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)

To explore the susceptibility of the extracellular protozoan, Entamoeba histolytica, to toxic oxygen intermediates, trophozoites were exposed to fluxes of O2, H2O2, and OH. generated enzymatically by the glucose oxidase and xanthine oxidase reactions. HM-1 trophozoites were resistant to O2, but were readily killed by H2O2 alone. OH. and 1O2 were not required for effective amebicidal activity. The addition of peroxidase and halide enhanced trophozoite killing by H2O2. Sonicates of amebae contained virtually no catalase and little glutathione peroxidase activity which may contribute to susceptibility to H2O2. Coupled with our previous studies with Toxoplasma gondii and Leishmania spp. these observations indicate that there is a broad spectrum of susceptibility of intra- and extracellular pathogenic protozoa to killing by oxygen intermediates.
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PMID:Susceptibility of Entamoeba histolytica to oxygen intermediates. 627 8

We describe a one-step kinetic method for the determination of 5'-nucleotidase (EC 3.1.3.5). Inosine is formed by the hydrolysis of inosine 5'-monophosphate which is catalyzed by seric 5'-nucleotidase, and then is converted to hypoxanthine by nucleoside phosphorylase. Two moles of hydrogen peroxide are formed for each mole of hypoxanthine oxidized to urate by xanthine oxidase. The rate formation of hydrogen peroxide is monitored at 510 nm using the oxidation of the chromogenic system 3,5-dichloro-2-hydroxybenzenesulfonic acid/4-aminophenazone in the presence of peroxidase. beta-Glycerophosphate inhibits the unspecific cleavage of the substrate by alkaline phosphatases. Inorganic phosphate is added to improve the reagent stability, and ferrocyanide to reduce bilirubin interference. Automation of the technique requiring 20 microliter of serum on a centrifugal analyzer is also described.
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PMID:A one-step determination of serum 5'-nucleotidase using a centrifugal analyzer. 627 35

1. Iron-dependent free radical damage to DNA and deoxyribose results in the formation of thiobarbituric acid (TBA) reactive intermediates. 2. These intermediates have been compared chromatographically and spectrophotometrically after incubation with the enzymes xanthine oxidase and peroxidase. 3. Loss of TBA-reactivity occurred in the bleomycin-iron(II) derived products incubated with xanthine oxidase and in a standard solution of sodium malondialdehyde incubated with peroxidase.
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PMID:Iron-dependent free radical damage to DNA and deoxyribose. Separation of TBA-reactive intermediates. 629 Feb 80

Effects of protizinic acid (PRT) on prostaglandins (PG) and the production of oxygen radicals were compared with those of other non-steroidal anti-inflammatory agents. Oral administration of 30 mg/kg of PRT, indomethacin (IM), or ibuprofen (IB) significantly inhibited arachidonic acid-induced erythema in guinea pigs. Although 30 mg/kg of PRT significantly inhibited PGE2-induced erythema, IM and IB did not significantly inhibit it. PRT inhibited phospholipase A2 (PLA2) activity, and the IC50 value was 2.1 X 10-4 M. On the other hand, IM and IB exerted no effect on the PLA2 activity at 3 X 10-4 M. These results suggest that PRT possesses a broader pharmacological activity on the PG system than IM and IB. As for effects on the production of oxygen radicals, in order of relative inhibitory potency was PRT greater than metiazinic acid (MA) = IM greater than IB = phenylbutazone (PB) in the xanthine oxidase assay, PB great than IM greater than PRT greater than MA = IB in the rabbit neutrophil myeloperoxidase assay, and IM greater than PB greater than PRT greater than MA greater than IB in the guinea pig macrophage assay. In the rabbit neutrophil and aggregated IgG-bound micropore filter assay, the order was PRT greater than MA greater than PB greater than IM = IB. Thus, the inhibitory effects of PRT was verified in all experiments on the production of oxygen radicals in contrast to IB. In particular, it could be especially meaningful that PRT showed the most potent activity in the aggregated IgG-bound micropore filter assay which has been reported to be a good model for studying the pathogenesis of inflammatory diseases believed to be caused by immune complexes.
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PMID:[Effects of protizinic acid on the prostaglandins system and the production of oxygen radicals]. 629 Mar 56

Our previous studies established that human neutrophils could damage and probably kill hyphae of Aspergillus fumigatus and Rhizopus oryzae in vitro, primarily by oxygen-dependent mechanisms active at the cell surface. These studies were extended, again quantitating hyphal damage by reduction in uptake of (14)C-labeled uracil or glutamine. Neither A. fumigatus nor R. oryzae hyphae were damaged by neutrophils from patients with chronic granulomatous disease, confirming the importance of oxidative mechanisms in damage to hyphae. In contrast, neutrophils from one patient with hereditary myeloperoxidase deficiency damaged R. oryzae but not A. fumigatus hyphae. Cell-free, in vitro systems were then used to help determine the relative importance of several potentially fungicidal products of neutrophils. Both A. fumigatus and R. oryzae hyphae were damaged by the myeloperoxidase-hydrogen peroxide-halide system either with reagent hydrogen peroxide or enzymatic systems for generating hydrogen peroxide (glucose oxidase with glucose, or xanthine oxidase with either hypoxanthine or acetaldehyde). Iodide with or without chloride supported the reaction, but damage was less with chloride alone as the halide cofactor. Hydrogen peroxide alone damaged hyphae only in concentrations >/=1 mM, but 0.01 mM hypochlorous acid, a potential product of the myeloperoxidase system, significantly damaged R. oryzae hyphae (a 1 mM concentration was required for significant damage to A. fumigatus hyphae). Damage to hyphae by the myeloperoxidase system was inhibited by azide, cyanide, catalase, histidine, and tryptophan, but not by superoxide dismutase, dimethyl sulfoxide, or mannitol. Photoactivation of the dye rose bengal resulted in hyphal damage which was inhibited by histidine, tryptophan, and 1,4-diazobicyclo(2,2,2)octane. Lysates of neutrophils or separated neutrophil granules did not affect A. fumigatus hyphae, but did damage R. oryzae hyphae. Similarly, three preparations of cationic proteins purified from human neutrophil granules were more active in damaging R. oryzae than A. fumigatus hyphae. This damage, as with the separated granules and whole cell lysates, was inhibited by the polyanion heparin. Damage to R. oryzae hyphae by neutrophil cationic proteins was enhanced by activity of the complete myeloperoxidase system or by hydrogen peroxide alone in subinhibitory concentrations. These data support the importance of oxidative products in general and the myeloperoxidase system in particular in damage to hyphae by neutrophils. Cationic proteins may also contribute significantly to neutrophil-mediated damage to R. oryzae hyphae.
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PMID:Damage to Aspergillus fumigatus and Rhizopus oryzae hyphae by oxidative and nonoxidative microbicidal products of human neutrophils in vitro. 629 3

Legionella pneumophila was susceptible to the antimicrobial action of oxygen metabolites generated by both the myeloperoxidase-H(2)O(2)-halide and the xanthine oxidase systems.
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PMID:Effect of oxygen-dependent antimicrobial systems on Legionella pneumophila. 629 60

Chemotactic factors, which are important in attracting neutrophils to inflammatory sites, have also been shown to stimulate oxidative metabolism, resulting in increased chemiluminescence and release of superoxide anion (O2-). We observed a unique bimodal chemiluminescence pattern upon stimulation with either the complement-derived factor C5a or formyl-methionyl-leucyl-phenylalanine. A sharp peak of activity occurred within 1 to 2 min, and a second more extended peak was seen between 3 and 6 min. Enhancement of both peaks occurred when the cells were pretreated with cytochalasin B. Expression of both peaks was found to be related to cell density, and expression of the second peak was not dependent upon extracellular metabolites released during the first peak. Cells preincubated in luminol and then thoroughly washed responded with only a single peak coincident with the second peak. Together these findings indicate that the first peak is extracellular in origin, whereas the second peak is cell associated. Studies with scavengers of oxygen intermediates and inhibitors of myeloperoxidase for the oxidation of luminol, which may occur in part through the formation of HOCl as well as through a non-HOCl-mediated mechanism. Evidence for a non-HOCl-mediated mechanism comes from experiments in which luminol, myeloperoxidase, and O2- generated by xanthine-xanthine oxidase produce luminescence in the absence of chloride ion. These studies provide further insight into the sequence of events which occur during the stimulation of neutrophils with chemotactic factors and the nature of neutrophil chemiluminescence.
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PMID:Analysis of the bimodal chemiluminescence pattern stimulated in human neutrophils by chemotactic factors. 630 58

Appropriately stimulated neutrophils release peroxidase and undergo a respiratory burst to form hydrogen peroxide (H2O2) and hydroxyl radicals (OH). We report here that both the myeloperoxidase-H2O2-halide system and OH released in this way can degrade the leukotrienes (LT) formed by neutrophils. More LTB4 and LTC4 were recovered from the supernatants of chronic granulomatous disease neutrophils (which are unable to respond to stimulation with a respiratory burst) than from normal or myeloperoxidase-deficient neutrophils when stimulated with the calcium ionophore A23187. When radiolabeled LTC4 was added, 72% of the LTC4 was recovered from the chronic granulomatous disease cells in contrast to 0% from the myeloperoxidase-deficient and normal cells. Inhibitor studies using catalase, superoxide dismutase, azide, mannitol, or ethanol suggested that LTC4 degradation was mediated primarily by the myeloperoxidase system in normal cells and by OH in myeloperoxidase-deficient cells. LTC4 degradation by the cell-free myeloperoxidase-H2O2-halide system and the OH -generating acetaldehyde-xanthine oxidase-Fe2+ system had inhibitor profiles comparable to normal and myeloperoxidase-deficient neutrophils, respectively. LTC4 degradation products formed by the stimulated neutrophils and model systems included the 5-(S), 12-(R)- and 5-(S), 12-(S)-6-trans-isomers of LTB4. Thus phagocytes may modulate LT activity in inflammatory sites by the inactivation of these potent biologic mediators by at least two oxidative mechanisms.
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PMID:Leukotriene production and inactivation by normal, chronic granulomatous disease and myeloperoxidase-deficient neutrophils. 631

Sickle cell anemia and other chronic hemolytic anemias are associated with an increased frequency of bacterial infections. There is evidence to suggest that in hemolytic states massive erythrocyte (RBC) ingestion by macrophages interferes with their antibacterial function, thereby predisposing infection. Stimulated by this possibility, we recently demonstrated that erythrophagocytosis by macrophages markedly inhibited intracellular killing of bacteria, and that zymosan-stimulated superoxide generation and chemiluminescence were also suppressed by RBC ingestion. We examined the effects of RBC components on generation of chemiluminescence, superoxide, and bactericidal activity by cell-free oxidative systems. Generation of chemiluminescence by hypoxanthine-xanthine oxidase was depressed in the presence of human RBC lysate or column-fractionated hemoglobin but not crystallized human hemoglobin (methemoglobin) (peak cpms of 15,522 [P = 0.00024], 28,360 [P = 0.0088], and 50,041 [P = 0.37], respectively, compared with 59,898 for positive controls). Similarly, hypoxanthine-xanthine oxidase production of superoxide was inhibited in the presence of column-fractionated human hemoglobin (43.8 versus 17.4 nmol per tube, P = 0.000001). A cell-free bactericidal system, acetaldehyde and xanthine oxidase with or without myeloperoxidase and Cl-, was markedly inhibited by column-purified hemoglobin. For example, after 2 h of incubation, surviving numbers of Staphylococcus aureus were: control (buffer only), 2.5 X 10(6)/ml; bactericidal system, none; bactericidal system plus hemoglobin, 2.2 X 10(6)/ml (P less than or equal to 0.03, bactericidal system versus other systems). Our studies have documented that interactions between RBC (hemoglobin) and reactive products of oxygen metabolism inhibit oxidative bactericidal mechanisms in cell-free systems as well as in macrophages.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Inhibition of cell-free oxidative bactericidal activity by erythrocytes and hemoglobin. 632 49

The interaction of imipramine with both resting and zymosan-activated human polymorphonuclear leukocytes (PMNs) resulted in the generation of chemiluminescence (CL). This CL was not accompanied, however, by an enhanced release of superoxide anion. CL was also observed following the interaction of imipramine with either a xanthine oxidase or a horseradish peroxidase catalyzed system. Collectively, these observations support the concept that the CL elicited from these interactions is reflective of the electronic excitation of the imipramine molecule. In contrast to the response seen with PMNs, addition of imipramine to resting alveolar macrophages (AMs) failed to yield CL. However, CL from imipramine was observed with resting AMs upon supplementation with exogenous horseradish peroxidase. The lack of response with control AMs and the significant inhibition of the imipramine-PMN CL by the myeloperoxidase inhibitor azide suggests that a peroxidase-derived oxidant facilitated the oxidation of imipramine, yielding a product in an electronically excited state. In addition to PMNs, CL was elicited from imipramine by rat or rabbit liver microsomes, suggesting that PMNs may be a useful model system to predict a xenobiotic effect on the CL response elicited by other cellular oxidant-generating systems. Moreover, these observations underscore the possibility that the metabolic activation of drugs by PMNs may be of pharmacologic and toxicologic importance.
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PMID:Oxidant-mediated electronic excitation of imipramine. 632 28


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