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)

Free radical generation, including reactive nitrogen and reactive oxygen species, is known to participate in cell physiology in both a positive and negative manner. Moreover, alterations in their concentrations are implicated in a number of renal diseases. However, there is evidence that high concentration of nitric oxide (NO) occurring as a result of iNOS induction and peroxynitrite formation, is capable of causing lipid peroxidation and protein oxidation in cyclosporine A (CsA) induced cellular damage. The present study was conducted to investigate the possible protective role of Lipoic acid (LA) in nitric oxide mediated cellular abnormalities induced by CsA in rat kidney. Adult male albino rats of Wistar strain were given CsA at a dose of 25 mg/kg body weight, orally for 21 days. An extensive elevation in the activities of xanthine oxidase was noted in the renal tissue of the CsA administered rats. These changes were associated with significant increase in the levels of plasma lipid peroxidation with high protein carbonyl contents and 3-nitrotyrosine formation coupled with diminished protein thiols. In addition, plasma nitrite/nitrate (NO(x)), RT-PCR for inducible NOS (iNOS) mRNA, and immunohistochemically demonstrable iNOS protein were evaluated to assess peroxidative damage. Concomitant treatment with LA (20 mg/kg body weight, orally for 21 days showed that the oxidative stress alteration were significantly decreased in CsA treated renal tissue. While the expression of iNOS and the amounts of NO(x) were decreased simultaneously. These results indicate that the antioxidant LA might have a protective effect against CsA-induced peroxidative changes and cellular damage of the renal tissue of the rat.
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PMID:Protective effect of lipoic acid on oxidative and peroxidative damage in cyclosporine A-induced renal toxicity. 1776 48

Reduction of nitrite to nitric oxide during ischemia protects the heart against injury from ischemia/reperfusion. However the optimal dose of nitrite and the mechanisms underlying nitrite-induced cardioprotection are not known. We determined the ability of nitrite and nitrate to confer protection against myocardial infarction in two rat models of ischemia/reperfusion injury and the role of xanthine oxidoreductase, NADPH oxidase, nitric oxide synthase and K(ATP) channels in mediating nitrite-induced cardioprotection. In vivo and in vitro rat models of myocardial ischemia/reperfusion injury were used to cause infarction. Hearts (n=6/group) were treated with nitrite or nitrate for 15 min prior to 30 min regional ischemia and 180 min reperfusion. Xanthine oxidoreductase activity was measured after 15 min aerobic perfusion and 30 min ischemia. Nitrite reduced myocardial necrosis and decline in ventricular function following ischemia/reperfusion in the intact and isolated rat heart in a dose- or concentration-dependent manner with an optimal dose of 4 mg/kg in vivo and concentration of 10 microM in vitro. Nitrate had no effect on protection. Reduction in infarction by nitrite was abolished by the inhibition of flavoprotein reductases and the molybdenum site of xanthine oxidoreductase and was associated with an increase in activity of xanthine dehydrogenase and xanthine oxidase during ischemia. Inhibition of nitric oxide synthase had no effect on nitrite-induced cardioprotection. Inhibition of NADPH oxidase and K(ATP) channels abolished nitrite-induced cardioprotection. Nitrite but not nitrate protects against infarction by a mechanism involving xanthine oxidoreductase, NADPH oxidase and K(ATP) channels.
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PMID:Nitrite confers protection against myocardial infarction: role of xanthine oxidoreductase, NADPH oxidase and K(ATP) channels. 1776 19

This work reports on the direct electrochemistry of the xanthine oxidase (XO) from buttermilk, a mononuclear molybdenum enzyme that comprises four redox active cofactors: a five-coordinate mononuclear Mo ion, two [2Fe-2S] clusters, and a flavin adenine dinucleotide (FAD) group. The Mo, [2Fe-2S] and FAD redox responses are obtained from the enzyme immobilized on an activated single-wall carbon nanotubes (SWNTs) modified glassy carbon electrode using protein film voltammetry. The formal potentials of which are -0.61 V, -0.47 V and -0.37 V (vs. SCE) at pH 5.0, respectively. Upon addition of nitrate to the electrochemical cell, a steady-state voltammogram and i-t amprometric response were observed, indicating XO can catalyze the reduction of nitrate.
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PMID:Direct electron transfer of xanthine oxidase and its catalytic reduction to nitrate. 1793 2

Sesbania grandiflora, commonly known as "sesbania" and "agathi," is widely used in Indian traditional medicine for the treatment of a broad spectrum of diseases. In the present study, we evaluated the possible protective effect of an aqueous suspension of S. grandiflora (ASSG) leaves against cigarette smoke-induced oxidative damage in rats. Adult Wistar-Kyoto rats were exposed to cigarette smoke for a period of 90 days and treated with ASSG (1,000 mg/kg of body weight/day, p.o) for a period of 3 weeks. The levels of protein carbonyl and activities of cytochrome P450, NADPH oxidase, and xanthine oxidase were significantly increased, whereas the levels of total thiol, protein thiol, non-protein thiol, nucleic acids, and tissue protein were significantly reduced in lung, liver, kidney, and heart of cigarette smoke-exposed rats as compared with control rats. Plasma nitric oxide levels, measured as nitrite plus nitrate, were significantly increased in cigarette smoke-exposed rats when compared to the control rats. The above changes were ameliorated to near control in the treatment group. These results suggest that supplementation with ASSG reversed the cigarette smoke-induced oxidative damage in rats through its antioxidant potential. These results provide further support for the traditional use of S. grandiflora in the treatment of smoke-related diseases.
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PMID:Protective effect of Sesbania grandiflora against cigarette smoke-induced oxidative damage in rats. 1859 82

Nitrite (NO(2)(-)) recycling to nitric oxide (NO) is catalysed by a number of enzymes and induces a protective vasodilation effect under hypoxia/ischaemia. In the present work, we tested the in vitro ability of the three NOS (nitric oxide synthase) isoforms to release NO from nitrite under anoxia using electrochemical detection, chemiluminescence and absorption spectroscopy. The release of free NO from anoxic nitrite solutions at 15 muM was specific to the endothelial NOS isoform (eNOS) and did not occur with the neuronal (nNOS) or inducible (iNOS) isoforms. Unlike xanthine oxidase, the eNOS reductase domain did not recycle nitrite to NO, and wild-type eNOS did not reduce nitrate. Our data suggest that structural and, by inference, dynamic differences between nNOS and eNOS in the distal haem side account for eNOS being the only isoform capable of converting nitrite into NO at pH 7.6. In human dermal microvascular endothelial cells under careful control of oxygen tension, the rates of NO formation determined by chemiluminescence were enhanced approximately 3.6- and approximately 8.3-fold under hypoxia (2 p.p.m. O(2)) and anoxia (argon) respectively compared with normoxia ( approximately 22 p.p.m. O(2)) using 10 muM extracellular nitrite. NOS inhibitors inhibited this hypoxic NO release. Our data show that eNOS is unique in that it releases NO under all oxygen levels from normoxia to complete anoxia at physiological micromolar nitrite concentrations. The magnitude of the hypoxic NO release by the endothelial cells suggest that the endothelium could provide an appropriate response to acute episodic ischaemia and may explain the observed eNOS-expression-specific protective effect as a short-term response in animal models of acute hypoxia.
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PMID:Isoform-specific differences in the nitrite reductase activity of nitric oxide synthases under hypoxia. 1904 40

In this study, we investigated whether inflammatory responses contribute to oxidative/nitrosative stress in patients with Chagas' disease. We used three tests (enzyme-linked immunosorbent assay, immuno-flow cytometry, and STAT-PAK immunochromatography) to screen human serum samples (n = 1,481) originating from Chiapas, Mexico, for Trypanosoma cruzi-specific antibodies. We identified 121 subjects who were seropositive for T. cruzi-specific antibodies, a finding indicative of an 8.5% seroprevalence in the rural population from Chiapas. Seropositive and seronegative subjects were examined for plasma levels of biomarkers of inflammation, i.e., myeloperoxidase (MPO), inducible nitric oxide synthase (iNOS), and xanthine oxidase (XOD), as well as for oxidative (advanced oxidation protein products [AOPPs]) and nitrosative (3-nitrotyrosine [3NT]) biomarkers. The seropositive subjects exhibited a significant increase in MPO activity and protein level, the indicator of neutrophil activation. Subsequently, a corresponding increase in AOPP contents, formed by MPO-dependent hypochlorous acid and chloramine formation, was noted in seropositive subjects. The plasma level of 3NT was significantly increased in seropositive subjects, yet we observed no change in XOD activity (O(2)(-) source) and nitrate/nitrite contents (denotes iNOS activation and NO production), which implied that direct peroxynitrite formation does not contribute to increased nitrosative damage in chagasic subjects. Instead, a positive correlation between increased MPO activity and protein 3NT formation was observed, which suggested to us that MPO-dependent formation of nitrylchloride that occurs in the presence of physiological NO and O(2)(-) concentrations contributes to protein nitration. Overall, our data demonstrate that T. cruzi-induced neutrophil activation is pathological and contributes to MPO-mediated collateral protein oxidative and nitrosative damage in human patients with Chagas' disease. Therapies capable of suppressing MPO activity may be useful in controlling the inflammation and oxidative/nitrosative pathology in chagasic cardiomyopathy.
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PMID:Increased myeloperoxidase activity and protein nitration are indicators of inflammation in patients with Chagas' disease. 1929 13

The immune response can be triggered by molecules derived from microorganisms (PAMP) or from molecules derived from damaged or dead host cells, known as the damage-associated molecular-pattern molecules (DAMP). Their immune effects are accompanied by altered redox environment. The level of stable end products of nitric oxide (NO)- plasma nitrate and nitrite (NOx), carbonyl groups (PCO) and nitrotyrosine (NTY), in relation to the metabolism of dsRNAs (poly I:C and poly A:U) and xanthine oxidase (XO activity), in plasma of type2 diabetic patients was determined. Thirty-six patients with type 2 diabetes (age group 34-66 years, 19 male and 17 female) were allocated to the study. Diabetic patients had a significantly higher level of plasma NOx products, NTY and PCO, fructosamine (FA) and XO activity indicating about altered redox environment. The concentration of circulating ribonucleic acids (CNAs) was significantly higher in type 2 diabetic patients, which was accompanied by a significantly decreased activity of RNase against double stranded RNA forms (poly I:C and poly A:U), compared to control samples. To determine whether CNAs, as possible DAMP molecules, are capable of exerting effect on inflammatory and host antiviral response, the effect of isolated CNAs on NF-kappaB, Bcl-2, Bax, MDA-5 and IRF-3 regulation was evaluated in culture of fresh isolated thymocytes. Circulating nucleic acids isolated from type 2 diabetic patients were able to upregulate NF-kappaB more than control RNA samples. In the same experimental conditions the mild Bcl-2 upregulation, followed by the marked Bax upregulation, was demonstrated. Since the Bcl-2/Bax ratio was lower in type 2 diabetic samples, obtained results may implicate that CNAs may exert proapoptotic response in type 2 diabetes. The CNAs isolated from diabetic patients were able to downregulate MDA-5 and IRF-3, very important subjects of the surveillance and cellular anti-viral response. The major findings of the present study are that impaired dsRNA metabolism may lead to increased level of different sized RNAs in type 2 diabetic patients. Acting as possible DAMP molecules, they may contribute to higher susceptibility of immune cells to inflammatory cascade via NF-kappaB activation, and possible MDA-5/IRF-3 axis downregulation, what may have an influence on further ineffective response against different pathogens.
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PMID:Possible impact of impaired double-stranded RNA degradation and nitrosative stress on immuno-inflammatory cascade in type 2 diabetes. 1935 92

In this work, colloidal laponite nanoparticles were further expanded into the design of the third-generation biosensor. Direct electrochemistry of the complex molybdoenzyme xanthine oxidase (XnOx) immobilized on glassy carbon electrode (GCE) by laponite nanoparticles was investigated for the first time. XnOx/laponite thin film modified electrode showed only one pair of well defined and reversible cyclic voltammetric peaks attributed to XnOx-FAD cofactor at about -0.370 V vs. SCE (pH 5). The formal potential of XnOx-FAD/FADH(2) couple varied linearly with the increase of pH in the range of 4.0-8.0 with a slope of -54.3 mV pH(-1), which indicated that two-proton transfer was accompanied with two-electron transfer in the electrochemical reaction. More interestingly, the immobilized XnOx retained its biological activity well and displayed an excellent electrocatalytic performance to both the oxidation of xanthine and the reduction of nitrate. The electrocatalytic response showed a linear dependence on the xanthine concentration ranging from 3.9 x 10(-8) to 2.1 x 10(-5)M with a detection limit of 1.0 x 10(-8)M based on S/N=3.
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PMID:Xanthine oxidase/laponite nanoparticles immobilized on glassy carbon electrode: direct electron transfer and multielectrocatalysis. 1950 Sep 69

The enzyme catalase is well-known to catalyze the disintegration of hydrogen peroxide to water and oxygen; however, this study shows that its main function in bovine milk is oxidation of nitrite to nitrate. This process depends on hydrogen peroxide, of which the main source appears to be hydrogen peroxide formation that is coupled to the conversion of purines--xanthine in the present study--to uric acid by milk xanthine oxidase. However, additional secondary sources of hydrogen peroxide appear to be important during the relatively long storage of milk in the gland cistern. This paper demonstrates that the oxidation of nitrite to nitrate is necessary to prevent accumulation of free radicals and oxidative products during storage of milk in the gland and during the unavoidable delay between milking and pasteurization in dairy plants. Recommendations for minimizing the deterioration in milk quality during commercial storage are presented.
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PMID:Hydrogen peroxide-dependent conversion of nitrite to nitrate as a crucial feature of bovine milk catalase. 1972 11

The disturbance of endothelium-dependent and endothelium-independent vascular reactions of relaxation was registered in the preparations of aorta of radiosensitive BALB/c mice, exposed to chronic external gamma-irradiation (cumulative dose of 0.43 Sv). Low doses of radiation induced an intensive hydrolysis of membrane phospholipids by phospholipase A2, displayed by an increase in the level of eukosanoisds--LTC4 and TxB2, formed under effects of lipid oxidases (lipoxygenase and cyclooxygenase) at the same time with O2 generation. High doses of O2- can also be formed under the effect of low doses of radiation along xanthine oxidase pathway simultaneously with uric acid. In these conditions *OH-radical is formed not only at the expense of water radiolysis, which is observed under the effect of high doses, as well as along the two--NO-dependent and NO-independent--pathways. Significant increase in the content of lipid peroxidation products--dienic conjugates and valonic dialdehyde--in the organs of cardiovascular system is a confirmation of active generation of *OH and *NO2 under the effect of low doses of radiation. The latter induce significant changes in the pools of NO stable metabolites, which can cause disturbance of NO-dependent physiological functions of both heart and aorta. Significant decrease in the levels of nitrite and nitrozothiols in these conditions may result in an oxidative stress. In increased simultaneous generation of *O2- and NO they may bind and thus form a toxic substance peroxynitrite. This notion can be confirmed by the low doses of nitrite, which are formed spontaneously in the presence of molecular oxygen against the background of increased or control levels of nitrate, which is formed mainly at the degradation of peroxynitrite, i.e. at high levels of superoxide anion.
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PMID:[Vascular reactivity and metabolism of the reactive oxygen species and nitrogen in effects of low doses of radiation]. 1979 69


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