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 is the pathological form of xanthine oxidoreductase, which generates free oxygen radicals, when it converts (hypo)xanthine to urate. We studied 1. developmental changes in rat heart, 2. urate production in catheterized patients, and 3. species differences of cardiac xanthine oxidase. First, we measured the activity of the enzyme at various ages. In rat-heart homogenate, xanthine oxidoreductase increased from 0.5 mU/g (newborn) to 25 mU/g (15 weeks, P less than 0.001). In the second part of the study, we demonstrated that patients undergoing coronary angioplasty showed some cardiac urate production. In the last part of our investigations we showed that in explanted human hearts perfused with hypoxanthine, the enzymatic activity was low, contrasting findings in some other species. The apparent xanthine oxidoreductase activity (mU/g) was: 33 (mouse), 28 (rat), 14 (guinea pig), 0.59 (rabbit), less than 0.1 (pig), 0.31 (man) and 3.7 (cow). We conclude that in several species, cardiac damage due to xanthine oxidase cannot be excluded; however in man it is unlikely to occur.
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PMID:Does xanthine oxidase cause damage during myocardial ischemia? 202 65

A study has been made of counteracting the stress organ injury in Plasmodium infection by means of antioxidants on the premise that free radicals are responsible for causing the injury to stress organs. This was evidenced by drastically altered biochemical parameters in liver and spleen of the host in terms of elevated levels of lipid peroxides and xanthine oxidase (XO) activity, and a fall in superoxide dismutase activity coupled with other drastic biochemical changes. The cardinal factor responsible for the above was considered to be XO which engenders free radicals purportedly responsible for the stress organ (biochemical) injury. Results demonstrate a lowering of lipid peroxide levels, xanthine oxidase activity, liver weight and modulation of protein level in liver of the host (mouse) in Plasmodium infection when treated with catechin, glutathione and propylgallate.
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PMID:The antioxidants as protectors of host stress organ injury in mice infected with Plasmodium berghei. 269 64

Oxypurines (hypoxanthine + xanthine, HX) were measured polarographically in the mixed umbilical cord blood plasma, the maternal venous blood plasma and in the anterior amniotic fluid of 104 deliveries. The HX increase was found in groups with clinical signs of perinatal hypoxia. The HX concentration in the mixed umbilical plasma above 15 umol/l (i.e., means +/- 2 S.D.) should be considered as pathological. The following results of experiments on animals suggested a possible pathogenic significance of xanthine oxidase (XOD) reaction on hypoxic injury: The higher the plasma XOD activity of different species (guinea pig, hamster, rat, mouse) the shorter was the survival time of the species in the interrupted hypoxia. Administration of hypoxanthine decreased the survival time of rats in the interrupted hypoxia, while the administration of allopurinol increased it. Allopurinol suppressed the post-hypoxic autoimmune response of the rats to brain tissue.
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PMID:Hypoxanthine in diagnosis, prognosis and pathogeny of hypoxic injury. 273 Jun 7

Male C57Bl/10 mice were chronically fed hexachlorobenzene (HCB) (0.02% of the diet) alone or in combination with a single subcutaneous dose of iron (12.5 mg iron per mouse). After eight weeks the group of mice pretreated with the iron overload was highly sensitized to the porphyrogenic effect of HCB, as shown by liver porphyrin accumulation. A synergistic effect of iron was evident on other parameters too, such as HCB-induced hepatic damage, activation of type O of xanthine oxidase, and decreased activity of copper zinc superoxide dismutase and glutathione peroxidase(s). None of these parameters was affected by iron alone. Iron alone and in association with HCB markedly raised the level of lipid peroxides, the increase in the HCB group being smaller. The combined treatment resulted in a significant reduction of HCB's inductive effects on microsomal heme and cytochromes P-450 and b5 and on the activity of aryl hydrocarbon hydroxylase. The content of nonprotein sulfhydryl groups was reduced to the same extent in mice treated with HCB or HCB plus iron. The results suggest that reactive intermediates such as are formed by lipid peroxidation are not sufficient on their own to create the conditions for uroporphyrinogen decarboxylase impairment, as evident in the group of mice receiving iron overload alone. Conversely, HCB administration induced a specific condition of imbalance in the liver between formation and inactivation of reactive intermediates which was associated with hepatic porphyrin accumulation and was potentiated by concomitant administration of iron.
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PMID:Investigations on the role of free radical processes in hexachlorobenzene-induced porphyria in mice. 323 39