Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.17.3.2 (xanthine oxidase)
 8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive oxygen species have been implicated as mediators of inflammation in ulcerative colitis. Chemiluminescence is a reliable means of estimating reactive oxygen species in biological media. Increased reactive oxygen species values in the inflamed colonic mucosa in rats were seen by chemiluminescence. The aims of the study were to find out if chemiluminescence is raised in the colonic mucosa of patients with ulcerative colitis and correlates with disease activity, and to elucidate the sources of the chemiluminescence. It was found that reactive oxygen species, as measured by the chemiluminescence technique, are raised in inflamed colonic mucosa and correlates with symptom score, sigmoidoscopic score, disease activity, and activity of the neutrophil enzyme myeloperoxidase. Chemiluminescence was inhibited by a myeloperoxidase inhibitor (azide) and an H2O2 scavenger (catalase) but not by allopurinol, an inhibitor of the enzyme xanthine oxidase. Chemiluminescence was also inhibited by indomethacin, but this did not seem to be related to inhibition of cyclo-oxygenase. These findings suggest that a likely cellular source of reactive oxygen species in the inflamed colon of patients with ulcerative colitis is the neutrophil and that myeloperoxidase conversion of H2O2 to hypochlorous acid, contributes to the chemiluminescence signal and possibly, to the tissue injury. Neither cyclo-oxygenase nor lipoxygenase seem to play a part as sources for the chemiluminescence.
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PMID:Increased production of luminol enhanced chemiluminescence by the inflamed colonic mucosa in patients with ulcerative colitis. 840 52

The ability of reactive oxygen species produced by triggered neutrophilic leukocytes, hypoxanthine/xanthine oxidase (HX/XAO), hydrogen peroxide, and hypochlorous acid/myeloperoxidase (HOCl/MPO) systems to degrade hyaluronate (HA) in human synovial fluid (SF) and purified umbilical cord HA was compared by measuring the molecular weight distribution of HA using high-performance liquid chromatography with a size-exclusion column. The exposure of noninflammatory SF to phorbol myristic acetate (PMA)-activated neutrophils or to hydrogen peroxide (H2O2) caused depolymerization of SF HA to the degree corresponding to that found in rheumatoid SFs. When HX/XAO was used as radical generator, the molecular weight of SF HA decreased from 3.42 x 10(6) to 1.40 x 10(4) daltons with concomitant decrease of SF viscosity to 36% from the original value. The HOCl/MPO system caused no depolymerization of SF HA, even at very high unphysiological HOCl concentrations that induced the precipitation of SF HA together with SF proteins. This effect was found to be comparable to conventional mucin clot formation in SF. However, purified human umbilical cord HA was easily depolymerized with HOCl/MPO or with H2O2, but these effects were sensitive to the hydroxyl radical scavenger mannitol and iron chelator desferrioxamine, indicating that the formation of reactive hydroxyl radical (OH.) is likely to participate in these reactions. Thus we conclude that in inflammatory SF HA is mainly depolymerized by OH. produced by decomposition of H2O2 catalyzed by iron, free or locally bound to HA itself. In contrast to what has been reported earlier, HOCl/MPO only depolymerizes purified umbilical cord HA (in a hydroxyl radical-dependent manner) but does not depolymerize HA in SF. As a matter of fact, HOCl/MPO has a scavenging action on SF HA by consuming H2O2 and thus preventing the formation of reactive hydroxyl radicals.
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PMID:Differential effects of reactive oxygen species on native synovial fluid and purified human umbilical cord hyaluronate. 840 85

In the present investigation alterations in the free radical generating and scavenging enzymes in platelets, neutrophils (PMNLs), heart and lung homogenates following rat pulmonary thromboembolism have been studied. Thrombosis was induced by intravenous infusion of collagen and adrenaline. Levels of malonaldehyde (MDA) were elevated in the PMNLs after thrombosis. Activities of superoxide dismutase (SOD) and catalase (CAT) were found to increase in platelets and PMNLs respectively. However, there was no significant alteration in the lactate dehydrogenase (LDH), lysozyme (LYS), ratio of xanthine oxidase to dehydrogenase (XO/XH) and PMNLs O2- generation before and after thrombosis. Migration of PMNLs following thrombosis was indicated by increased activity of myeloperoxidase (MPO) in the heart. In addition, pretreatment with allopurinol, a xanthine oxidase inhibitor and indomethacin, a cyclooxygenase inhibitor offered protection against thromboembolism induced death/paralysis. Results suggest the involvement of free radicals in thrombosis.
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PMID:Free radical scavenging mechanisms during pulmonary thromboembolism in rats. 846 69

Xanthine oxidoreductase exists in two functionally distinct forms. Under normal conditions, the larger part of the enzyme occurs as an NAD(+)-dependent dehydrogenase form which produces NADH and urate. The dehydrogenase can be transformed under various (patho)physiological conditions to an oxygen-dependent oxidase form which produces oxygen radicals and/or hydrogen peroxide and urate. Tetrazolium salts are used to demonstrate the total activity of both the dehydrogenase and the oxidase form of the enzyme. We have developed a procedure to detect the oxidase form only in unfixed cryostat sections with the use of cerium on the basis of the semipermeable membrane technique. The incubation medium contained hypoxanthine as substrate, cerium ions, and sodium azide to inhibit catalase and peroxidase activity. In a second-step reaction, diaminobenzidine was polymerized in the presence of cobalt ions by decomposition of cerium perhydroxide. Large amounts of final reaction product were found in milk droplets in the acini of lactating bovine mammary gland, whereas milk-secreting epithelial cells contained hardly any final reaction product. In rat duodenum, enzyme activity was found in the cytoplasm of enterocytes and goblet cells but not in the mucus. Control reactions performed in the absence of substrate or in the presence of substrate and allopurinol, a specific inhibitor of xanthine oxidase, were completely negative in both tissues, with the exception of polymorphonuclear leukocytes in the lamina propria of duodenum. The positive nonspecific reaction in these cells was caused by myeloperoxidase activity. We conclude that the present method is specific for the detection of xanthine oxidase activity. Moreover, conversion of the dehydrogenase form into the oxidase form can be prevented by omission of chemical fixation of the tissue in the present procedure.
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PMID:A histochemical procedure for light microscopic demonstration of xanthine oxidase activity in unfixed cryostat sections using cerium ions and a semipermeable membrane technique. 846 47

The aim of this study was to determine whether lipids are damaged by myeloperoxidase (MP) not only with hydrogen peroxide (H2O2), but also with a H2O2-generating system. Using the hypoxanthine-xanthine oxidase-Cu,Zn-superoxide dismutase (HX-XO-SOD) system as an effective H2O2-generating system, we observed a reduction in the ability of MP to produce peroxylipids in the HX-XO-SOD-MP system, compared with the H2O2-MP system. We also noted that MP inhibited the production of monoepoxide by the H2O2-cytochrome c (Cyt c) system. These results suggest that MP plays a role as an absorber of active oxygen species and prevents phagocytes from self-destruction.
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PMID:Superoxide anion reduces the ability of myeloperoxidase to damage lipids. 860 38

A chemiluminescence (CL) procedure was developed to determine the time course of the release of myeloperoxidase (MPO) from activated human neutrophils using two CL probes, luminol, and MCLA. Luminol-dependent CL (LDCL) and MCLA-dependent CL (MDCL) in a hypoxanthine (HX)/xanthine oxidase (XOD) system, both of which were completely inhibited by superoxide dismutase, were a linear function of the XOD concentration, with the relationship formula being LDCL = 0.003 x MDCL. Under the same conditions, MPO could enhance LDCL in a dose-dependent manner, without influencing MDCL. There was a linear correlation between the MPO concentrations and the values of (LDCL-0.003 x DCL) (coefficient of correlation = 0.004). This correlation made it possible to determine the release of MPO in the neutrophil/stimulus system by simultaneously monitoring the generation of LDCL and MDCL. By this CL procedure, it was revealed that there were variations in both neutrophil MPO releasing patterns and levels depending on the stimulating agent used.
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PMID:A chemiluminescence procedure for determination of the release of myeloperoxidase from activated human neutrophils. 866 97

Aromatic amines are mammary carcinogens in rodents and exposure to aromatic amines may be associated with increased risk of breast cancer in women. Peroxidases present in milk can oxidize aromatic amines to reactive electrophiles which bind to DNA and induce mutations. Hydrogen peroxide, required for peroxidase-dependent oxidations, is supplied by milk xanthine oxidase and by the respiratory burst of neutrophils, cells which are present in milk and activated by exposure to it. In this paper, I propose that lactoperoxidase and myeloperoxidase activate aromatic amines, within the breast ducts, and that these enzymes play a crucial role in the chemical induction of breast cancer.
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PMID:The role of peroxidase-catalyzed activation of aromatic amines in breast cancer. 867 8

Cultured human umbilical vein endothelial cells (HUVECs) treated with reactive oxygen species (ROS) show increased adherence of polymorphonuclear leukocytes (PMNs). Because pentoxifylline (PTX) is known to inhibit cell interactions, we studied PMN adherence to ROS-stimulated HUVECs pretreated with PTX. ROS were generated by the oxidation of hypoxanthine by xanthine oxidase, giving rise to superoxide anion and hydrogen peroxide. Human PMNs were then added to HUVEC monolayers. After various times, the cultures were washed and the number of adherent PMNs was estimated by measuring myeloperoxidase in the total cell homogenate. PTX inhibited adherence in a concentration-dependent manner. Moreover, the increase in intracellular cAMP content varied with the PTX concentration. Isobutylmethylxanthine (IBMX) and isoproterenol (ISO) which increase intracellular cAMP content, also inhibited the adherence of PMNs to ROS-stimulated HUVECs. We conclude that cAMP is probably involved in the intracellular regulation of ROS-mediated PMN adherence to endothelial cells.
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PMID:Effects of pentoxifylline on the adherence of polymorphonuclear neutrophils to oxidant-stimulated human endothelial cells: involvement of cyclic AMP. 869 72

Tissue destruction in atherosclerosis is partly due to uncontrolled protease and oxygen radical release. In this study we investigated the release of elastase and myeloperoxidase, as well as the production of reactive oxygen species by polymorphonuclear leukocytes (PMNLs) obtained from patients with obliterative atherosclerotic of the lower legs. In addition we measured the plasma concentration of xanthine oxidase. PMNLs of atherosclerotic patients have a greater ability to increase elastase and myeloperoxidase release after their stimulation with formyl-methionin-leucyl-phenylalanin (fMLP) and calcium ionophore, A23187, independently of their age, than PMNLs of healthy middle-aged subjects. Similarly to healthy elderly subjects there was an increased superoxide anion (O2-) production under basal condition in both atherosclerotic patient age-groups. The activation of PMNLs with fMLP and A23187 enhanced O2- formation both in healthy subjects and in patients with atherosclerotic disease of the lower legs, however the increase was significantly less in the latter group. No biochemical parameters showed significant correlation with patient's risk factors, however myeloperoxidase production was significantly higher in less severe stage of the disease (P < 0.05). We found that patients with atherosclerotic disease of the lower legs have higher plasma xanthine oxidase level than control subjects. This study indicates an other piece of evidence suggesting the activation and involvement of neutrophils in the pathogenesis of atherosclerosis of the lower legs. The similar tendencies in the reactivity of neutrophils during aging and in atherosclerosis suggest that atherosclerosis may be an early aging process.
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PMID:Neutrophils obtained from obliterative atherosclerotic patients exhibit enhanced resting respiratory burst and increased degranulation in response to various stimuli. 878 40

In the present investigation we studied the concerted role of superoxide anion, platelet activating factor (PAF) and leukotriene B4 (LTB4) in the mechanism that results in polymorphonuclear leucocyte accumulation induced by oxygen free radicals in rat pancreas. This was done by comparing the effects of a PAF antagonist (BN-52021), a LTB4 inhibitor (MK-886) and superoxide dismutase (SOD) in a experimental rat model of inflammation elicited by the oxygen free radicals induced via infusion of xanthine/xanthine oxidase. Also, the effect of independent LTB4 infusion has been studied. The results show that increases in polymorphonuclear cell infiltration (evaluated by tissue histology), myeloperoxidase and LTB4 levels induced in pancreas by infusion of xanthine/xanthine oxidase were abolished by the administration of either the PAF antagonist, the LTB4 inhibitor, or SOD. The fact that BN-52021 could prevent neutrophil recruitment and LTB4 synthesis suggests that PAF is a necessary step for subsequent LTB4 synthesis and polymorphonuclear leucocyte accumulation.
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PMID:Free radical enhancement promotes leucocyte recruitment through a PAF and LTB4 dependent mechanism. 903 33


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