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)

Feeding calculi producing diet (CPD) to rats for 4 weeks produced calcium oxaltate stones. Supplementation of sodium citrate to CPD (c-CPD) prevented stone formation. Except oxalate, the excretion of calcium, phosphorus and magnesium was restored to normal in c-CPD fed rats. The CPD fed rats exhibited increase in glycolic acid oxidase (GAO) and lactate dehydrogenase (LDH) activities and only GAO activity was partially restored in c-CPD fed rats. Kidney sub-cellular fractions of calculi producing diet (CPD) fed rats showed increased susceptibility for lipid peroxidation in presence of promotors. Antioxidant enzyme activities of superoxide dismutase (SOD), catalase and glutathione peroxidase and antioxidant concentrations of reduced glutathione, total thiols, ascorbic acid and vitamin E were significantly decreased while the xanthine oxidase activity, and concentrations of hydroxyl radical, diene conjugates and hydroperoxides were significantly increased in CPD fed rats. The susceptibility to lipid peroxidation, activities of antioxidant enzymes, and the concentration of antioxidants were not normalized by feeding citrate.
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PMID:Effect of citrate feeding on free radical induced changes in experimental urolithiasis. 145 50

The effect of the plant alkaloid ryanodine on the cardiac sarcoplasmic reticulum (SR) function, which plays a major role in the regulation of intracellular calcium and thereby in the generation of force, was studied by determining oxalate-supported calcium uptake, steady-state calcium load, calcium permeability, intravesicular-free calcium and Ca,Mg-adenosine triphosphatase (ATPase) activity of "heavy" vesicles in the presence or absence of the oxygen-free radical-generating system. In vitro generation of oxygen-free radicals by xanthine oxidase (0.09 u/ml), acting on xanthine (25 microM) as a substrate, increased the permeability of the vesicles to calcium, determined by measuring net efflux of calcium after stopping pump-mediated fluxes, and decreased oxalate-supported calcium uptake and steady-state calcium load with no effect on Ca,Mg-ATPase activity. This effect of oxygen-free radicals was inhibited completely by superoxide dismutase, which eliminated completely superoxide anion radical production and caused an anticipated increase in hydrogen peroxide from the xanthine-xanthine oxidase reaction in our system. The xanthine-xanthine oxidase reaction decreased intravesicular-free calcium. The diminished level of intravesicular-free calcium, which was reflected by the decreased steady-state calcium load induced by oxygen-free radicals, was prevented by specific closure of the SR calcium release channel by ryanodine under established optimal conditions; under the same conditions, ryanodine also prevented superoxide dismutase-inhibitable reduction of calcium uptake induced by oxygen-free radicals in the presence or absence of oxalate. Ryanodine was without effect on Ca,Mg-ATPase activity by itself and had no effect on any of the changes in calcium permeability mediated by the generation of oxygen-free radicals under the experimental conditions used.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of ryanodine on oxygen free radical-induced dysfunction of cardiac sarcoplasmic reticulum. 184 30

In this study, we attempted to elucidate the metabolic pathway and enzymes actually involved in oxalate formation from glycolate in rat and human liver. In rat liver, the formation of oxalate from glycolate appeared to take place predominantly via glyoxylate. The oxalate formation from glycolate observed with crude enzyme preparations was almost entirely accounted for by the sequential actions of glycolate oxidase and xanthine oxidase (XOD) or lactate dehydrogenase (LDH). Under the conditions used, no significant activity was attributable to glycolate dehydrogenase, an enzyme reported to catalyze the direct oxidation of glycolate to oxalate. Among the three enzymes known to catalyze the oxidation of glyoxylate to oxalate, glycolate oxidase and XOD showed much lower activities (a higher Km and lower Vmax) toward glyoxylate than those with the respective primary substrates. As to LDH, none of the LDH subunit-deficient patients examined showed profoundly lowered urinary oxalate excretion. Based on the results obtained, the presumed efficacies in vivo of individual enzymes, as catalysts of glyoxylate oxidation, and the in vivo conditions assumed to allow their catalysis of oxalate production are discussed.
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PMID:The formation of oxalate from glycolate in rat and human liver. 222 23

In a retrospective study two patient groups suffering from recurrent calcium oxalate lithiasis are compared before and after antirheumatic therapy using Diclofenac-Natrium alone or in combination with xanthine oxidase inhibitors and/or hydrochlorothiazides. The examination of concentration and excretion of lithogenic important parameters show a partly significant reduction of the concentration mean values of calcium, oxalic acid and uric acid. The influence of non-steroidal antiphlogistics (NSAP) on calculus recurrence rate in calcium oxalate lithiasis is recognized.
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PMID:[Urinary calculus protective side effects of anti-rheumatic therapy]. 237 78

The effect of superoxide radical on the azide-insensitive ATP-dependent Ca2+-transport by a plasma membrane (PM)-enriched fraction (F2) and an endoplasmic reticulum (ER)-enriched fraction (F3) isolated from pig coronary artery was examined using xanthine oxidase plus xanthine to generate superoxide ions. A preincubation with xanthine oxidase plus xanthine at 37 degrees C preferentially inactivated the oxalate-stimulated Ca2+ uptake by the F3 fraction rather than the phosphate-stimulated uptake by the F2 fraction, indicating that the Ca2+ pump in the ER was more susceptible to this free radical. The inactivation of the Ca2+ uptake depended on the concentrations of xanthine oxidase and xanthine in the preincubation mixture as well as on the preincubation time. Furthermore, the inclusion of superoxide dismutase in the preincubation mixture prevented the inactivation. Thus the inactivation was caused by superoxide radical. Preincubation with xanthine oxidase plus xanthine, however, altered the half-life of efflux of Ca2+ from these vesicles only marginally. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, the F3 fraction showed formation of a Ca2+-dependent acid stable phosphoenzyme at 0 degree C predominantly at a protein band corresponding to 100 kDa. The level of the 100-kDa acylphosphate intermediate was inhibited in parallel with the inhibition of the Ca2+ uptake by preincubation with xanthine oxidase plus xanthine. We conclude that superoxide radical inactivates the ER Ca2+ transport by lowering the level of the phosphoenzyme.
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PMID:Effect of superoxide radical on Ca2+ pumps of coronary artery. 284 93

Precipitation of calcium oxalate was studied in a group of ten patients who underwent transurethral prostatectomy with glycine irrigation. Post operatively all patients showed hyperoxaluria; 60% with oxaluria higher than 10 times the critical concentration of calcium oxalate in urine. Other factors, known to favour crystallogenesis were modified during the same period: low urinary output, relative hypercalciuria and uraturia and hypomagnesuria. Thus, conditions for intraluminal precipitation of calcium oxalate were present post operatively. We suggest the use of a xanthine oxidase inhibitor to prevent hyperoxaluria.
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PMID:Calcium oxalate precipitation in urine following T.U.R. with glycine as irrigation fluid. 367 69

Disturbances in purine metabolism with hyperuricaemia and/or hyperuricosuria are a risk factor in uric acid and Ca oxalate stone formation. By way of a competitive xanthine oxidase inhibition, the formation of uric acid is reduced by allopurinol. In investigations on two groups of patients, Milurit could be demonstrated to decrease the uric acid levels in serum and urine. No differences could be seen in the dosages of 3 x 100 mg or 1 x 300 mg Milurit. Therefore, in stone recurrence prevention, the administration of Milurit 300 is recommended.
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PMID:Prevention of recurrent uric acid and calcium oxalate stones by administration of the xanthine oxidase inhibitors Milurit 100 and Milurit 300. 668

Superoxide (O2-)-dependent lipid peroxidation on addition of xanthine oxidase (XO) and Fe(3+)-ADP was induced in egg phosphatidylcholine (PC) liposomes containing dicetylphosphate (DCP), which are negatively charged like biological membranes, but not in uncharged egg PC liposomes. Positively charged Fe(3+)-ADP interacted more with negatively charged egg PC-DCP liposomes than with uncharged egg PC liposomes. The activities of Fe(3+)-chelates for initiating O(2-)-dependent lipid peroxidation were in the order Fe(3+)-ADP > Fe(3+)-citrate > Fe(3+)-oxalate = Fe(3+)-malonate > Fe(3+)-EDTA = 0. This order was the same as that for the reduction rates of these Fe(3+)-chelates to Fe(2+)-chelates by O(2-)-generated by XO. Lineweaver-Burk plots showed that the chelators inhibited XO by different mechanisms: uncompetitively by ADP and adenosine and non-competitively by organic acid chelators (citrate and oxalate) and EDTA. These results suggest that ADP interacts with XO in a manner different from the other chelators. Lipid peroxidation by XO-xanthine and Fe(3+)-ADP was induced in egg PC liposomes containing a trace (0.31-0.35 mol%) of peroxidized egg PC (PC-OOH), but not in PC-OOH-free liposomes of egg PC obtained by their pretreatment with triphenylphosphine. PC-OOH incorporated into dimyristoyl phosphatidylcholine (DMPC) liposomes was degraded on addition of both XO-xanthine and Fe(3+)-chelate, but not of either one alone. alpha-Tocopherol in DMPC liposomes was oxidized on addition of XO-xanthine and Fe(3+)-chelates in the presence, but not in the absence of PC-OOH. Furthermore, PC-OOH was required for decrease of the ESR spectrum of the spin probe 12-(N-oxyl-4,4'-dimethyloxazolidin-2-yl)stearic acid, which labels the hydrophobic region of egg PC liposome membranes, on addition of XO-xanthine and Fe(3+)-chelates. These results indicate that the "induction message of lipid peroxidation," which is associated with reduction of Fe(3+)-ADP by O2- and concurrent degradation of PC-OOH, must be transferred from the membrane surface to the inner hydrophobic region of the membranes.
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PMID:Dynamics of xanthine oxidase- and Fe(3+)-ADP-dependent lipid peroxidation in negatively charged phospholipid vesicles. 784 Jun 82

Oxalate, the major stone-forming constituent induces lipid peroxidation during lithogenesis. In experimental condition oxalate formation was induced by the administration of its precursor glycollate. Glycollate-fed rats showed increased susceptibility to lipid peroxidation in the presence of promoters. In addition, antioxidant enzymes-catalase, superoxide dismutase and glutathione peroxidase also showed decreased activity. Reduced glutathione, total thiols and ascorbic acid were also significantly decreased. On the other hand, an increased xanthine oxidase and decreased glucose-6-phosphate dehydrogenase activity was also observed upon glycollate administration. Cysteine, a sulphydryl compound, is known to inhibit free radical toxicity in various pathologies. Cysteine administration to glycollate-fed rats brought about a significant decrease in the peroxidative level, with an increase in the antioxidant status.
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PMID:Effect of L-cysteine on lipid peroxidation in experimental urolithiatic rats. 874 47

This study aimed to evaluate whether administration of cyclosporin to hyperoxaluric rats affects liver antioxidant status, and whether pretreatment with vitamin E reverses the effect. Male Wistar rats were divided into two major groups of 40. One group was given vitamin E. Both major groups were then divided into four subgroups which received vehicle (olive oil), cyclosporin in olive oil (50 mg kg(-1)), 3% ammonium oxalate or cyclosporin + 3% ammonium oxalate for three days. The activities of liver lactate dehydrogenase, glycolic acid oxidase and xanthine oxidase, and the level of malondialdehyde, an indicator of lipid peroxidation, increased when cyclosporin was administered to hyperoxaluric rats. The levels of antioxidants ascorbic acid, vitamin E and reduced glutathione and the activities of glutathione-metabolizing enzymes were altered significantly when hyperoxaluric rats were treated with cyclosporin. All these enzymes and antioxidants showed highly significant correlation values, r. These changes were restored to near normal by pretreatment with vitamin E. These findings suggest that cyclosporin-induced hepatotoxicity is aggravated in hyperoxaluria. This was almost totally prevented by pretreatment with vitamin E.
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PMID:Effect of cyclosporin on liver antioxidants and the protective role of vitamin E in hyperoxaluria in rats. 964 43


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