Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granulocytes engaged in the phagocytosis of opsonized zymosan emit light by a process that is inhibited by superoxide dismutase and catalase. In the present report is is shown that light emission is the result of reactions between certain unspecified constituents of the ingested particles and some or all of the oxidizing agents (H2O2, O2),and possibly the hydroxyl radical and singlet oxygen) produced by the activated cells. This conclusion is based on a study of light emission by both activated cells ans artificial O2 generating system containing xanthine oxidase and purine. With these two systems light production required the presence of both zymosan and oxidizing agent, suggesting that the oxidation of particle components is necessary for luminescence to occur. The characteristics of the emission spectrum as well as the finding that granulocytes activated by a nonparticulate agent (F-) fail to liminesce show that light emission by the relaxation of singlet oxygen to the ground state does not contribute in a major way to the chemiluminescence of phagocytosing granulocytes; whether singlet oxygen contributes to chemiluminescence in other ways cannot be decided from the data available. Inasmuch as the oxidation of constituents of ingested particles is an important bacterial killing mechanism in the granulocyte, chemiluminescence may be viewed as a manifestation of the microbicidal activity of the cell.
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PMID:The origin of the chemiluminescence of phagocytosing granulocytes. 96 86

Incubation of either Staphylococcus epidermidis or Escherichia coli with a sufficiently high concentration of xanthine oxidase, an enzyme capable of reducing oxygen to superoxide (O2-), resulted in the death of the microorganisms. Protection against the killing os S. epidermidis by xanthine oxidase was afforded by superoxide dismutase, an enzyme which converts O2- to O2 and H2O2, and also by catalase, which destroys H2O2. These findings indicate that neither O2- nor H2O2 were able to kill S. epidermidis under the experimental conditions, but that the bactericidal agent was the product of a reaction between O2- and H2O2. By contrast, E. coli was protected by catalase but not by superoxide dismutase. With this organism, therefore, H2O2 appears to have been the bactericidal agent.
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PMID:Biological defense mechanisms. Evidence for the participation of superoxide in bacterial killing by xanthine oxidase. 108 40

Erythrocytes are hemolyzed by myeloperoxidase, an H2O2-generating system (glucose + glucose oxidase; hypoxanthine + xanthine oxidase) and an oxidizable cofactor (chloride, iodide, thyroxine, triiodothyronine). The combined effect of chloride and either iodide or the thyroid hormones is greater than additive. Myeloperoxidase can be replaced by lactoperoxidase in the iodide-, thyroxine and triiodothyronine-dependent, but not in the chloride-dependent, systems. Hemolysis is is inhibited by the peroxidase inhibitors, azide and cyanide, and by catalase and is stimulated by superoxide dismutase when the xanthine oxidase system is employed as the source of H2O2. Hemolysis by the iodide-dependent system is associated with the iodination of erythrocyte components.
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PMID:Hemolysis and iodination of erythrocyte components by a myeloperoxidase-mediated system. 117 52

Isolated pancreatic acini were incubated with either a combination of xanthine and xanthine oxidase which generates superoxide (O2), or hydrogen peroxide (H2O2), and the direct cytotoxic effect of active oxygen species on the pancreatic acini was examined in vitro in the isolated pancreatic acini system of the rat. Both amylase secretion and lactic dehydrogenase discharge were increased dose-dependently by the addition of xanthine and xanthine oxidase, and suppressed by the addition of a superoxide scavenger, superoxide dismutase. In addition, amylase and lectate dehydrogenase discharge was increased dose-dependently by hydrogen peroxide and decreased by catalase. These results suggest that superoxide and hydrogen peroxide directly injure pancreatic acinar cells and that active oxygen species are involved in the pathogenesis of acute pancreatitis.
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PMID:Toxic effects of oxygen-derived free radicals on rat pancreatic acini; an in vitro study. 128 95

To understand the role of the superoxide (O-2) radical in chromate-related genotoxicity, we investigated whether Cr(VI) can catalyze the Haber-Weiss cycle in vitro: O-2 + Cr(VI)----Cr(V) + O2 Cr(V) + H2O2----Cr(VI) + .OH + OH-. ESR and spin trapping techniques were utilized to monitor the O-2 (produced using xanthine/xanthine oxidase), .OH, and Cr(V) species. Superoxide dismutase as well as catalase inhibited the .OH radical radical formation, attesting to the direct involvement of O-2 and H2O2 in the process. ESR measurements also provided direct evidence for the formation of Cr(V). Kinetic measurements were consistent with the role of Cr(V) and H2O2 as intermediates in .OH formation. These results indicate that in cellular media, especially during chromate phagocytosis, the O-2 radical can become a significant source of .OH radicals and hence a significant factor in the biochemical mechanism of cellular damage due to Cr(VI) exposure.
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PMID:The role of superoxide radical in chromium (VI)-generated hydroxyl radical: the Cr(VI) Haber-Weiss cycle. 130 99

Neutrophils which accumulate at sites of inflammation secrete a number of injurious oxidants which are highly reactive with protein sulfhydryls. The present study examined the possibility that this reactivity with thiols may cause protein damage by mobilizing zinc from cellular metalloproteins in which the metal is bound to cysteine. The ability of the three principal neutrophil oxidants, hypochlorous acid (HOCl), superoxide (.O2-), and hydrogen peroxide (H2O2), to cleave thiolate bonds and mobilize complexed zinc was compared using two model compounds (2,3-dimercaptopropanol and metallothionein peptide fragment 56-61), as well as metallothionein. With all compounds, 50 microM HOCl caused high rates of Zn2+ mobilization as measured spectrophotometrically with the metallochromic indicator 4-(2-pyridylazo)resorcinol. Xanthine (500 microM) plus xanthine oxidase (30 mU), which produced a similar concentration of .O2-, also effected a rapid rate of Zn2+ mobilization which was inhibited by superoxide dismutase but not catalase, indicating that .O2- is also highly reactive with thiolate bonds. In contrast, H2O2 alone was much less reactive at comparable concentrations. These data suggest that HOCl and .O2- can cause damage to cellular metalloproteins through the mobilization of complexed zinc. In view of the essential role played by zinc in numerous cellular processes, Zn2+ mobilization by neutrophil oxidants may cause significant cellular injury at sites of inflammation.
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PMID:Oxidant-induced mobilization of zinc from metallothionein. 130 84

Reactive oxygen intermediates (ROI) have been implicated in a variety of pathophysiological conditions, and vascular smooth muscle may be a site of damage in such oxygen toxicity. Mechanisms of the effects of these intermediates on vascular smooth muscle at the cellular level, however, have not been well studied. We have previously shown that xanthine oxidase (XO)-generated superoxide radicals (O2-.) inhibited the Ca(2+)-adenosine triphosphatase of vascular smooth muscle sarcoplasmic reticulum (SR) through mechanisms that do not involve H2O2 or hydroxyl radicals. In the present study, we report that the D-myo-inositol 1,4,5-trisphosphate (IP3)-induced Ca2+ release from bovine aortic SR was also affected by O2-(.). Hypoxanthine (100 microM) plus XO (10 mU/ml) in the presence of catalase (100 U/ml) stimulated the IP3-induced Ca2+ release from SR monitored using arsenazo III. At 10 microM IP3, the release was doubled by O2-. treatment. As a consequence of using the higher SR protein concentrations required to observe the Ca2+ release, this effect was independent of Ca2+ uptake inhibition induced by O2-(.). Since the effect of O2-. was not seen when a nonhydrolyzable analogue of IP3 was used to induce Ca2+ release, O-2. may be inhibiting the degradation processes of IP3.
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PMID:Superoxide stimulates IP3-induced Ca2+ release from vascular smooth muscle sarcoplasmic reticulum. 131 Feb 31

The effects of clinically used protease inhibitors (aprotinin, nafamostat mesilate, gabexate mesilate) on the production of oxygen-derived free radicals (O2-, H2O2, .OH) by human polymorphonuclear leukocytes were examined. Nafamostat mesilate and gabexate mesilate markedly and dose-dependently inhibited zymosan-stimulated O2- production by human polymorphonuclear leukocytes. However, aprotinin had a slight scavenging effect on O2- produced by the xanthine-xanthine oxidase system. All the protease inhibitors inhibited H2O2 production, but had no significant scavenging effect on H2O2. Nafamostat mesilate and gabexate mesilate slightly inhibited .OH production. These results indicate that the synthetic protease inhibitors nafamostat mesilate and gabexate mesilate inhibit the production of various activated oxygen radicals by human polymorphonuclear leukocytes, and the differences in their inhibitory effects suggest that each synthetic protease inhibitor is specific for a particular oxygen-derived free radical.
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PMID:Effect of synthetic protease inhibitors on superoxide (O2-), hydrogen peroxide (H2O2) and hydroxyl radical production by human polymorphonuclear leukocytes. 131 67

Two free radical generating systems, xanthine oxidase/hypoxanthine or phenazine methosulfate/NADH, were exposed to air plus He, N2, or Ar at partial pressures ranging from 0.2 to 6.0 MPa, and the rates of production of superoxide, hydroxyl, singlet O2, and H2O2 were measured. All three inert gases acted similarly to enhance the production of superoxide radicals by facilitating interactions between iron and H2O2, or O2 and organic radicals. These reactions occurred at quite low gas partial pressures, only 0.28 MPa, and hydrostatic pressures of up to 6.0 MPa had no effect on radical reactions. Enhanced radical production may be the basis for the inhibition of cellular growth mediated by inert gases, and inert gas enhancement of O2 toxicity.
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PMID:Inert gas enhancement of superoxide radical production. 131 38

The purpose of this study was to explore the role of singlet oxygen in cardiovascular injury. To accomplish this objective, we investigated the effect of singlet oxygen [generated from photoactivation of rose-bengal] on the calcium transport and Ca(2+)-ATPase activity of cardiac sarcoplasmic reticulum and compared these results with those obtained by superoxide radical, hydrogen peroxide and hydroxyl radical. Isolated cardiac SR exposed to rose bengal (10 nM) irradiated at (560 nm) produced a significant inhibition of Ca2+ uptake; from 2.27 +/- 0.05 to 0.62 +/- 0.05 mumol Ca2+/mg.min (mean +/- SE) (P less than 0.01) and Ca(2+)-ATPase activity from 2.08 +/- 0.05 mumol Pi/min.mg to 0.28 +/- 0.04 mumol Pi/min.mg (mean +/- SE) (P less than 0.01). The inhibition of calcium uptake and Ca(2+)-ATPase activity by rose bengal derived activated oxygen (singlet oxygen) was dependent on the duration of exposure and intensity of light. The singlet oxygen scavengers ascorbic acid and histidine significantly protected SR Ca(2+)-ATPase against rose bengal derived activated oxygen species but superoxide dismutase and catalase did not attenuate the inhibition. SDS-polyacrylamide gel electrophoresis of SR exposed to photoactivated rose bengal up to 14 min, demonstrated complete loss of Ca(2+)-ATPase monomer band which was significantly protected by histidine. Irradiation of rose bengal also caused an 18% loss of total sulfhydryl groups of SR. On the other hand, superoxide (generated from xanthine oxidase action on xanthine) and hydroxyl radical (0.5 mM H2O2 + Fe(2+)-EDTA) as well as H2O2 (12 mM) were without any effect on the 97,000 dalton Ca(2+)-ATPase band of sarcoplasmic reticulum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Singlet oxygen: a potential culprit in myocardial injury? 131 3


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