The species distribution of xanthine oxidase

Al-Khalidi, Usama; Chaglassian, T. H.

doi:10.1042/bj0970318

Cited by 245 publications

(92 citation statements)

References 4 publications

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“…• " Xanthine oxidase is relatively low in the whole brain. 12 - 13 However, a recent immunocytochemical study demonstrated the presence of substantial xanthine oxidase in various vascular endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Effect of allopurinol on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats.

Itoh¹,

Kawakami²,

Yamauchi³

et al. 1986

Stroke

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In spontaneously hypertensive rats, we studied the participation of xanthine oxidase-linked free radical in ischemia and reperfusion-induced cerebral injury, using allopurinol, a xanthine oxidase inhibitor. The loss of righting reflex was noted in some animals after a 4 hour occlusion of bilateral common carotid arteries and 19 of 25 animals died within 72 hours after reperfusion. One hour after reperfusion, the cerebral water content increased significantly, with an increase in sodium content and a decrease in potassium content. In 7 animals treated with oral administrations of allopurinol (200 mg/kg) 24 hours and 1 hour before occlusion, no death was found either during occlusion or after reperfusion, and the loss of righting reflex was noted in only one animal 24-72 hours following reperfusion. The increase in cerebral water content and accompanied changes in electrolyte contents were clearly prevented by allopurinol. These results suggest the possibility that the production of xanthine oxidase-linked free radical participates in cerebral injury due to ischemia and reperfusion in spontaneously hypertensive rats.

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Section: Discussionmentioning

confidence: 99%

Effect of allopurinol on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats.

Itoh¹,

Kawakami²,

Yamauchi³

et al. 1986

Stroke

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“…2B) and catalytic activity (Table 1), was observed even under normoxic conditions. Even though rodents have much greater XOR-specific activities in plasma than humans (49), release of this enzyme from XOR-replete human splanchnic tissues can still have potent pathophysiologic effects. Present evidence supports that not only the extent of XOdependent tissue O 2 ⅐Ϫ production, but also its anatomic location, will determine whether or not vascular ⅐ NO-dependent signaling is adversely affected (50).…”

Section: Discussionmentioning

confidence: 99%

Oxygen radical inhibition of nitric oxide-dependent vascular function in sickle cell disease

Aslan

Ryan

Adler

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

349

337

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“…Infarcts were produced by 40 min of coronary occlusion followed by reperfusion. After the initial surgical preparations but approximately 35 Postmortem studies. Area at risk.…”

Section: Methodsmentioning

confidence: 99%

Failure of the xanthine oxidase inhibitor allopurinol to limit infarct size after ischemia and reperfusion in dogs.

Reimer¹,

Jennings²

1985

Circulation

164

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During the acute phase of myocardial ischemia, adenine nucleotides are degraded to nucleosides and bases, especially inosine and hypoxanthine. Simultaneously, xanthine dehydrogenase is converted to xanthine oxidase, an enzyme that converts hypoxanthine to xanthine, and xanthine to uric acid, producing a superoxide anion for each molecule of hypoxanthine or xanthine oxidized. To determine if free radicals via this enzymatic source contribute to cell death in myocardial ischemia, we determined whether allopurinol, an inhibitor of xanthine oxidase, could limit infarct size in a reperfusion preparation of myocardial infarction. The circumflex coronary artery of each of 34 dogs was occluded for 40 min, followed by reperfusion for 4 days. Infarct size then was measured by histologic methods and was related to major baseline predictors of infarct size, including anatomic area at risk and collateral blood flow. Infarct size was larger (NS) in the allopurinol (n = 8) than in the control (n = 1 1) group, a trend that was related to slightly higher (NS) collateral blood flow in the control group. We conclude that allopurinol has no beneficial effect in this preparation of experimental myocardial infarction. The results oppose the hypothesis that free radicals, produced via the xanthine oxidase reaction, are an important contributing factor in myocardial ischemic cell death.Circulation 71, No. 5, 1069-1075, 1985. FR1EE RADICALS, including the superoxide anion (02-) and the hydroxyl radical (OH), have been implicated as causal or contributing factors in a variety of types of cell injury, including myocardial ischemia.`-Several metabolic pathways may lead to production of free radicals during ischemia,5'6 including the xanthine oxidase reaction in which hypoxanthine is oxidized to xanthine or xanthine is oxidized to uric acid.' '°The xanthine oxidase reaction is of particular interest because large quantities of hypoxanthine, and its precursor inosine, accumulate rapidly in severely ischemic myocardium as a consequence of the degradation of the purine nucleotides."' 12 Especially when reperfusion is established, the xanthine oxidase reaction, fueled by an initially large substrate supply plus abundant oxygen resulting from reactive hyperemia, might produce an excessive load of superoxide anion. The latter might cause death of myocytes that would otherwise have survived the temporary period of ischemia. If this hypothesis is valid, inhibition of the xanthine oxidase reaction should prevent some or all of the cell death, and thereby limit infarct size in a temporary occlusion/reperfusion setting. Accordingly, the purpose of the present study was to test whether allopurinol, a xanthine oxidase inhibitor, alters myocardial infarct size in a coronary occlusion/reperfusion preparation of ischemic injury.

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The species distribution of xanthine oxidase

Cited by 245 publications

References 4 publications

Effect of allopurinol on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats.

Effect of allopurinol on ischemia and reperfusion-induced cerebral injury in spontaneously hypertensive rats.

Oxygen radical inhibition of nitric oxide-dependent vascular function in sickle cell disease

Failure of the xanthine oxidase inhibitor allopurinol to limit infarct size after ischemia and reperfusion in dogs.

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