Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P47989 (xanthine oxidase)
 8,633 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The synthesis of thromboxane B2 is increased in platelets from rabbits with experimental hypercholesterolemia, but the increase is not due to increased phospholipids hydrolysis. We have clarified the mechanism for the increased thromboxane synthesis. The biosyntheses of prostaglandin H2 and thromboxane B2 were unaffected by superoxide dismutase, xanthine oxidase, mannitol, or benzoate in other experiments designed to study the possible involvement of reactive oxygen species. These results suggest that O2.- and OH were not likely to be involved as intermediates in the synthesis of prostaglandin H2 and thromboxane B2 in platelets. The rate of prostaglandin H2 biosynthesis was promoted in deuterium oxide, and this deuterium oxide enhancement effect was reversed by 2,5-diphenylfuran, suggesting that singlet oxygen may be involved in prostaglandin H2 biosynthesis. The biosynthesis of prostaglandin H2 was promoted by ADP-Fe3+ but inhibited by EDTA and EDTA-Fe3+. The effect of ADP-Fe3+ could not be replaced by EDTA-Fe3+. The effects of glutathione, glutathione peroxidase and H2O2 on cyclooxygenase and thromboxane synthetase were studied by using partially purified enzymes and platelet microsomes. Glutathione and glutathione peroxidase inhibited the activity of cyclooxygenase but did not inhibit that of thromboxane synthetase. H2O2 caused the inactivation of cyclooxygenase, but the addition of H2O2 did not inhibit the formation of thromboxane B2 from prostaglandin H2. An examination of glutathione concentration and glutathione peroxidase activity in platelets from normal and experimentally hypercholesterolemic rabbits demonstrated that both were decreased in platelets from later group. The observed alterations in glutathione levels and glutathione peroxidase activity are large enough to cause increased thromboxane B2 synthesis in platelets but the possibility that other unidentified factors may also contribute cannot be excluded.
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PMID:Increased thromboxane B2 biosynthesis in platelets. 681 1

Examination of hearts and livers of rats fed ethanol for 25-30 weeks showed significant increases in catalase and glutathione peroxidase activity. Further examination revealed that the xanthine dehydrogenase/oxidase activity ratio in both tissues were decreased, suggesting that an interconversion of the dehydrogenase into oxidase might have occurred. Such an interconversion would be expected to enhance the formation of superoxide anions during acetaldehyde metabolism by xanthine oxidase. Since a role of oxidative or free radical damage in the etiology of ethanol-induced liver pathology is becoming increasingly apparent, the observation that the biochemical changes in the heart and liver are comparable suggests that oxidative damage is involved in alcoholic pathology of the heart as well as liver.
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PMID:A possible role of xanthine oxidase in producing oxidative stress in the heart of chronically ethanol treated rats. 689 81

In this comprehensive approach, inhibition of autoxidation of PUFA by SOD or other enzymes has been studied. The systems used were: 1) in miscible media in which enzyme, substrat, and peroxidation products are soluble; 2) in non-miscible media such as emulsions; 3) in heterogenous media containing subcellular fragments or whole blended tissue. Depending on experimental conditions, inhibition or activation of peroxidation by SOD can be observed in miscible systems. Other enzymes such as phospholipase A, xanthine oxidase, or horseradish peroxidase are protective in heterogeneous media. Moreover, PUFA hydroperoxide are scavenged by glutathione peroxidase which thus could lessen the autocatalytic effects encountered during peroxidation. Enzymatic inhibition of autoxidation in emulsions was not observed. We conclude that superoxide ion does not play a major role in the initiation of peroxidation and that it may very well act as a free radical chain terminator. In addition, other enzymes such as xanthine oxidase, horseradish peroxidase or phospholipase A show an effective although empirical protection against autoxidation in homogenates of tissues.
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PMID:[Inhibition of the autoxidation of polyunsaturated fatty acids by superoxide dismutase]. 700 94

This study demonstrates that the promastigote form of virulent Leishmania donovani and Leishmania tropica are both deficient in endogenous enzymatic scavengers of H(2)0(2) (catalase, glutathione peroxidase) and susceptible to low fluxes of H(2)O(2) in a cell-free model. In addition, the killing of promastigotes by H(2)0(2) is markedly enhanced in the presence of a peroxidase and halide. Promastigotes also readily trigger the macrophage oxidative burst including the generation of H(2)0(2), and most intracellular promastigotes are killed within 18 h by unstimulated normal resident cells. Catalase, but not scavengers or quenchers of O(2)(-), OHx, or (1)O(2), protected promastigotes in a cell-free xanthine oxidase microbicidal system, and catalase also partially inhibited the leishmanicidal activity of resident macrophages. Thus, amongst various oxygen intermediates, H(2)0(2) alone appeared to be both necessary and sufficient for promastigote killing. Depriving macrophages of exogenous glucose, which inhibits the generation of oxygen intermediates, achieved effects similar to catalase treatment. These observations directly contrast with the intracellular parasite, T. gondii which is richly endowed with catalase and glutathione peroxidase, highly resistant to H(2)0(2), and requires products of O(2)(-)-H(2)0(2) interaction for effective oxidative killing. Toxoplasmas also fail to trigger the respiratory burst of normal macrophages, and readily multiply within these cells (1-5). Macrophages first activated by in vivo or in vitro immunologic stimuli, however, display an enhanced capacity to generate oxygen intermediates beyond O(2)(-) and H(2)0(2), and are able to kill toxoplasmas or inhibit their intracellular replication (1, 2). These studies illustrate the wide spectrum of susceptibility to oxidative products which appears to exist for virulent intracellular protozoans, and indicate that such differences may be reflected in contrasting fates of parasites within cell-free oxidative environments and the cytoplasm of normal resident macrophages. In addition, these observations also demonstrate that nonactivated phagocytes may display effective microbicidal activity against certain intracellular pathogens utilizing an oxygen-dependent mechanism.
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PMID:Susceptibility of Leishmania to oxygen intermediates and killing by normal macrophages. 725 18

Previous studies have demonstrated that reactive oxygen species are involved in ischemic injury. The present work was undertaken to determine in vivo the role of xanthine oxidase in the oxygen free radical production during rat liver ischemia and to examine the activity of antioxidant enzymes (superoxide dismutase, catalase and glutathione peroxidase) during the same period. Our results indicate a 4-fold increase in xanthine oxidase activity between 2 and 3 hours of normothermic ischemia, in parallel with a decrease in cell viability. Moderate hypothermia delays both events. Under the same conditions, the activity of oxygen radical scavenging enzymes remains unchanged. Moreover, we have compared in vitro the susceptibility of isolated liver cells to an oxidative stress induced by O2.-, H2O2 and .OH. Our results reveal that endothelial cells are much more susceptible to reactive oxygen species than hepatocytes, probably because they lack H2O2-detoxifying enzymes. These findings suggest that xanthine oxidase might play a major role in the ischemic injury mainly at the level of the sinusoidal space where most endothelial cells are located.
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PMID:Deleterious effects of xanthine oxidase on rat liver endothelial cells after ischemia/reperfusion. 748 47

The reactive oxygen species, hydrogen peroxide (H2O2) and superoxide anion (O2o-), were generated with a xanthine-xanthine oxidase system and their effect on human sperm function was studied. The action of reactive oxygen species on selected human spermatozoa resulted in a decreased capacity for ionophore-induced acrosome reaction, a decrease in sperm motility, an increase in the concentration of lipid hydroperoxides and a loss of membrane polyunsaturated fatty acids. H2O2 was the key intermediate of the deleterious effects exerted by the xanthine and xanthine oxidase. Among these parameters, the acrosome reaction appeared most susceptible to the reactive oxygen species generated by the xanthine-xanthine oxidase system, and was decreased without sperm motility being affected. Treatment with H2O2 was shown to inactivate several enzymatic activities involved in the antioxidant defence of spermatozoa: glutathione peroxidase, superoxide dismutase and glucose-6-phosphate dehydrogenase. H2O2 and O2o- were shown to be involved in the lipid alterations triggered by the xanthine-xanthine oxidase system. Singlet oxygen is proposed to intervene in the lipoperoxidation process. The inefficacy of mannitol in protecting spermatozoa suggests that hydroxyl radicals were not produced in the extracellular medium.
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PMID:Reactive oxygen species, lipid peroxidation and enzymatic defence systems in human spermatozoa. 770 95

It has been documented that cytokines can induce the formation of reactive oxygen species (ROS) in the liver, and that an inflammatory reaction can locally increase the production of ROS, but it remains unknown whether in vivo a subcutaneous (s.c.) inflammatory reaction can induce the formation of ROS in the liver. To determine in vivo whether an inflammatory reaction, able to decrease the amount of hepatic cytochrome P450, enhances the presence of ROS in the liver, turpentine was injected s.c. to rabbits, which were sacrificed 48 hours later. Control rabbits received saline s.c. The amount and activity of cytochrome P450, as well as several parameters reflecting the presence of ROS were assessed in the liver. Total amount of cytochrome P450 was reduced, as was its activity, assessed by the rates of hydroxylation of aniline and of demethylation of aminopyrine. Moreover, lipid peroxidation increased, while the activity of the enzymatic scavengers, i.e. catalase, glutathione peroxidase and superoxide dismutase decreased. In addition, hepatic concentrations of reduced glutathione were diminished. On the other hand, the activity of the xanthine oxidase system was enhanced by almost 200%. These results strongly suggest an increased presence of ROS. The changes in the amount of cytochrome P450 were inversely correlated with lipid peroxidation. In conclusion, these results show that in vivo an inflammatory reaction, that reduces total cytochrome P450 and its activity, produces simultaneously an oxidative stress in the liver.
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PMID:Inflammation-induced decrease in hepatic cytochrome P450 in conscious rabbits is accompanied by an increase in hepatic oxidative stress. 774 59

In the present study, it was observed that somatostatin could significantly protect rat gastric mucosa from injury induced by cold-restraint stress and inhibit the stress induced increase of malonaldehyde (MDA) content. In the gastric mucosa of stress rats, the xanthine oxidase (XO) activity were increased and the glutathione peroxidase (GSH-Px) activity were decreased respectively, while the superoxide dismutase (SOD) activity showed no change. After pretreatment with somatostatin, the decrease of GSH-Px activity was significantly reversed, whereas XO and SOD activities were not significantly affected. The above results show that the protective effect of somatostatin against the stress-induced injury of gastric mucosa may be related to an enhancement of the ability of gastric mucosa to scavenge oxygen-derived free radicals.
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PMID:[Protective effect of somatostatin against stress injury of gastric mucosa may be related to the scavenge of free radicals]. 797 28

To assess right colic artery blood flow and relevance of xanthine dehydrogenase/xanthine oxidase after experimentally induced strangulation obstruction and reperfusion of the colon, 5 ponies were subjected to 2.5 hours of complete ischemia of the left dorsal and ventral colons, allowed to recover from surgery, and monitored during a 48-hour reperfusion period. Five ponies were subjected to sham surgery and served as controls. All ponies had a Doppler ultrasound blood flow monitor implanted on the right colic artery near the pelvic flexure 10 to 14 days prior to the ischemic period. Colic artery blood flow was monitored prior to, during, and for 4 hours after surgery. Blood samples from the right colic artery and vein distal to the obstruction site were collected during surgery (prior to ischemia, after 1 and 2 hours of ischemia, and after 10 and 60 minutes of reperfusion) for determination of arterial and venous blood gas tensions and electrolytes. Prior to surgery, blood selenium and plasma vitamin E (alpha-tocopherol) concentrations and blood glutathione peroxidase (GPX) activity were determined to assess the status of endogenous antioxidants. Combined xanthine dehydrogenase (XDH) plus xanthine oxidase (XO) activity, and XO activity alone (nanomoles per minute per gram of tissue) were determined, using a dual-spectrophotometric technique. Xanthine dehydrogenase and oxidase activities were determined prior to ischemia, after 1 and 2 hours of ischemia, and at 1 and 48 hours after reperfusion. Median blood flow in the experimental and control groups (156 ml/min and 110 ml/min, respectively) was not statistically different before surgery, and was significantly (P < 0.02) lower in the experimental (4 ml/min) vs the control group (72.5 ml/min) during the ischemic period. Experimental ponies had significantly (P < 0.03) lower right colic artery blood flow during the 4 hours immediately after recovery from anesthesia. Significant difference was not observed in right colonic venous bicarbonate concentration between groups at any time. Median right colonic venous PCO2, pH, and standard base excess were different (P < 0.001) between groups during the ischemic period only. Median venous oxygen saturation and median venous PO2 were significantly (P < 0.001) lower in the experimental ponies at the end of 2 hours of ischemia, but were significantly (P < 0.05) increased during the reperfusion phase. Median venous potassium concentration was significantly (P < 0.01) higher in experimental ponies during the ischemic and reperfusion phases. Vitamin E and GPX values were within normal limits for all ponies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Measurements of blood flow and xanthine oxidase activity during postischemic reperfusion of the large colon of ponies. 797 59

The presence of cancer induces metabolic alterations in distant, tumor-free tissues and organs of the host. A remote humoral effect of cancer growing extrahepatically is an increase in the activity of oxidant and a decrease of antioxidant enzymes in the liver of the tumor-bearing animal. We speculated that TNF-alpha, produced by host cells, the cancer, or both, is responsible for these changes. When human recombinant TNF-alpha, 100 micrograms/kg/d i.p. for 5 days, was injected in groups of rats fed ad libitum, starved, or pair-fed, a decrease in the activity of superoxide dismutase and glutathione peroxidase and an increase in xanthine oxidase was observed, particularly with pair-fed controls. It is concluded that TNF-alpha, directly or indirectly, causes these enzyme alterations in the tumor-free liver of a tumor-bearing host.
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PMID:TNF-alpha effect on oxygen free radical scavenging and generating enzymes in rat liver. 808 Dec 9


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