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)

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

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

Membrane injury facilitated the fixation of calcium oxalate crystals and subsequent growth into kidney stones. Oxalate-induced membrane injury was mediated by lipid peroxidation reaction through the generation of oxygen free radicals. In urolithic rat kidney or oxalate exposed cultured cells, both superoxide anion and hydroxyl radicals were generated in excess, causing cellular injury. In hyperoxaluric rat kidney, both superoxide and H2O2-generating enzymes such as glycolic acid oxidase (GAO) and xanthine oxidase (XO) were increased, and hydroxyl radical and transition metal ions, iron, and copper were accumulated. The lipid peroxidation products, thiobarbituric acid-reactive substances (TBARS), hydroperoxides, and diene conjugates were excessively released in tissues of urolithic rats and in plasma of rats as well as stone patients. The accumulation of these products was concomitant with the decrease in the antioxidant enzymes, superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), and glucose-6 phosphate dehydrogenase (G6PD) as well as radical scavengers, vitamin E, ascorbic acid, reduced glutathione (GSH), and protein thiol. All the above parameters were decreased in urolithic condition, irrespective of the agents used for the induction of urolithiasis. Oxalate binding activity and calcium oxalate crystal deposition were markedly pronounced, along with decreased adenosine triphosphatase (ATPase) activity. Lipid peroxidation positively correlated with cellular oxalate, oxalate binding, gamma-glutamyl carboxylase, and calcium level and negatively correlated with GSH, vitamin E. ascorbic acid, and total protein thiol. Antioxidant therapy to urolithic rats with vitamin E, glutathione monoester, methionine, lipoic acid, or fish oil normalised the cellular antioxidant system, enzymes and scavengers, and interrupted membrane lipid and protein peroxidation reaction, ATPase inactivation, and its associated calcium accumulation. Antioxidant therapy prevented calcium oxalate precipitation in the rat kidney and reduced oxalate excretion in stone patients. Similarly, calcium oxalate crystal deposition in vitro to urothelium was prevented by free radical scavengers such as phytic acid and mannitol by protecting the membrane from free radical-mediated damage. All these observations were suggestive of the active involvement of free radical-mediated lipid peroxidation-induced membrane damage in the pathogenesis of calcium oxalate crystal deposition and retention.
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PMID:Calcium oxalate stone disease: role of lipid peroxidation and antioxidants. 1194 24

Exhaustive exercise is a generator of free radicals and reactive species in mammals. Allopurinol is a known inhibitor of xanthine oxidase, a source of free radicals during exercise. In this study, the influence of allopurinol on the metabolic profile of blood plasma of rats that had undergone exhaustive swimming was investigated by GC-MS. Rats were divided into four groups: (i) placebo administration, no exercise; (ii) placebo administration followed by exercise until exhaustion; (iii) allopurinol administration, no exercise; and (iv) allopurinol administration followed by exercise until exhaustion. Samples obtained following the aforementioned treatments were analyzed on GC-MS after two-step derivatization (methoxymation and silylation). GC-MS analysis in full scan acquisition achieved the quantitation of 86 metabolites in 45min. GC-MS data were analyzed using univariate and multivariate statistical analysis methods. Safe classification/prediction of the samples was accomplished according to exercise and allopurinol administration. Separation of the study groups according to exercise was mainly due to lactic acid, pyruvic acid, 2-hydroxybutyric acid, uracil, oxalic acid, pyroglutamic acid and stearic acid (p<0.05). Separation according to allopurinol administration was mainly due to compounds of the purine catabolic pathway and amino acids. Allopurinol administration was not found to modulate the metabolic responses to exercise.
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PMID:GC-MS analysis of blood for the metabonomic investigation of the effects of physical exercise and allopurinol administration on rats. 2461 30