PMID:Biochemistry of reoxygenation injury. 284 73

The direct effect of oxygen metabolites was studied on isolated perfused rat hearts. Superoxide anion (O2-.) and hydrogen peroxide (H2O2) were generated by adding purine (2.3 mM) and purified xanthine oxidase (0.06 U/ml) to Krebs-Henseleit buffer (pH 7.4). Xanthine oxidase was added to the purine-containing perfusate either near the aorta (group A, which gave H2O2 less than 10 microM) or at a distant point from the aorta (group B, which gave 250 to 300 microM H2O2). The generation rate of O2-. was 31.7 +/- 1.0 nmol/ml/min in the experimental conditions. Contractile function, tissue adenosine triphosphate (ATP), and ultrastructure were not affected in group A. In contrast, hearts in group B showed marked decrease in contractility (+dP/dt) to 24.4 +/- 4.3% of control values. ATP levels were also markedly reduced from control values of 23.4 +/- 0.7 to 7.4 +/- 0.7 mumol/g dry tissue. Ultrastructure in group B hearts revealed "wavy" and disintegrated sarcolemma, depletion of glycogen deposits, and swelling and disruption of mitochondria. Release of the thiobarbituric acid reactive products including malondialdehyde was significant in the effluent (1.68 +/- 0.17 nmol/min/g wet tissue). These changes were almost completely prevented by catalase, but not by superoxide dismutase and deferoxamine. Moreover, exogenous H2O2 perfusion (300 microM) showed results similar to group B hearts. These observations suggest that H2O2 plays a major role in the injury. O2- does not appear to damage hearts directly, although it is important as a precursor of H2O2 and other radical species including hydroxyl radical.
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PMID:Myocardial dysfunction and ultrastructural alterations mediated by oxygen metabolites. 285 30

It has been postulated that changes in the availability of partially reduced O2 species, such as O2 radicals, could serve as a link between PO2 in the alveolus and pulmonary vascular tone (Herz 11: 127-141, 1986). To assess this hypothesis, the hemodynamic effects of acute changes in the balance between the production of O2 radicals and availability of antioxidant enzymes were studied in the isolated perfused rat lung. Intravascular generation of O2 radicals, by administration of xanthine-xanthine oxidase, decreased the pulmonary vascular pressor response to alveolar hypoxia (-55 +/- 5%) and angiotensin II (-58 +/- 10%, P less than 0.01 for each) in isolated perfused rat lungs without increasing the lung wet-to-dry weight ratio. Decreases in pulmonary vascular reactivity were inhibited by pretreatment of the lung with desferrioxamine or a mixture of catalase and superoxide dismutase. Catalase and superoxide dismutase preserved the hypoxic pressor response whether given in liposomes or in dissolved form. Superoxide dismutase administered free in solution, or combined with catalase in liposomes, increased the normoxic pulmonary arterial pressure and enhanced vascular reactivity to angiotensin II and hypoxia. Lungs treated with antioxidant enzymes in liposomes had 50% higher lung catalase levels than control lungs (P less than 0.05). These findings demonstrate that exogenous partially reduced O2 species can decrease pulmonary vascular reactivity and suggest that endogenous radicals, superoxide radical in particular, might be important in modulating pulmonary vascular tone.
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PMID:Oxygen radicals and antioxidant enzymes alter pulmonary vascular reactivity in the rat lung. 291 13

Oxygen-derived free radicals such as the hydroxyl radical (.OH) have been shown to mediate the oxidation of ethanol by a variety of oxy radical-generating systems. Among these are microsomal electron transport systems (both intact and purified, reconstituted systems), the coupled oxidation of hypoxanthine or xanthine by xanthine oxidase, and the model iron-ascorbate system. The sequence of reactions leading to the oxy radical-dependent oxidation of ethanol as well as other hydroxyl radical-scavenging agents by these various systems is believed to proceed through the formation of a common intermediate, namely, hydrogen peroxide (H2O2), after dismutation of the superoxide anion radical (O2-.). The presence of iron, especially chelated iron, greatly enhances the production of .OH by serving as an oxidant for O2-. or a reductant for H2O2. Experiments were carried out to evaluate the role of iron, the chelating agent, O2-., and H2O2 in the oxidation of ethanol by a variety of in vitro systems (chemical, enzymatic, and intact membrane bound) that can produce oxy radicals via different mechanisms. The generation of .OH by all the systems studied was sensitive to catalase, which indicates that H2O2 is the precursor of .OH. Superoxide radical appears to be the reducing agent in the hypoxanthine-xanthine oxidase system, indicating an iron-catalyzed Haber-Weiss reaction. In the ascorbate, reductase, and microsomal systems, superoxide radical does not appear to be the reducing agent. However, superoxide radical probably is the precursor of H2O2. While iron plays an important role in the production of .OH by the various systems, the effect of iron depends on the nature of the iron chelate.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ethanol oxidation by hydroxyl radicals: role of iron chelates, superoxide, and hydrogen peroxide. 298 64

The effects of free radicals on the isolated tracheal chains from guinea pigs were examined in in vitro experiments. When isolated tracheal chains were exposed to the hypoxanthine plus xanthine oxidase system, biphasic contraction was observed. This contraction was prevented by adding superoxide dismutase. However, catalase, mannitol, and indomethacin were ineffective in preventing the contraction due to free radicals. The uric acid plus uricase system had no effect on tracheal muscle tension. These results suggest that superoxide radical contracts tracheal chains.
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PMID:Biphasic contraction of isolated guinea pig tracheal chains by superoxide radical. 299 55

Spin-trapping of superoxide ion, O2-, which is produced from two different sources (OH(-)-DMSO and xanthine-xanthine oxidase systems), was investigated by use of a water-soluble, notroso-aromatic spin trap, sodium 3,5-dibromo-4-nitrosobenzene-sulfonate (DBNBS). It was found that O2- from all sources was easily trapped by DBNBS to yield the stable O2- adduct showing the ESR spectrum consisting of a triplet of a triplet [aN (1) = 12.63 G and aH (2) = 0.71 G]. Hydroperoxy radical (HO2.), which can be generated from the oxidation of hydrogen peroxide with Ce4+ ion, was not trapped by DBNBS. These results indicate that the trapped radical is O2-, but not HO2..
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PMID:Spin-trapping of superoxide ion by a water-soluble, nitroso-aromatic spin-trap. 301 Sep 90

Effect of superoxide radical (O2-) produced extracellularly by hypoxanthine (HX) and xanthine oxidase (XO) on invasive capacity of rat ascites hepatoma cells was studied. Invasive capacity was estimated in vitro by counting the number of tumor cell colonies penetrated underneath cultured mesothelial cell monolayer. When the tumor cells had been treated with non-toxic doses of HX and XO, the formation of penetrated colonies increased with increasing concentrations of XO. This increment was completely inhibited by scavengers of active oxygen radicals, superoxide dismutase (SOD) in combination with catalase (CAT) added simultaneously at the time of HX-XO treatment.
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PMID:Superoxide radical potentiates invasive capacity of rat ascites hepatoma cells in vitro. 301 47

Methylguanidine (MG), a toxin reported in uremia, is thought to be a product of creatinine oxidation. This study is designed to demonstrate the role of active oxygen in the oxidation of creatinine under conditions compatible with those found in uremia. MG synthesis is moderately stimulated by the superoxide radical derived from 3 mM hypoxanthine and 0.015 units/ml xanthine oxidase and inhibited by the addition of superoxide dismutase. This is increased markedly by the addition of 0.05% hydrogen peroxide and augmented to about 56,000 times the control rate in the presence of hydroxyl radicals derived from the reaction of 10 mM FeSO4 and 0.05% hydrogen peroxide. In addition, MG synthesis is inhibited by the addition of sorbitol, lactulose or ethanol, the scavengers of hydroxyl radicals. These results indicate that creatinine can be oxidized to MG by various species of active oxygen and that one of the mechanisms of MG synthesis is such oxidation. MG, therefore, may be a useful indicator of peroxidation in vivo.
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PMID:Active oxygen in methylguanidine synthesis. 302 53

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


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