Serum xanthine oxidase

Shamma'a, Munir H.; Nasrallah, Salah M.; Al-Khalidi, Usama

doi:10.1007/bf01072233

Cited by 25 publications

(11 citation statements)

References 8 publications

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“…High levels of circulating XO are mostly seen with conditions involving liver damage, particularly acute viral hepatitis [18–20]; there has been at least one report of high levels of circulating XO in inflammatory rheumatic diseases [21]. In general, XO activity in normal human serum is very low [18, 22]; in contrast, synovial fluid XO concentrations in acutely injured knees were very high.…”

Section: Discussionmentioning

confidence: 99%

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Xanthine oxidase injurious response in acute joint injury

Stäbler

Zura

Hsueh

et al. 2015

Clinica Chimica Acta

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Background While acute trauma is a major cause of osteoarthritis, its etiology is poorly understood. We sought to determine whether xanthine oxidase (XO), a major producer of reactive oxygen species, plays a role in the early events of acute joint injury. Methods We analyzed synovial fluid from 23 subjects with recent severe acute knee injury. As a control we evaluated SF from 23 individuals with no or minimal knee osteoarthritis. We measured XO activity, reactive oxygen+reactive nitrogen species (ROS+RNS), protein oxidative damage (carbonyl), the type II collagen synthesis marker procollagen II c-propeptide (CPII) and the type II collagen degradation marker collagen type II telopeptide (CTx-II). We also measured the proinflammatory cytokine IL-6. Results XO and ROS+RNS were higher (p=0.02 and p=0.001 respectively) in acute injury than control and were strongly positively associated (r=0.62, p=0.004). Carbonyl was higher in acute injury than control (p=0.0002) and was positively correlated with XO (r=0.68, p=0.0007) as well as with ROS+RNS (r=0.71, p=0.004). CPII was higher in acute injury than control (p<0.0001) and was negatively correlated with XO (r=−0.49, p=0.017). While CTxII was not significantly higher in acute injury than control, it was positively correlated with CPII (r=0.71, p=0.0002). IL-6 was higher in acute injury than control (p<0.0001). Conclusions These results are consistent with a potentially injurious effect of XO activity in acute joint injury characterized by excess free radical production and oxidative damage. These effects are associated with an inhibition of type II collagen production that may impede the ability of the injured joint to repair.

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Section: Discussionmentioning

confidence: 99%

“…In general, XO activity in normal human serum is very low [18, 22]; in contrast, synovial fluid XO concentrations in acutely injured knees were very high. High XO activity in injured joints could be due to high local production and/or slow clearance.…”

Section: Discussionmentioning

confidence: 99%

Xanthine oxidase injurious response in acute joint injury

Stäbler

Zura

Hsueh

et al. 2015

Clinica Chimica Acta

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“…The combination of hypoxanthine and 100% 0 2 appeared to have a damaging effect on the rat lung [24]. It has been reported that xanthine oxidase is liberated from the liver and is found in plasma in several diseases [28]. In sich newborns, xanthine oxidase could well be found in plasma^ although this has never been measured.…”

Section: Discussionmentioning

confidence: 99%

Plasma hypoxanthine levels in newbom infants: A specific indicator of hypoxia

Saugstad¹,

Gluck²

1982

Journal of Perinatal Medicine

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“…The rat was chosen as an experimental animal because its lung contains xanthine oxidase in contrast to humans (1,36). There is, however, evidence that xanthine oxidase is quite easily released from the liver of sick adult humans (29) and could thus react with hypoxanthine in any part of the body to create oxygen radicals. Plasma xanthine oxidase has, however, not yet been determined in sick newborn infants.…”

Section: Discussionmentioning

confidence: 99%

Hypoxanthine and Oxygen Induced Lung Injury: A Possible Basic Mechanism of Tissue Damage?

et al. 1984

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Summaryoxygen exposure with simultaneous intravenous hypoxanthine infusion. Lung injury was induced in young rats by a continuous infusion of hypoxanthine intravenously and breathing 100% oxygen for 48 h (group 1). Control animals were rats infused glucose and MATERIALS AND METHODSbreathing 100% oxygen (group 2), rats infused hypoxanthine in room air (group 3), and untreated rats (group 4). In group 1 rats interstitial and alveolar edema was found with a tendency toward marked margination of polymorphonuclear neutrophils in small vessels (P < 0.025 compared with group 2). The main elastase inhibitor alphal-antitrypsin (a-1-PI) was significantly elevated in group 1; 2-, 3-and 5-fold, respectively, when compared with groups 2, 3, and 4. The surfactant phopholipids from alveolar lavage were normal in all groups. The protein-rich fraction of the lavage fluid from group I rats inactivated, however, the surface properties of lung surfactant. Minimum surface tension in group 1 rats was 14.5 dyn/cm compared with 7.0 dyn/cm in group 2, 2.9 dyn/cm in group 3 and 3.5 dyn/cm in group 4 (P < 0.05, group 1 and 2 versus 4). We conclude that the combination of hypoxanthine and high levels of oxygen causes lung injury, possibly via free oxygen radicals. We discuss the possibility that these findings demonstrate a basic pathogenetic mechanism for the hypoxic-hyperoxic insult and can contribute to the understanding of pathogenesis of a variety of diseases both in pediatrics and adult medicine. AbbreviationFree oxygen radicals have been shown to destroy cell membranes by lipid peroxidation (3, 8, 1 1, 2 1). It has been suggested that such radicals play an important role in the pathogenesis of the acute and chronic lung damage among patients treated with oxygen. Many authors have, however, suggested that oxygen must be combined with other more or less unknown factors, before injury occurs ( 14,27).Recently, it has been shown that the hypoxanthine/xanthine oxidase system generates free radicals (7), and that this system potently induces inflammatory changes both in the hamster cheek pouch (22) and the rat lung (16). Further, it has, by now, been well established that hypoxanthine accumulates in tissues (33), plasma (30,32,34,35), and other body fluids (12,23,25) during hypoxia. When high concentrations of oxygen are administered to the hypoxic patient, large amounts of free radicals may be produced by the hypoxanthine/xanthine oxidase system. We, therefore, have raised the question whether the combination of hypoxanthine and oxygen is more damaging than high oxygen alone to the lung. In the present study we evaluated this by investigating experimentally the effect on the rat lung to 100% Young female rats of the Wistar strain, weighing 170-230 g, were used. Four groups were investigated. Group 1, rats infused continuously with 5 mM hypoxanthine dissolved in 5% glucose and exposed to 98-100% oxygen (n = 10). Group 2, rats infused continuously with 5% glucose and exposed to 98-100% oxygen (n = 9). Group 3, rats infused continuously wit...

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Serum xanthine oxidase

Cited by 25 publications

References 8 publications

Xanthine oxidase injurious response in acute joint injury

Xanthine oxidase injurious response in acute joint injury

Plasma hypoxanthine levels in newbom infants: A specific indicator of hypoxia

Hypoxanthine and Oxygen Induced Lung Injury: A Possible Basic Mechanism of Tissue Damage?

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