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)

Creatine kinase is a sulfhydryl containing enzyme that is particularly susceptible to oxidative inactivation. This enzyme is potentially vulnerable to inactivation under conditions when it would be used as a diagnostic marker of tissue damage such as during cardiac ischemia/reperfusion or other oxidative tissue injury. Oxidative stress in tissues can induce the release of iron from its storage proteins, making it an available catalyst for free radical reactions. Although creatinine kinase inactivation in a heart reperfusion model has been documented, the mechanism has not been fully described, particularly with regard to the role of iron. We have investigated the inactivation of rabbit muscle creatine kinase by hydrogen peroxide and by xanthine oxidase generated superoxide or Adriamycin radicals in the presence of iron catalysts. As shown previously, creatine kinase was inactivated by hydrogen peroxide. Ferrous iron enhanced the inactivation. In addition, micromolar levels of iron and iron chelates that were reduced and recycled by superoxide or Adriamycin radicals were effective catalysts of creatinine kinase inactivation. Of the physiological iron chelates studied, Fe(ATP) was an especially effective catalyst of inactivation by what appeared to be a site-localized reaction. Fe(ICRF-198), a non-physiological chelate of interest because of its putative role in alleviating Adriamycin-induced cardiotoxicity, also catalyzed the inactivation. Scavenger studies implicated hydroxyl radical as the oxidant involved in iron-dependent creatine kinase inactivation. Loss of protein thiols accompanied loss of creatine kinase activity. Reduced glutathione (GSH) provided marked protection from oxidative inactivation, suggesting that enzyme inactivation under physiological conditions would occur only after GSH depletion.
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PMID:Free radical inactivation of rabbit muscle creatinine kinase: catalysis by physiological and hydrolyzed ICRF-187 (ICRF-198) iron chelates. 783 53

The scavenging effect of Chinonin on NO and oxygen free radicals and its protective effect on myocardium from the ischemia-reperfusion injury was studied with electron spin resonance (ESR) and chemiluminescence techniques. Chinonin can effectively inhibit the oxidative activity of ONOO-, (the IC50 = 7 x 10 (-5) mmol/L) and scavenge oxygen free radicals generated from the reaction of xanthine and xanthine oxidase (the IC50 = 2/5 x 10(-4) mmol/l). It is difficult to find another antioxidant which can scavenge so effectively both ONOO- and oxygen free radicals simultaneously. In the system of ischemia-reperfusion injury of myocardium, Chinonin can, in parallel, scavenge the NO and oxygen free radicals generated from the ischemia-reperfused myocardium, and decrease the activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary artery effluent of ischemia-reperfused heart and therefore protect the heart from ischemia-reperfusion injury. The protective effect of 0.1 mmol/l Chinonin is similar to that of 1500 U/ml SOD and catalase.
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PMID:Scavenging effect of Chinonin on NO and oxygen free radicals and its protective effect on the myocardium from the injury of ischemia-reperfusion. 860 70

Reactive oxygen species (ROS) have been reported to alter cardiac myofibrillar function as well as myofibrillar enzymes such as myosin ATPase and creatine kinase (CK). To understand their precise mode and site of action in myofibrils, the effects of the xanthine/xanthine oxidase (X/XO) system or of hydrogen peroxide (H2O2) have been studied in the presence and in the absence of phosphocreatine (PCr) in Triton X-100-treated cardiac fibers. We found that xanthine oxidase (XO), with or without xanthine, induced a decrease in maximal Ca(2+)-activated tension. We attributed this effect to the high contaminating proteolytic activity in commercial XO preparations, since it could be prevented a protease inhibitor, phenylmethylsulfonyl fluoride (PMSF), and it could be mimicked by trypsin. In further experiments, XO was pre-treated with 1 mmo1/L PMSF. Superoxide anion production by the X/XO system, characterized by electron paramagnetic resonance spin-trapping technique, was not altered by PMSF. A slight increase in maximal force was then observed either with X/XO (100 mumol/L per 30 mIU/mL) or H2O2. pMgATP-rigor tension relationships have been established in the presence and in the absence of PCr to separate the effects of ROS on myosin ATPase and myofibrillar-bound CK. In the absence of PCr, pMgATP50, the pMgATP necessary to induce half-maximal rigor tension, was reduced from 5.03 +/- 0.17 (n = 21) to 4.22 +/- 0.22 (n = 4) after 25 minutes of incubation in the presence one of 30 mIU/mL. XO and 100 mumol/L xanthine or to 4.04 +/- 0.1 (n = 11) after incubation in the presence of 2.5 mmol/L H2O2. The ROS effects were partially prevented or antagonized by 1 mmol/L dithiothreitol. No effect was observed on pMgATP50 when PCr was absent. pCa-tension relationships have been evaluated to assess the effects of ROS on active tension development. Incubations with H2O2 induced on increase in Ca2+ sensitivity and resting tension when MgATP was provided through myofibrillar CK (PCr and MgADP as substrates) but not when MgATP was added directly. These results suggest that myofibrillar CK was inhibited by ROS. Active stiffness and the time constant of tension changes after quick stretches applied to the fibers were dose-dependently increased by H2O2 only in the presence of PCr. In addition, myofibrillar CK but not myosin ATPase enzymatic activity was depressed after incubation with either ROS. These results suggest that ROS mainly alters CK in myofibrils, probably by the oxidation of its essential sulfhydryl groups. Such CK inactivation results in a decrease in the intramyofibrillar ATP-to-ADP ratio. The effects of ROS on cytosolic and bound CKs may take part in the overall process of myocardial stunning after cardiac ischemia and reperfusion.
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PMID:Creatine kinase is the main target of reactive oxygen species in cardiac myofibrils. 863 32

New Zealand rabbits were assigned randomly to three groups: sham operation, intestinal simple obstruction, and strangulation obstruction. To relate possible changes in the body fluid content of biochemical markers to the strangulation process, subsequent samples of blood and peritoneal fluid, for the determination of levels of creatine kinase (CK), lactic acid (LA), xanthine oxidase (XO), and inorganic phosphate (IP), were obtained at 1-, 2-, 4-, and 6-hour intervals, and intestinal histological specimens were graded blindly. Significant increases in plasma LA (3.93 +/- 0.26 v 2.99 +/- 0.37; P < .05), peritoneal LA (5.03 +/- 1.14 V 3.33 +/- 0.86; P < .05), and CK (940 +/- 146 v 772 +/- 165, P < .05) occurred after 1 hour of ischemic injury. Except for serum CK, all parameters in the blood and peritoneal fluid in group 3 were markedly elevated within 4 hours. The serum CK remained almost unchanged throughout the 6-hour study period. The results suggest that plasma LA, peritoneal LA, and CK are sensitive indicators in the early diagnosis of bowel ischemia; the determination of both serum and peritoneal XO and IP was also helpful for early diagnosis; in contrast, serum CK was not a useful indicator. The value of any biochemical marker as an early diagnostic tool for intestinal ischemia depends not only on its quantity but also on its location and mechanism of release.
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PMID:Changes in body fluid markers in intestinal ischemia. 878 76

The present study investigated the effect of 7 days of strenuous exercise on the quantity of xanthine oxidase and IGF-I in muscle. Fifteen male military trainees performed 1 week of terrain marching and warfare exercises. Muscle biopsies and blood samples were obtained prior to and after the week. After the week, the number of xanthine oxidase immunoreactive cells, identified as capillary endothelial cells and leucocytes, and the number of IGF-I immunoreactive cells, mainly vascular cells but also cells tentatively identified as satellite cells, were higher in the muscle (P < 0.05). Plasma creatine kinase activity was 650% higher after the week (P < 0.001) and the muscle content of hydroxyproline was elevated by 160% 2 months post-exercise (P < 0.05), both findings implying injury to the muscle. The present data provide a first observation of an elevated level of xanthine oxidase and IGF-I in human skeletal muscle after exercise. It is proposed that both substances increased as a result of cellular damage: xanthine oxidase because of the influence of immunomodulators, and IGF-I in association with regenerative processes. The increased expression of IGF-I in the muscle could, however, also reflect cellular growth in response to an elevated load on the muscle and the vascular bed.
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PMID:Increased expression of xanthine oxidase and insulin-like growth factor I (IGF-I) immunoreactivity in skeletal muscle after strenuous exercise in humans. 880 Mar 59

1. The present study tested the hypothesis that the level of xanthine oxidase is elevated in injured human skeletal muscle in association with inflammatory events. Seven male subjects performed five bouts of strenuous one-legged eccentric exercise. Muscle biopsies from both the exercised and the control leg, together with venous blood samples, were obtained prior to exercise and at 45 min, 24, 48 and 96 h after exercise. The time courses of xanthine oxidase immunoreactivity and indicators of muscle damage and inflammation were examined. 2. The number of xanthine oxidase structures observed by immunohistological methods in the exercised muscle was up to eightfold higher than control from day 1 to day 4 after exercise (P < 0.05). The increase was attributed to an enhanced expression of xanthine oxidase in microvascular endothelial cells and an invasion of leucocytes containing xanthine oxidase. 3. The concentration of plasma interleukin-6 was significantly higher 90 min after exercise than before exercise (P < 0.05) and remained higher than pre-exercise levels throughout the 4 days. On day 4 the plasma creatine kinase activity was approximately 150-fold higher (P < 0.05) than resting levels. 4. Despite the increase in xanthine oxidase in the muscle there were no detectable changes in the levels of muscle malondialdehyde or in plasma antioxidant capacity up to 4 days post-exercise. 5. It is concluded that eccentric exercise leads to an increased level of xanthine oxidase in human muscle and that the increase is associated with secondary inflammatory processes. The increase in xanthine oxidase in the muscle occurs mainly in microvascular endothelial cells, but occurs also via infiltrating leucocytes containing xanthine oxidase. A role for leucocytes in xanthine oxidase induction in endothelium is proposed.
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PMID:Xanthine oxidase in human skeletal muscle following eccentric exercise: a role in inflammation. 902 82

To study the mechanism of the protective effect of gamma-glutamylcysteine ethyl ester, mitochondrial creatine kinase activity of rat heart was measured. Gamma-glutamylcysteine ethyl ester had a protective effect against the depression of creatine kinase activity induced by xanthine + xanthine oxidase or hydrogen peroxide. Gamma-glutamylcysteine ethyl ester also prevented the depression of creatine kinase activity induced by N-ethylmaleimide. It is suggested that the protective effect of gamma-glutamylcysteine ethyl ester is related to oxygen free radicals or to reduction of the sulfhydryl groups of the enzyme which were previously oxidized by oxygen free radicals.
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PMID:Effects of gamma-glutamylcysteine ethyl ester on heart mitochondrial creatine kinase activity: involvement of sulfhydryl groups. 966 7

The ESR signal of NO bound to hemoglobin was detected during the ischemia-reperfusion of myocardium with low temperature ESR technique, and the synergic effects of NO and oxygen free radicals in the injury of the process were studied with this technique. Oxygen free radicals and NO bound to beta-subunit of hemoglobin (beta-NO complex) could be detected simultaneously in the ischemia-reperfused myocardium. Those signals could not be detected from the normal myocardium even in the presence of L-arginine. However, those signals could be detected and were dose-dependent with L-arginine in the ischemia-reperfused myocardiums and the signal could be suppressed with the inhibitor of NO synthetase, NG-nitro-L-arginine methylester (NAME). Measurement of the activities of lactate dehydrogenase (LDH) and creatine kinase (CK) in the coronary artery effluent of ischemia-reperfused heart showed that L-arginine at lower concentration (< 1 mmol/L) could protect the heart form the ischemia-reperfusion injury but at higher concentration aggravate the injury. Addition of NAME to the reperfusion solution could also protect the myocardium. Addition of xanthine (X)/xanthine oxidase (XO) or Fe2+/H2O2 to the reperfusion solution increased the production of NO and oxygen free radicals and the ischemia-reperfused injury simultaneously. Addition of superoxide dismutase (SOD) and catalase decreased the production of NO and oxygen free radicals and the ischemia-reperfusion injury.
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PMID:Synergic effects of NO and oxygen free radicals in the injury of ischemia-reperfused myocardium--ESR studies on NO free radicals generated from ischemia-reperfused myocardium. 977 52

The main purpose of this study was to investigate the effect of free radicals and experimental diabetes on cytosolic creatine kinase activity in rat heart, muscle and brain. Hydrogen peroxide decreased creatine kinase activity in a dose dependent manner which was reversed by catalase. Xanthine/xanthine oxidase, which produces superoxide anion, lowered the creatine kinase activity in the same manner whose effect was protected by superoxide dismutase. N-acetylcysteine and dithiothreitol also significantly ameliorated the effect of Xanthine/xanthine oxidase and hydrogen peroxide. Experimental diabetes of twenty-one days (induced by alloxan), also caused a similar decrease in the activity of creatine kinase. This led us to the conclusion that the decrease in creatine kinase activity during diabetes could be due to the production of reactive oxygen species. The free radical effect could be on the sulfhydryl groups of the enzyme at the active sites, since addition of sulfhydryl groups like N-acetylcysteine and dithiothreitol showed a significant reversal effect.
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PMID:Effects of free radicals on cytosolic creatine kinase activities and protection by antioxidant enzymes and sulfhydryl compounds. 1097 54

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


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