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

---

Query: EC:1.17.3.2 (xanthine oxidase)
8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute phase protein, C-reactive protein (CRP), when heat-aggregated (Agg-CRP), potentiates immunoglobulin G (IgG) Fc receptor-mediated luminol-enhanced chemiluminescence (CL) in human monocytes and neutrophils. Luminol-CL is a sensitive measure of phagocyte respiratory burst activity; however, the nature of oxidative products contributing to the light emission and their site of generation remain incompletely defined. To more precisely describe the oxidative burst of monocytes and neutrophils to Agg-CRP, superoxide anion release was measured by cytochrome c reduction. In addition, the extracellular release of hydrogen peroxide was distinguished from hydrogen peroxide generation using a phenol red oxidation assay. Finally, a flow cytometric determination of dichlorofluorescein (DCFH) oxidation was employed as an index of intracellular peroxide production. Although Agg-CRP alone did not stimulate hydrogen peroxide generation by either monocytes or neutrophils, it significantly enhanced hydrogen peroxide generation in response to heat-aggregated IgG (Agg-IgG). In contrast, Agg-CRP did not enhance the extracellular release of either hydrogen peroxide or superoxide anion from Agg-IgG-stimulated cells. The capacity of Agg-CRP to enhance selectively intracellular oxidative product generation was confirmed when measuring DCFH oxidation in Agg-IgG-stimulated cells. To evaluate whether this selective enhancement of intracellular oxidative events could be attributed, at least in part, to a scavenging effect of Agg-CRP, a cell-free oxygen radical-generating system was employed. Agg-CRP did not significantly diminish the lucigenin-amplified CL response induced by the xanthine/xanthine oxidase reaction. These results indicate that although Agg-CRP enhances the intracellular generation of reactive oxygen intermediates by monocytes and neutrophils, extracellular release of those products is not influenced by cell interaction with Agg-CRP. It is tempting to speculate that CRP can selectively boost the microbicidal activities of monocytes and neutrophils within an inflammatory site by amplifying the intracellular generation of reactive oxygen products without increasing damage to surrounding normal tissues.
...
PMID:C-reactive protein selectively enhances the intracellular generation of reactive oxygen products by IgG-stimulated monocytes and neutrophils. 132 45

The means by which neutrophils within the body ward off infectious and neoplastic processes by the activation of molecular oxygen, as well as how such mechanisms dysfunction, is the subject of extensive ongoing research. Most previous studies of neutrophil activation indicate that there is a transient production of reactive oxygen species. Luminol-amplified chemiluminescence surveillance of O2-. and H2O2 supported these general findings. Yet, recent studies showed that production of reactive oxygen species by PMA-stimulated neutrophils is not transient but persistent; however, luminol-dependent methods do not corroborate such findings. The kinetics of O2-. production by human neutrophils were studied using luminol-amplified chemiluminescence (CL), spin trapping combined with electron spin resonance detection, and ferricytochrome c reduction. The effects of pH and O2 level on luminol-amplified CL were determined using hypoxanthine/xanthine oxidase to produce O2-. and H2O2 in cell-free systems. As we have found by electron spin resonance and ferricytochrome c reduction, stimulated neutrophils continued to generate O2-. for several hours, yet when luminol-amplified CL was used to continuously follow radical production, CL was shortly lost. Similar loss of CL was observed with continuous enzymatic formation of O2-. and H2O2. The failure of the CL assay to report O2-. and H2O2 formation results from some luminol reaction product which interferes with the light reaction. Our results show that the cells are operative for long periods indicating that cell exposure to prolonged O2-. fluxes does not terminate radical production, and even when pH, [O2], and reagents are optimized, the use of luminol-amplified CL is not a valid assay for continuous monitoring of O2-. and H2O2 generated by either stimulated neutrophils or in cell-free systems.
...
PMID:On radical production by PMA-stimulated neutrophils as monitored by luminol-amplified chemiluminescence. 164 85

The effects of cimetidine, ranitidine, histamine and histidine, as well as of their copper complexes, have been examined in an enzymic and chemical O2- generated systems. Copper complexes like CuZnSOD inhibited both the reduction of cytochrome c and NBT2+ in xanthine-xanthine oxidase systems, but their inhibitory action was due to a certain extent to the copper-induced inhibition of xanthine oxidase. EDTA abolished the inhibitory effect of all copper complexes studied. Luminol chemiluminescence in NADH2-PMS system was inhibited by CuZnSOD while it was enhanced by copper complexes. The copper-accelerating effect gradually increased up to about 1 microM Cu and decreased, reaching the control values up to 10 microM Cu. In the presence of low copper concentrations chemiluminescence was inhibited by CuZnSOD only, while in the presence of high copper concentrations it was inhibited by catalase and mannitol, but not by CuZnSOD. The ligands however, have been ineffective in the two O2- generated systems.
...
PMID:Do the copper complexes of histamine, histidine and of two H2-antagonists react with O2-? 167 75

Luminol chemiluminescence induced by the xanthine or hypoxanthine-O2-xanthine oxidase system is analyzed and compared. Characteristics of the light emission curves were examined considering the conventional reaction scheme for the oxidation of both substrates in the presence of xanthine oxidase. The ratio of the areas of the rate of superoxide production during substrate oxidation to uric acid. The O2-. to uric acid ratio for each substrate can account for differences in xanthine and hypoxanthine-supported light emission, since uric acid is a strong inhibitor of O2-.-dependent luminol chemiluminescence. These results are consistent with a free radical scavenging role for uric acid. A similar but weaker scavenging effect of xanthine may also contribute to the observed differences in chemiluminescent yields between both substrates.
...
PMID:Luminol chemiluminescence using xanthine and hypoxanthine as xanthine oxidase substrates. 215 34

Superoxide dismutase (superoxide: superoxide oxidoreductase, EC 1.15.1.1) (SOD) and ferricytochrome c are used to check the effects on luminol chemiluminescence induced by a xanthine or hypoxanthine/xanthine oxidase/oxygen system. Luminol chemiluminescence has been attributed to superoxide anion radical (O2.-) in this system. From kinetic studies on the light intensity vs. time curves it is demonstrated that addition of SOD into the system does not affect the mechanism of O2.- generation, whilst ferricytochrome c dramatically alters the time-course of the reaction. This is interpreted as the effect of cytochrome c redox cycling by reaction with H2O2, modifying oxy-radical generation in the reaction medium. Also, an alternative mechanism for luminol chemiexcitation is proposed under certain experimental conditions.
...
PMID:Comparison of the effects of superoxide dismutase and cytochrome c on luminol chemiluminescence produced by xanthine oxidase-catalyzed reactions. 253 90

Eu3+-tetracycline complex (EuT) increased the chemiluminescence (CL) intensity of linolenic acid micells (UFA-somes) oxidized with lipoxygenase and CL of the lecithin liposomes peroxidized with Fe2+ ions by 3 orders of magnitude. In the systems producing oxygen radicals (xanthine + xanthine oxidase and Fenton's reagent) EuT was ineffective. Luminol increased CL intensity up to 4 orders of magnitude in Fenton's reagent and by 2 orders of magnitude in xanthine oxidase reaction. The sensitization of CL in Fe2+-induced lipid peroxidation (LPO) of liposomes was by a factor 40, while in lipoxygenase reaction very low sensitization was observed. By means of cut-off light filter OS-12 (Soviet) having short wave-length transmittance limit at 560 nm it was possible to measure separately in the same sample the luminol-sensitized CL (maximal emission near 480 nm) and EuT-sensitized CL (maximum at 620 nm); these two CL components reflect, correspondingly, the production rate of oxygen- and lipid-free radicals. Mannitol, the OH radical scavenger, inhibited luminol-dependent component of CL in peroxidized liposomes and did not inhibited EuT sensitized CL in the same system. Apparently, hydroxyl radicals are produced in LPO reactions and responsible for the effect of CL sensitization by luminol, but are not involved in the chain LPO process.
...
PMID:Selective sensitization of chemiluminescence resulted from lipid and oxygen radical reactions. 257 Jul 36

We tested the effects of generally used chemiluminescence inhibitors on an example of luminol chemiluminescence elicited by xanthine oxidase/hypoxanthine system, and attempted to assess their capabilities in discovering the reaction pathways leading to chemiluminescence. Luminol itself is a xanthine oxidase inhibitor and its concentration affects the reaction mechanism. Maximal chemiluminescence response was observed at luminol concentration inhibiting urate production. Chemiluminescence was totally inhibited by superoxide dismutase, the inhibition by catalase depended on luminol concentration. Ferricytochrome c, a detector of superoxide, either stimulated or inhibited chemiluminescence in a concentration-dependent manner. Chemiluminescence was highly stimulated by peroxidases. A pronounced inhibition of chemiluminescence was caused by chelators; 1 mM desferal and 0.01 mM diethyldithiocarbamate. It is suggested that measurement of luminol chemiluminescence is not a suitable method for discrimination among individual reactive oxygen species and their quantitative determination in biological systems.
...
PMID:Variables in xanthine oxidase-initiated luminol chemiluminescence: implications for chemiluminescence measurements in biological systems. 379 63

The origin of luminol-dependent chemiluminescence (CL) in neutrophils stimulated by immune complexes (IC) was investigated. It was found that CL induced by soluble IC and aggregated human gamma globulin (AHG) was glucose-independent, while insoluble IC-induced CL was diminished in the absence of glucose. AHG-induced CL was not inhibited by superoxide dismutase, catalase or 2,5-dimethyl furan, but was suppressed in the presence of phenol, sodium benzoate, sodium formate and mannitol. The CL was also inhibited by inhibitors of arachidonic acid (AA) metabolism including 5,8,11,14-eicosatetraynoic acid, nordihydroguaiaretic acid, quinacrine, indomethacin and aspirin, and by prostaglandins E1 and E2, theophylline and dibutyryl cyclic AMP. Luminol-dependent CL was also studied in cell-free systems including AA plus soybean lipoxygenase, hydroperoxyeicosatetraenoic acid plus peroxidase and xanthine oxidase plus xanthine. Our results indicate that, in neutrophils exposed to soluble IC and AHG, CL is produced and this is closely linked to the formation of free radicals during the metabolism of AA. The radical(s) involved is likely to include the hydroxyl radical. In neutrophils stimulated by large aggregates of IC or micro-organisms, superoxide anion, H2O2 and singlet oxygen are also produced as a result of activation of NAD(P)H oxidase. These oxygen species function as oxidizing agents for AA metabolism and amplify the production of hydroxyl radical along the lipoxygenase (and possibly cyclooxygenase) pathway(s).
...
PMID:Luminol-dependent chemiluminescence produced by neutrophils stimulated by immune complexes. 608 70

Luminol-dependent chemiluminescence of normal human polymorphonuclear leucocytes (PMN) which were resting, or stimulated by unopsonized latex beads, opsonized zymosan or the chemotactic peptide N-formyl-met-leu-phe was decreased more than 80% in the presence of physiological concentrations of albumin (4%, w/v). This inhibition did not result from impairment of light transmission, cellular toxicity, luminol excited-state quenching or a dialysable contaminant in the albumin preparation, but was reduced by 30% when the fall induced by albumin in extracellular free Ca2+ concentration was corrected. The inhibition was most apparent in the larger second phase of the PMN chemiluminescent response to chemotactic peptide or opsonized zymosan stimulation. The smaller first phase of these responses was in fact enhanced by low concentrations of albumin (0.05-0.5%, w/v) and only inhibited up to 50% by 4% (w/v) albumin. Albumin in the range 0.1-4% (w/v) exerted a similar effect on chemiluminescence resulting from superoxide anion (O-2) and hydrogen peroxide (H2O2) production by xanthine oxidase catalysed oxidation of xanthine in the presence of luminol. We suggest that the effect of albumin on PMN luminol-dependent chemiluminescence is mediated by modification of the oxygen radical generating pathway, or oxygen radical scavenging. This previously undocumented property of the major extracellular protein requires further examination if oxygen radicals are to be established as important mediators of inflammation.
...
PMID:Albumin inhibits human polymorphonuclear leucocyte luminol-dependent chemiluminescence: evidence for oxygen radical scavenging. 671 82

In vivo oxidative change was visualized in the gastric mucosa of rats and the alteration was analysed by using a fluorescence microscope equipped with a digital imaging processor during the development of mucosal damage. Dichlorofluorescein (DCF)-associated fluorescence increased after the repeated electrical stimulation on the gastric artery (irritation), suggesting the occurrence of lipid peroxidation. The increase was enhanced in the mid-zone of two adjacent collecting venules. Allopurinol attenuated the oxidative stress in mucosa, showing the involvement of xanthine oxidase. Luminol-dependent chemiluminescence value in the blood taken from gastric vein was elevated by the irritation, suggesting that leucocyte-generated oxygen radicals also participate in this oxidative process. alpha-Tocopherol attenuated both the DCF activation and the increase in chemiluminescence value and prevented gastric mucosal injury. The present results suggest that alpha-tocopherol may be useful for the prevention of oxidative alteration in gastric mucosa.
...
PMID:Fluorographic study on the oxidative stress in the process of gastric mucosal injury: attenuating effect of vitamin E. 851 96


1 2 Next >>

---