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 dismutating activity of the D-penicillamine copper complex was determined and compared with the activities of Cu-Zn and Mn superoxide dismutase in four O2 ground negative earth generating systems. I. Nitrite formation from hydroxylamine. II. Crocin destruction by xanthine/xanthine oxidase. III. Ethylene production by isolated chloroplasts. IV. Nitrite formation from hydroxylamine by chloroplasts in the presence of diquat (1, 1'-dimethylene-2,2'-bipyridylium dibromide). In all four test systems a high dismutative activity of the complex was found, which is not sensitive to KCN as demonstrated with test system III. The results are discussed with regard to the antiinflammatory activity of D-penicillamine.
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PMID:Determination of the superoxide dismutating activity of D-penicillamine copper. 66 84

To demonstrate whether there are any pathways of nitrite formation from N-nitrosamines other than reductive denitrosation by cytochrome P-450 we performed the following experiments. An esterified alpha-hydroxylated nitrosamine was incubated in a microsomal system to test if nitrite generation is coupled with or linked to the oxidative bioactivation pathway. Simultaneously, inhibitors of microsomal esterases were added to test if the intact molecule or a metabolite from the oxidative metabolism was responsible for nitrite formation. To check if the superoxide radical anion could be related to the mechanism of nitrite generation, nitrosamines were incubated with a xanthine oxidase/hypoxanthine system. To test if the OH radical was involved in nitrite formation, nitrosamines were incubated with an artificial hydroxy-radical generating system (xanthine oxidase/hypoxanthine system supplemented with Fe2+/EDTA). Measurable amounts of nitrite were detected after incubation of the esterified-hydroxylated N-nitrosamine when the hydrolysis by microsomal esterases was inhibited by diisopropylfluorophosphate or paraoxon and when the N-nitrosamines were incubated with the artificial hydroxy-radical generating system. Nitrite formation could not be detected in the O2(-)-generating system (xanthine oxidase/hypoxanthine) or when the esterified alpha-hydroxylated N-nitrosamine was incubated without inhibition of the microsomal esterases. These results demonstrate that besides reductive denitrosation by cytochrome P-450, nitrite generation from N-nitrosamines can also be caused by hydroxy-radicals. The importance of this possible pathway for the in vivo situation of nitrosamine metabolism is discussed.
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PMID:Metabolic nitrite formation from N-nitrosamines: are there other pathways than reductive denitrosation by cytochrome P-450? 375 94

Nitroreductase enzymes generally catalyze the reduction of nitroaromatic compounds to the corresponding amines. In contrast, ferredoxin NADP oxidoreductase (FNR), glutathione reductase, xanthine oxidase, and cytochrome c reductase catalyze the NADPH dependent elimination of the nitramine nitro group from 2,4,6-trinitrophenylmethylnitramine to form N-methylpicramide (NMP). Nitrite elimination was inhibited under aerobic conditions. Our results suggest that under aerobic conditions, tetryl is enzymatically reduced to the nitroanion radical which is then involved in the reduction of molecular oxygen. Under anaerobic conditions, the radical is reduced to NMP and nitrite is eliminated.
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PMID:Elimination of nitrite from the explosive 2,4,6-trinitrophenylmethylnitramine (tetryl) catalyzed by ferredoxin NADP oxidoreductase from spinach. 860 4

Nitrogen dioxide's rats' inhalations with injections per os of pyrazole, amidopyrine and sodium nitrite lead to considerable increasing of endogenic N-nitrosodimethylamine formation, which had been determined by system gas chromatograph-thermal energetic analyser. This increasing essentially didn't depend on the rats' immunisation by vaccine BCG, which leads to the intensification of NO synthesis by peritoneal macrophages and others manifestations of their metabolic activation: increasing of creatine kinase and adenosine desaminase activities. It hadn't been brought to light the obvious dependent between changes of xanthine oxidase and xanthine dehydrogenase activities in the liver and blood serum and intensification of lipids peroxidation and also the amount of N-nitrosodimethylamine in the rats in the conditions of endogenic and exogenic nitrosation factors' influence.
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PMID:[Effect of exogenous and endogenous nitrosation factors on formation of N-nitrosodimethylamine in rats depending on the status of purine catabolism]. 1097 64

The authors have previously reported that intratracheal instillation of staphylococcal enterotoxin-B (SEB) induced interstitial pneumonia (IP) in autoimmune-prone mice. SEB-reactive T-cells were critically involved in the development of IP in this model. Concern has arisen about the hazards of reactive oxygen species (ROS) and reactive nitrogen species (RNS) in the process of lung injury and fibrosis. Therefore, the involvement of nitric oxide (NO) and superoxide anion (O2-) in the pathogenesis of IP in this autoimmune-prone model has been investigated. Nitrite/nitrate levels were increased in bronchoalveolar lavage (BAL) fluid and serum from SEB-injected mice. The signal of the NO-(N-(dithiocarboxy) sarcosine)2-Fe2+ complex was detected in the SEB-injected lung and whole blood by electron paramagnetic resonance (EPR) spectroscopy. NO production was significantly decreased by aminoguanidine (AG) treatment. Xanthine oxidase (XO) activity in the lung, BAL fluid, and plasma was increased with instillation of SEB, and 4-amino-6-hydroxypyrazolo(3,4-d)-pyrimidine (AHPP) significantly inhibited XO activity. Moreover, both AG and AHPP significantly decreased production of pro-inflammatory cytokines, numbers of infiltrated cells in BAL fluid, and the area of thickened alveolar septa in the SEB-injected lung. In conclusion, the overproduction of nitric oxide and super oxide anion were implicated in the pathogenesis of interstitial pneumonia, and inducible nitric oxide synthase and xanthine oxidase inhibitors had protective effects against interstitial pneumonia in this model.
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PMID:Effects of inducible nitric oxide synthase and xanthine oxidase inhibitors on SEB-induced interstitial pneumonia in mice. 1193 21

Enzyme catalyzed biotransformation of the energetic chemical octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine (HMX) is not known. The present study describes a xanthine oxidase (XO) catalyzed biotransformation of HMX to provide insight into the biodegradation pathway of this energetic chemical. The rates of biotransformation under aerobic and anaerobic conditions were 1.6+/-0.2 and 10.5+/-0.9 nmolh(-1)mgprotein(-1), respectively, indicating that anaerobic conditions favored the reaction. The biotransformation rate was about 6-fold higher using NADH as an electron-donor compared to xanthine. During the course of reaction, the products obtained were nitrite (NO(2)(-)), methylenedinitramine (MDNA), 4-nitro-2,4-diazabutanal (NDAB), formaldehyde (HCHO), nitrous oxide (N(2)O), formic acid (HCOOH), and ammonium (NH(4)(+)). The product distribution gave carbon and nitrogen mass-balances of 91% and 88%, respectively. A comparative study with native-, deflavo-, and desulfo-XO and the site-specific inhibition studies showed that HMX biotransformation occurred at the FAD-site of XO. Nitrite stoichiometry revealed that an initial single N-denitration step was sufficient for the spontaneous decomposition of HMX.
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PMID:Mechanism of xanthine oxidase catalyzed biotransformation of HMX under anaerobic conditions. 1280 94

The aims of this study were to test whether xanthine oxidase, lactoperoxidase, and NO are components of the innate immune system of mammary secretion during active involution in dairy cows, and whether the innate immune system is activated by casein hydrolysates. Our laboratory has shown recently that infusion of CNH into mammary glands induced involution and was associated with earlier increases in the concentrations of components of the innate immune system. Intact casein is inactive and served as control. Half of the glands of 8 Holstein cows scheduled for dry off (approximately 60 days before parturition) were injected for 3 days with a single dose of casein hydrolyzates and the contralateral glands with a single dose of intact casein with the same concentration. Involution elicited marked increases in xanthine oxidase and lactoperoxidase activities, and accumulation of urate and nitrate. NO and H(2)O(2) were constantly produced in the mammary gland secretion. Nitrite formed either by autooxidation of NO or by conversion of nitrate to nitrite by xanthine oxidase was converted into the powerful nitric dioxide radical by lactoperoxidase and H(2)O(2) that is derived from the metabolism of xanthine oxidase. Nitric dioxide is most likely responsible for the formation of nitrosothiols on thiol-bearing groups, which allows an extended NO presence in mammary secretion. Nitrite is effectively converted to nitrate, which accumulated in the range of approximately 25 microM -1 mM from the start of the experiment to the complete involution of glands. The mammary secretion in all glands was bactericidal and bacteriostatic during established involution, and this appeared sooner and more acutely in glands treated with casein hydrolyzates, within 8 to 24 h. It is concluded that xanthine oxidase, lactoperoxidase, and NO are components of the mammary innate immune system that form bactericidal and bacteriostatic activities in mammary secretions. The innate immune system play a major role in preventing intramammary infection during milk stasis and its activation may increase its effectiveness.
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PMID:Role of xanthine oxidase, lactoperoxidase, and NO in the innate immune system of mammary secretion during active involution in dairy cows: manipulation with casein hydrolyzates. 1580 11

Nitrite represents a circulating and tissue storage form of NO whose bioactivation is mediated by the enzymatic action of xanthine oxidoreductase, nonenzymatic disproportionation, and reduction by deoxyhemoglobin, myoglobin, and tissue heme proteins. Because the rate of NO generation from nitrite is linearly dependent on reductions in oxygen and pH levels, we hypothesized that nitrite would be reduced to NO in ischemic tissue and exert NO-dependent protective effects. Solutions of sodium nitrite were administered in the setting of hepatic and cardiac ischemia-reperfusion (I/R) injury in mice. In hepatic I/R, nitrite exerted profound dose-dependent protective effects on cellular necrosis and apoptosis, with highly significant protective effects observed at near-physiological nitrite concentrations. In myocardial I/R injury, nitrite reduced cardiac infarct size by 67%. Consistent with hypoxia-dependent nitrite bioactivation, nitrite was reduced to NO, S-nitrosothiols, N-nitros-amines, and iron-nitrosylated heme proteins within 1-30 minutes of reperfusion. Nitrite-mediated protection of both the liver and the heart was dependent on NO generation and independent of eNOS and heme oxygenase-1 enzyme activities. These results suggest that nitrite is a biological storage reserve of NO subserving a critical function in tissue protection from ischemic injury. These studies reveal an unexpected and novel therapy for diseases such as myocardial infarction, organ preservation and transplantation, and shock states.
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PMID:Cytoprotective effects of nitrite during in vivo ischemia-reperfusion of the heart and liver. 1584 Dec 16

Nitrones such as 5,5-dimethyl-1-pyrroline N-oxide (DMPO), 5-diethoxyphosphoryl-5-methyl-1-pyrroline N-oxide (DEPMPO) and 5-ethoxycarbonyl-5-methyl-1-pyrroline N-oxide (EMPO) have become the spin-traps of choice for the detection of transient radical species in chemical and biological systems using electron paramagnetic resonance (EPR) spectroscopy. The mechanism of decomposition of the superoxide radical anion (O2(.-)) adducts of DMPO, DEPMPO and EMPO in aqueous solutions was investigated. Our findings suggest that nitric oxide (NO) was formed during the decomposition of the O2(.-) adduct as detected by EPR spin trapping using Fe(II)N-methyl-d-glucamine dithiocarbamate (MGD). Nitric oxide release was observed from the O2(.-) adduct formed from hypoxanthine-xanthine oxidase, PMA-activated human neutrophils, and DMSO solution of KO2. Nitric oxide formation was not observed from the independently generated hydroxyl radical adduct. Formation of nitric oxide was also indirectly detected as nitrite (NO2(.-)) utilizing the Griess assay. Nitrite concentration increases with increasing O2(.-) concentration at constant DMPO concentration, while NO2(.-) formation is suppressed at anaerobic conditions. Moreover, large excess of DMPO also inhibits NO2(.-) formation which can be attributed to the oxidation of DMPO to hydroxamic acid nitroxide (DMPO-X) by nitrogen dioxide (NO2), a precursor to NO2(.-). Product analysis was also conducted to further elucidate the mechanism of adduct decay using gas chromatography-mass spectrometry (GC-MS) technique.
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PMID:Nitric oxide release from the unimolecular decomposition of the superoxide radical anion adduct of cyclic nitrones in aqueous medium. 1610 5

Nitrite reduction to nitric oxide (NO) may be potentiated by a nitrite reductase activity of deoxyHb and contribute to systemic hypoxic vasodilation. The effect of nitrite on the pulmonary circulation has not been well characterized. We explored the effect of nitrite on hypoxic pulmonary vasoconstriction (HPV) and the role of the red blood cell (RBC) in nitrite reduction and nitrite-mediated vasodilation. As to method, isolated rat lungs were perfused with buffer, or buffer with RBCs, and subjected to repeated hypoxic challenges, with or without nitrite. As a result, in buffer-perfused lungs, HPV was reduced at nitrite concentrations of 7 muM and above. Nitrite inhibition of HPV was prevented by excess free Hb and RBCs, suggesting that vasodilation was mediated by free NO. Nitrite-inhibition of HPV was not potentiated by mild acidosis (pH = 7.2) or xanthine oxidase activity. RBCs at 15% but not 1% hematocrit prevented inhibition of HPV by nitrite (maximum nitrite concentration of approximately 35 muM) independent of perfusate Po(2). Degradation of nitrite was accelerated by hypoxia in the presence of RBCs but not during buffer perfusion. In conclusion, low micromolar concentrations of nitrite inhibit HPV in buffer-perfused lungs and when RBC concentration is subphysiological. This effect is lost when RBC concentration approaches physiological levels, despite enhanced nitrite degradation in the presence of RBCs. These data suggest that, although deoxyHb may generate NO from nitrite, insufficient NO escapes the RBC to cause vasodilation in the pulmonary circulation under the dynamic conditions of blood flow through the lungs and that RBCs are net scavengers of NO.
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PMID:Red blood cells prevent inhibition of hypoxic pulmonary vasoconstriction by nitrite in isolated, perfused rat lungs. 1701 49


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