Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.17.3.2 (xanthine oxidase)
8,383 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 role of endogenous nitric oxide (NO) in modulating myocardial contractility is still unclear, in part because of unknown, secondary effects of blocking NO release. We hypothesized that the nonspecific inhibition of nitric oxide synthase (NOS) enhances endothelin-1 (ET-1) effects, which can play a role in ET-A receptor-dependent myocardial contractile responses. The myocardial contractility was estimated from the slope of the left ventricular end-systolic pressure-diameter relationship in closed-chest, pentobarbital-anesthetized dogs. Group 1 (n = 7) was the saline-treated control, while in groups 2 (n = 7) and 3 (n = 7) N-nitro-l-arginine (NNA, 4 mg kg(-1)), a nonselective NOS blocker, was administered with or without pretreatment with the ET-A receptor antagonist ETR-P1/fl peptide (100 nmol kg(-1) iv). Plasma ET-1, nitrite/nitrate (NO(x)) and blood superoxide levels were measured, and myocardial ET-1 content and xanthine oxidoreductase (XOR) activity were determined from myocardial biopsies. The infusion of NNA over 120 min decreased the plasma NO(x), significantly elevated the plasma ET-1 and blood superoxide levels, and in parallel greatly increased the left ventricular contractility as compared with the untreated controls [47.5 vs 30 mm Hg mm(-1)]. The myocardial ET-1 content decreased simultaneously, while the XOR activity and blood superoxide level were significantly elevated. These effects, including NNA-induced positive inotropy, were significantly suppressed by pretreatment with ETR-P1/fl peptide. These results demonstrate that a diminished NO synthesis leads to a preponderant ET-1 effect, which increases myocardial contractility through an ET-A receptor-dependent mechanism.
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PMID:Nonspecific inhibition of nitric oxide synthesis evokes endothelin-dependent increases in myocardial contractility. 1973 35

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

This study investigated the effect of astaxanthin (ASX; 3,3-dihydroxybeta, beta-carotene-4,4-dione), a water-dispersible synthetic carotenoid, on liver ischemia-reperfusion (IR) injury. Astaxanthin (5 mg/kg/day) or olive oil was administered to rats via intragastric intubation for 14 consecutive days before the induction of hepatic IR. On the 15th day, blood vessels supplying the median and left lateral hepatic lobes were occluded with an arterial clamp for 60 min, followed by 60 min reperfusion. At the end of the experimental period, blood samples were obtained from the right ventricule to determine plasma alanine aminotransferase (ALT) and xanthine oxidase (XO) activities and animals were sacrificed to obtain samples of nonischemic and postischemic liver tissue. The effects of ASX on IR injury were evaluated by assessing hepatic ultrastructure via transmission electron microscopy and by histopathological scoring. Hepatic conversion of xanthine dehygrogenase (XDH) to XO, total GSH and protein carbonyl levels were also measured as markers of oxidative stress. Expression of NOS2 was determined by immunohistochemistry and Western blot analysis while nitrate/nitrite levels were measured via spectral analysis. Total histopathological scoring of cellular damage was significantly decreased in hepatic IR injury following ASX treatment. Electron microscopy of postischemic tissue demonstrated parenchymal cell damage, swelling of mitochondria, disarrangement of rough endoplasmatic reticulum which was also partially reduced by ASX treatment. Astaxanthine treatment significantly decreased hepatic conversion of XDH to XO and tissue protein carbonyl levels following IR injury. The current results suggest that the mechanisms of action by which ASX reduces IR damage may include antioxidant protection against oxidative injury.
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PMID:Effect of astaxanthin on hepatocellular injury following ischemia/reperfusion. 1990 May

At sufficiently low oxygen concentrations, hemeproteins are deoxygenated and become capable of reducing nitrite to nitric oxide (NO), in a reversal of the reaction in which NO is converted to nitrate or nitrite by oxygenated hemeproteins. The maximum rates of NO production depend on the oxygen avidity. The hemeproteins with the highest avidity, such as hexacoordinate hemoglobins, retain oxygen even under anoxic conditions resulting in their being extremely effective NO scavengers but essentially incapable of producing NO. Deoxyhemeprotein-related NO production can be observed in mitochondria (at the levels of cytochrome c oxidase, cytochrome c, complex III and possibly other sites), in plasma membrane, cytosol, endoplasmic reticulum and peroxisomes. In mitochondria, the use of nitrite as an alternative electron acceptor can contribute to a limited rate of ATP synthesis. Non-heme metal-containing proteins such as nitrate reductase and xanthine oxidase can also be involved in NO production. This will result in a strong anoxic redox flux of nitrogen through the hemoglobin-NO cycle involving nitrate reductase, nitrite: NO reductase, and NO dioxygenase. In normoxic conditions, NO is produced in very low quantities, mainly for signaling purposes and this nitrogen cycling is inoperative.
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PMID:Anoxic nitric oxide cycling in plants: participating reactions and possible mechanisms. 1992 98

In this study, we examined the protective effects of vitamin E (VE) against gastric mucosal lesions induced by water immersion restraint stress (WIRS) in rats in comparison with that of vitamin C (VC). The gastric mucosa of rats with 6 h of WIRS showed lesions with bleeding, decrease in nonprotein SH, VC, VE, and adherent mucus concentrations and constitutive nitric oxide synthase activity, and increase in lipid peroxide and NOx (nitrite/nitrate) concentrations and myeloperoxidase, xanthine oxidase, and inducible nitric oxide synthase activities. Either VE (0.05 or 0.5 mmol/kg) or VC (0.5 or 1.5 mmol/kg) was orally administered to rats with 6 h of WIRS just before the onset of the stress. Both doses of pre-administered VE prevented gastric mucosal lesion development and attenuated all these changes in gastric mucosal components and enzymes studied, whereas only the higher dose of pre-administered VC suppressed the changes in all parameters studied. These results indicate that orally administered VE protects against WIRS-induced gastric mucosal lesions in rats more effectively than orally administered VC. These results also suggest that the administered VE protects against gastric mucosal lesions in rats with WIRS through its antioxidant and anti-inflammatory actions in the gastric mucosa in the same way as the administered VC.
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PMID:Vitamin E protects against stress-induced gastric mucosal lesions in rats more effectively than vitamin C. 2009 2

The present study investigated the modulatory role of phenolic extract of soybean (PESB) in a rat model of nephrotoxic acute renal failure induced by cisplatin. Cisplatin (2 mg/kg/day) was administered to the rats for 5 days and the animals were pretreated with PESB (250-1000 mg/kg). Blood urea nitrogen reduced by 49.8% and 59.0%, serum creatinine by 34.7% and 62.1% and urinary N-acetyl-beta-D-glucosaminidase also decreased by 37.7% and 49.2% following treatment with 250- and 500-mg/kg doses of the extract respectively in the cisplatin-treated rats. The extract also significantly increased renal myeloperoxidase activity by 26.8% and 40.6% at these doses. PESB also decreased renal xanthine oxidase activity and serum nitrate/nitrite in the cisplatin-treated rats. In addition, PESB significantly attenuated the marked renal oxidative damage that accompanied cisplatin treatment. The extract improved liver histology and significantly increased the activities of the antioxidant enzymes measured [superoxide dismutase, catalase, glutathione-S-transferase], prevented glutathione depletion and decreased malondialdehyde level following cisplatin treatment. Furthermore, cisplatin-induced decrease in the activities of glucose-6-phosphatase and 5'-nucleotidase in these rats was attenuated only at 250 mg/kg dose of the extract. We concluded therefore that PESB via antioxidant and possibly anti-inflammatory actions offered protective benefit against cisplatin-mediated acute toxic injury to the kidney.
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PMID:Phenolic extract of soybean (Glycine max) attenuates cisplatin-induced nephrotoxicity in rats. 2010 12

The nitrate-nitrite-NO pathway is emerging as an alternative to the l-arginine/NO-synthase pathway for the generation of NO in mammals. Bioactivation of the stable nitrate anion involves initial reduction to nitrite by commensal bacteria in the gastrointestinal tract. Nitrite is then further metabolized in blood and tissues to form nitric oxide (NO) and other bioactive nitrogen oxides. In addition to nitrate reduction by bacteria, a functional mammalian nitrate reductase activity was recently explored. It was demonstrated that xanthine oxidoreductase (XOR) and possibly other enzymes can catalyze nitrate reduction under normoxic conditions in vivo. In the present study, we compared nitrate reduction in germ free (GF) and conventional mice. One aim was to see if the complete lack of bacterial nitrate reduction in the GF mice would be associated with an upregulation of mammalian nitrate reductase activity. Sodium nitrate (NaNO(3)) or placebo (NaCl) was injected intraperitoneally and blood and tissues were collected 1.5-2h later for measurements of nitrate and nitrite and in some cases analyses of protein expression. Tissue and plasma levels of nitrate increased to a similar extent in conventional and GF animals after nitrate administration. Plasma nitrite was 3-fold higher in GF mice receiving nitrate compared to placebo while this effect of nitrate was absent in the conventional mice. In GF mice pretreated with the xanthine oxidase inhibitor allopurinol the increase in nitrite was attenuated. The levels of nitrite in the liver and small intestine increased after the nitrate load in GF mice but not in the conventional mice. Anaerobic nitrate reduction to nitrite in intestinal tissue homogenates was also accelerated in GF mice. Studies of tissue protein levels revealed increased expression of XOR in the livers of GF animals. We conclude that XOR expression in tissues is enhanced in germ free mice and this may explain the apparently greater tissue nitrate reductase activity observed in these animals. Future studies will reveal if this represents a compensatory functional response to uphold nitrite homeostasis in the absence of commensal bacteria.
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PMID:Enhanced xanthine oxidoreductase expression and tissue nitrate reduction in germ free mice. 2014 47


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