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)

Xanthine oxidase activity in blood from the ipsilateral femoral vein, and the relationship between xanthine oxidase production and the products of lipid peroxidation, were studied before operation and for 60 min following release of clamps after successful revascularization in two groups of patients with claudication or critical ischaemia. Before revascularization, detectable levels of xanthine oxidase were found only in patients with critical ischaemia. Clamping during bypass surgery led to release of xanthine oxidase in claudicants, but this activity reduced after 60 min. There was no evidence of lipid peroxidation during this time. Xanthine oxidase activity in brachial vein blood was higher than in femoral vein blood in patients with critical ischaemia before revascularization.
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PMID:Xanthine oxidase in critically ischaemic and claudicant limbs: profile of activity during early reperfusion. 869 45

We previously showed oxidative damage and edema within skeletal muscle after contractile claudication. To investigate the sources of this oxidative damage in the gastrocnemius muscle, we administered allopurinol (Allo, to inhibit xanthine oxidase) and cyclophosphamide (Cyclo, to deplete neutrophils) before inducing contractile claudication in male Sprague Dawley rats. Contractile claudication (ligated stimulated, LS) caused a significant increase in xanthine oxidase activity [sham ligated stimulated (SS) = 2.57 +/- 0.07; LS = 3.22 +/- 0.07] and neutrophil infiltration (SS = 0.47 +/- 0.03; LS = 0.91 +/- 0.10) compared with controls (SS), and this was associated with increased lipid peroxidation, protein oxidation, muscle damage, and edema. Pretreatment with Allo attenuated the increase in xanthine oxidase activity and attenuated lipid hydroperoxides (control LS = 12.85 +/- 0.50; Allo LS = 9.96 +/- 0.71), muscle damage, and neutrophil infiltration (control LS = 0.91 +/- 0.10; Allo LS = 0.61 +/- 0.07). This latter finding suggests that xanthine oxidase-derived oxidants are chemotactic to neutrophils. Pretreatment with Cyclo reduced neutrophil infiltration (control LS = 0.91 +/- 0.10; Cyclo LS = 0.55 +/- 0.02) and attenuated lipid peroxidation (control LS = 12.85 +/- 0.50; Cyclo LS = 6.462 +/- 0.62), protein oxidation (control LS = 2.59 +/- 0.47; Cyclo LS = 1.77 +/- 0.60), muscle damage, and edema. Together, these data indicate that contractile claudication causes an increase in xanthine oxidase activity and neutrophils in muscle and that inhibition of these oxidant sources protects against oxidative stress, muscle damage, and edema.
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PMID:Xanthine oxidase and activated neutrophils cause oxidative damage to skeletal muscle after contractile claudication. 1296 96

The purpose of this study was to determine the extent and sources of oxidative stress within skeletal muscle following an acute bout of contractile claudication. Twenty-four hours after unilateral ligation of the femoral artery, rat hind limbs were stimulated in vivo for 30 min, and force production measured. One-hour post-stimulation, animals were sacrificed and soleus and gastrocnemius muscles removed. There was significant reduction in force in the control limb (sham ligated/stimulated (SS)), while force in the ligated limb (ligated/stimulated (LS)) was reduced by 72%. There was an increase in skeletal muscle lipid hydroperoxides (53 and 47%) and protein carbonyls (57 and 54%) in the soleus and gastrocnemius muscles, respectively, and the muscle wet/dry weight ratio was increased in the gastrocnemius muscles. Total glutathione (GHS) was reduced, while xanthine oxidase (XO) activity and neutrophil levels were increased, in LS compared to SS in both soleus and gastrocnemius muscles. These data suggest that an acute bout of contractile claudication causes significant oxidative damage and edema to skeletal muscle. This is associated with both an increase in the activity of the radical-producing enzyme xanthine oxidase and an increase in activated neutrophils.
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PMID:Oxidative damage to skeletal muscle following an acute bout of contractile claudication. 1464 90

We have previously shown oxidative stress and oedema, caused by both xanthine oxidase-derived oxidants and infiltrating neutrophils, within skeletal muscle after contractile-induced claudication. The purpose of this study was to determine whether supplementation with antioxidant vitamins attenuates the oxidative stress, neutrophil infiltration and oedema associated with an acute bout of contractile-induced claudication. Rats received vehicle, vitamin C, vitamin E or vitamin C + E for 5 days prior to contractile-induced claudication. Force production was significantly reduced in the claudicant limbs of all groups compared with the control (sham) limb of control animals. Contractile-induced claudication caused a significant increase in protein oxidation, lipid peroxidation, neutrophil infiltration and oedema compared with sham muscles. Supplementation with vitamin C, E or C + E prevented the increases in each of these, and there were no differences between groups. These findings suggest that, in an animal model of exercise-induced claudication, neutrophil chemotaxis is caused by oxidizing species and that antioxidant supplementation can prevent oxidative damage, neutrophil infiltration and oedema following an acute bout of contractile-induced claudication.
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PMID:Antioxidants attenuate oxidative damage in rat skeletal muscle during mild ischaemia. 1822 25