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)

Amino acid compositions of the milk fat globule membrane protein and plasma membrane protein from other sources, as well as the compositions of milk fat globule membrane-derived xanthine oxidase and selected plasma membranes-associated proteins were compared by statistical difference index. Additionally, the average hydrophobicity of xanthine oxidase and selected membrane proteins were compared. These comparisons indicate high orders of apparent compositional homology between the various plasma membranes and membrane-associated proteins. Because the biological functions of membrane proteins are widely diverse, it is speculated that their "relatedness" may reflect on evolutionary convergence to similar amino acid compositions, necessitated by their in situ environment--the lipoidal bilayer. However, compositional relatedness should not imply sequential homology.
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PMID:Compositional homology of membrane-protein systems and membrane-associated proteins: comparison with milk fat globule membrane and "membrane"-derived xanthine oxidase. 90 34

The effect of mastitis on the milk fat globule membrane of milk samples from individual quarters was investigated. Wisconsin Mastitis Test positive (greater than 20mm) milk contained approximately 10% less milk fat globule membrane material than negative (smaller than 10mm) milk. The lipid portion of the milk fat globule membrane preparation from positive milk contained smaller amounts of phospholipids and larger amounts of cholesterol. Milk fat globule membrane preparations from positive milk had higher aldolase activity and lower xanthine oxidase activity. Dissociated membrane protein prepared from positive milk was resolved into five components by polyacrylamide gel electrophoresis while the membrane protein prepared from negative milk was resolved into three components.
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PMID:Influence of mastitis on properties of milk. XI. Fat globule membrane. 111 37

Diphenylene iodonium (Ph2I), a lipophilic reagent, is an efficient inhibitor of the production of O2- by the activated NADPH oxidase of bovine neutrophils. In a cell-free system of NADPH oxidase activation consisting of neutrophil membranes and cytosol from resting cells, supplemented with guanosine 5'-[gamma-thio]triphosphate, MgCl2 and arachidonic acid, or in membranes isolated from neutrophils activated by 4 beta-phorbol 12-myristate 13-acetate, addition of a reducing agent, e.g. NADPH or sodium dithionite, markedly enhanced inhibition of the NADPH oxidase by Ph2I. The membrane fraction was found to contain the Ph2I-sensitive component(s). In the presence of a concentration of Ph2I sufficient to fully inhibit O2- production (around 10 nmol/mg membrane protein), addition of catalytic amounts of the redox mediator dichloroindophenol (Cl2Ind) resulted in a by-pass of the electron flow to cytochrome c, the rate of which was about half of that determined in non-inhibited oxidase. A marked increase in the efficiency of this by-pass was achieved by addition of sodium deoxycholate. The Cl2-Ind-mediated cytochrome c reduction was negligible in membranes isolated from resting neutrophils. At a higher concentration of Ph2I (100 nmol/mg membrane protein), the Cl2Ind-mediated cytochrome c reductase activity was only half inhibited, which indicated that, in the NADPH oxidase complex, there are at least two Ph2I sensitive components, differing by their sensitivity to the inhibitor. At low concentrations of Ph2I (less than 10 nmol/mg protein), the spectrum of reduced cytochrome b558 in isolated neutrophil membranes was modified, suggesting that the component sensitive to low concentrations of Ph2I is the heme binding component of cytochrome b558. Higher concentrations of Ph2I were found to inhibit the isolated NADPH dehydrogenase component of the oxidase complex. A number of membrane and cytosolic proteins were labeled by [125I]Ph2I. However, the radiolabeling of a membrane-bound 24-kDa protein, which might be the small subunit of cytochrome b558, responded more specifically to the conditions of activation and reduction which are required for inhibition of O2- production by Ph2I. The O2(-)-generating form of xanthine oxidase was also inhibited by Ph2I. Inhibition of xanthine oxidase, a non-heme iron flavoprotein, by Ph2I had a number of features in common with that of the neutrophil NADPH oxidase, namely the requirement of reducing conditions for inhibition of O2- production by Ph2I and the induction of a by-pass of electron flow to cytochrome c by Cl2Ind in the inhibited enzyme, suggesting some similarity in the molecular organization of the two enzymes.
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PMID:Diphenylene iodonium as an inhibitor of the NADPH oxidase complex of bovine neutrophils. Factors controlling the inhibitory potency of diphenylene iodonium in a cell-free system of oxidase activation. 132 36

Incubation of human erythrocytes oxidized by iron catalysts, ADP/Fe3+ or xanthine/xanthine oxidase/Fe3+, with autologous IgG resulted in IgG binding as detected by enzyme immunoassay using protein A-beta-galactosidase conjugate. The binding of autologous IgG to ADP/Fe3(+)-treated erythrocytes maximized when the cells were treated with 1.8:0.1 mM ADP/Fe3+, and declined when treated above this concentration, suggesting that autologous IgG binds to moderately but not to excessively oxidized erythrocytes. The antibody involved in the binding was anti-Band 3, the autoantibody known to bind to aged erythrocytes, because isolated anti-Band 3 bound to the oxidized cells, but anti-Band 3-depleted autologous IgG did not. In addition, purified Band 3 inhibited the autologous IgG binding. Anti-alpha-galactosyl IgG, another natural antibody which has been reported to bind to aged erythrocytes, did not bind to the oxidized cells. Oxidation of membrane lipids, SH-groups of membrane proteins, and Hb of these cells was slight, but the cells contained an increased amount of membrane-bound native Hb, indicating that the oxidized cell membrane has an altered property. alpha-Tocopherol prevented the lipid oxidation and the subsequent IgG binding. Reduction of the oxidized erythrocytes with dithiothreitol resulted in a loss of the IgG binding. These results suggest that anti-Band 3 binding sites (Band 3 senescent antigen) are formed on moderately oxidized erythrocytes as a result of oxidation of membrane protein SH-groups which can be mediated by the membrane lipid oxidation and that formation of the anti-Band 3 binding sites on the oxidized cells is an essentially reversible membrane event which is linked to oxidation and restoration of the protein SH-groups.
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PMID:Binding of anti-band 3 autoantibody to oxidatively damaged erythrocytes. Formation of senescent antigen on erythrocyte surface by an oxidative mechanism. 230 47

1. Proteins of fat-globule membrane from bovine milk were solubilized with the non-ionic detergent Triton X-100 in the presence of protease inhibitors. Approximately 25% of the total membrane protein was solubilized and the extracts were shown to contain a sample of most of the major membrane proteins and glycoproteins. 2. The solubilized proteins were separated in flat-beds of Ultrodex by electrofocusing and the pI values for the major proteins, glycoproteins and certain enzymes determined. Several of the proteins displayed marked heterogeneity indicating the existence of protein variants and isoenzymes. Principal pI values for the enzymes assayed were as follows: xanthine oxidase, 7.35--7.55; NADH2: iodonitrotetrazolium reductase, less than 4.5; 5'-nucleotidase, 7.15--7.4; alkaline phosphatase, 5.4--5.7; phosphodiesterase, 4.6--4.8; gamma-glutamyl transpeptidase, 4.4--4.55. 3. Fractions after electrofocusing were analyzed by 'fused rocket' immunoelectrophoresis and crossed immunoelectrophoresis after separation in polyacrylamide gels containing sodium dodecyl sulphate. Major antigens of the membrane include xanthine oxidase and glycoproteins of apparent molecular weights 67 000, 49 500 and 46 000. The latter two components share common antigenic determinants and could not be separated by gel filtration, ion-exchange chromatography, lectin-affinity chromatography or preparative electrofocusing.
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PMID:Separation of the proteins of bovine milk-fat-globule membrane by electrofocusing with retention of enzymatic and immunological activity. 610 13

The role of membrane peroxidation in red cell aging was investigated by exposing rat erythrocytes to a peroxide-generating system of xanthine oxidase with hypoxanthine, and the resulting alterations were compared to those observed during in vivo aging. Erythrocyte incubation with peroxides decreased the activities of adenylate cyclase and protein kinase, enzymes which were found to be reliable markers reflecting differences between young and old cells. Membranes from age-separated erythrocytes were solubilized and subjected to electrophoresis on gradient polyacrylamide-sodium dodecyl sulfate gels. Electrophoretic patterns indicated that old erythrocytes contained higher amounts of several membrane proteins than young cells. These were proteins in bands 2.1 and 4.1, and proteins of molecular weight larger than 250,000. There was a relative increase in the amount of proteins in band 4.1 and the high molecular weight (greater than 250,000) proteins as a results of peroxidation. These studies demonstrate that cells incubated in vitro with a peroxide-generating system resemble senescent erythrocytes in membrane enzyme activities, cell density, and membrane protein composition. We propose that peroxidation plays an important role in red cell aging.
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PMID:Role of peroxidation in erythrocyte aging. 689 44

Exocytosis from Weibel-Palade bodies, the secretory granules of vascular endothelial cells, causes the rapid release of von Willebrand factor (vWF), an adhesive glycoprotein involved in primary hemostasis, and cell surface expression of P-selectin, a membrane protein involved in neutrophil binding. Thus, exocytosis may represent a link between hemostasis and inflammation. We investigated the effect of reactive oxygen intermediates (ROIs) on vWF secretion. Incubation of cultured endothelial cells with xanthine oxidase (XO), which generates superoxide anions (O2-), induces a potent, rapid secretory response. However, vWF release was not observed in response to H2O2. Extracellular, subendothelial vWF deposits typically seen after exocytosis from Weibel-Palade bodies were observed after exposure to XO. XO caused a rapid, sustained increase in intracellular free calcium concentration ([Ca2+]i). vWF secretion was markedly inhibited by BAPTA-AM, a cell-permeant calcium chelator. Removal of extracellular calcium did not inhibit vWF release, although the sustained phase of the [Ca2+]i increase was suppressed. These results suggest that XO-induced vWF release is mediated by the initial increase in [Ca2+]i which is caused by calcium mobilization from intracellular stores rather than by calcium influx. Exocytosis from Weibel-Palade bodies may contribute to the pathogenic effect of ROIs in atherosclerosis and inflammation.
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PMID:Reactive oxygen intermediates induce regulated secretion of von Willebrand factor from cultured human vascular endothelial cells. 775 49

The preventive effects of a traditional Chinese medicine Sho-saiko-to (Kampo prescription, TJ-9) were determined from oxygen toxicity and membrane damage in liver during endotoxemia. The liver lipid peroxide level and xanthine oxidase activity 18 h after administration of endotoxin (6 mg/kg, i.p.) to TJ-9 (500 mg/kg/d, p.o.)-pretreated mice were markedly lower than that in endotoxin-treated mice, whereas the administration of TJ-9 significantly increased superoxide dismutase and glutathione peroxide activities in liver of endotoxin-injected mice. In the mice pretreated with a TJ-9, the levels of alpha-tocopherol and nonprotein SH in liver tissue 18 h after endotoxin injection were markedly increased as compared to those in endotoxin-treated mice. Leakages of acid phosphatase and lactate dehydrogenase isozyme in serum were markedly lower in endotoxin-TJ-9-treated mice than those in mice given endotoxin. The administration of TJ-9 clearly prevented the membrane protein damage arising from endotoxin challenge. Kampo prescription Sho-saiko-to thus appears to protect the liver plasma membrane from injury by free radicals which occur in a tissue ischemic state during endotoxemia.
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PMID:Preventive effects of a traditional Chinese medicine (sho-saiko-to) against oxygen toxicity and membrane damage during endotoxemia. 822 Mar 25

Production of oxygen radicals by phagocytic cells and loss of surfactant function have each been implicated in the pathogenesis of acute lung injury. Therapeutic administration of exogenous surfactant to injured lungs in which neutrophils are the dominant cell type has been proposed. To understand the role of surfactant in modulating pulmonary inflammation and the impact of surfactant supplementation on diseased lungs, we studied the effect of native porcine and synthetic surfactant preparations on human neutrophil respiratory burst oxidase activity in vitro. We found that surfactant inhibited neutrophil superoxide production induced by either receptor-mediated [formylmethionylleucylphenylalanine (fMLP)] or non-receptor-mediated [phorbol myristate acetate (PMA)] agonists with an IC50 of approximately 0.015 mg phospholipid/ml for porcine surfactant or approximately 0.050 mg phospholipid/ml for synthetic surfactant. Surfactant had no effect on detection of superoxide generation in a noncellular system using xanthine and xanthine oxidase and only minimally inhibited superoxide generation by neutrophils that had been fully stimulated by prior exposure to PMA. There was no effect of surfactant on neutrophil calcium mobilization in response to fMLP, on lactoferrin release in response to PMA, or on membrane protein kinase C activity in response to PMA. Suspensions of dipalmitylphosphatidylcholine alone had no effect on neutrophil superoxide production. Taken together, these findings indicate that certain components of lung surfactant may effect relatively late steps in the activation of the respiratory burst or may alter subsequent steps involved in the assembly of the respiratory burst oxidase.
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PMID:Inhibition of the human neutrophil respiratory burst by native and synthetic surfactant. 862 55

In this experiment the protective effects of beta-carotene (beta-C) liposome against rat neutrophile membrane damage caused by extracellular or intracellular reactive oxygen were species (ROS) investigated by means of fluorescence labels 1, 6-diphenyl-1,3,5 hexatriane (DPH) and N-(3-pyrene) maleimide (N-(3p)M). The extracellular ROS include the singlet oxygen (1O2) generated by photoreaction of sensitizer rosebengal and the superoxide anion (O2-.) produced by xanthine/xanthine oxidase reactive system. The intracellular ROS was sensitizer rosebengal and superoxide anion (O2-.) produced by xanthine/xanthine oxidase reactive system while the intracellular oxygen was generated by stimulating neutrophile respiratory burst with opsonized zymosan. No change in the peak or shape of fluorescent excitation and emission spectra was found for either of the two labels. The results of fluorescent polarization value in the membrane showed that beta-C liposome could significantly inhibit the damage of rat neutrophile membrane protein reacted either by intracellular generated reactive oxygen species or by extracellular generated O2-. or 1O2. It could also inhibit the injury of the rat neutrophile membrane lipid reacted by extracellular reactive oxygen species. However, the protective effects of beta-C liposome against membrane lipid damage reacted by intracellular reactive oxygen species by at the same concentration as those on membrane protein were not significant, which could be partly explained by relatively higher damage level of rat neutrophile membrane lipid domain reacted by intracellular reactive oxygen species than that of the membrane protein domain.
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PMID:[Protective effects of beta-carotene liposome against rat neutrophile membrane damage caused by intra- or extra-cellular reactive oxygen species]. 938 68


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