Search results for "OXIDASE"

showing 10 items of 927 documents

Up-and-Coming Markers: Myeloperoxidase, a Novel Biomarker Test for Heart Failure and Acute Coronary Syndrome Application?

2008

Myeloperoxidase (MPO) is a mammalian enzyme responsible for generation of hypochlorite. The advantage of myeloperoxidase for use as a biomarker in the setting of heart failure and acute coronary syndrome is the early increase of MPO concentration in response to the acute event. In the setting of heart failure the reported independency of coronary artery disease and general inflammation, as indicated by MPO concentration in comparison to other inflammatory markers or in subgroups of patients with ischemic and non-ischemic cardiomyopathy, has to be highlighted. In terms of ACS, inclusion of MPO into a multiple marker strategy might add to enhance diagnosis and therapy decision making. Therefo…

medicine.medical_specialtyAcute coronary syndromeanimal diseasesCardiomyopathyInflammationDiseaseEmergency NursingDiagnosis DifferentialCoronary artery diseaseInternal medicinemedicineHumansAcute Coronary SyndromePeroxidaseHeart Failurebiologybusiness.industrymedicine.diseaseMyeloperoxidaseHeart failurebiology.proteinCardiologyEmergency MedicineBiomarker (medicine)medicine.symptombusinessCardiology and Cardiovascular MedicineBiomarkersCongestive Heart Failure
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Topical application of the adenosine A2Areceptor agonist CGS-21680 prevents phorbol-induced epidermal hyperplasia and inflammation in mice

2014

The nucleoside adenosine is a known regulator of immunity and inflammation that mediates, at least in part, the anti-inflammatory effect of methotrexate, an immunosuppressive agent widely used to treat autoimmune inflammatory diseases. Adenosine A2A receptors play a key role in the inhibition of the inflammatory process besides promoting wound healing. Therefore, we aimed to determine the topical effect of a selective agonist, CGS-21680, on a murine model of skin hyperplasia with a marked inflammatory component. Pretreatment with either CGS-21680 (5 μg per site) or the reference agent dexamethasone (200 μg/site) prevented the epidermal hyperplasia and inflammatory response induced by topica…

medicine.medical_specialtyAdenosineAdenosine A2 Receptor AgonistsAdministration Topicalmedicine.medical_treatmentAnti-Inflammatory AgentsAdenosine A2A receptorInflammationDermatologyPharmacologyBiologySkin DiseasesBiochemistryDexamethasoneMicechemistry.chemical_compoundInternal medicinePhenethylaminesmedicineAnimalsMolecular BiologyDexamethasoneCell ProliferationPeroxidaseCGS-21680InflammationHyperplasiaAdenosineAdenosine receptorDisease Models AnimalEndocrinologyCytokinechemistryCytokinesTetradecanoylphorbol AcetateFemaleCollagenEpidermismedicine.symptomWound healingmedicine.drugExperimental Dermatology
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Anti-gout drugs as potential therapy for atrial fibrillation.

2014

Atrial fibrillation (AF) is an important cardiovascular disease in theelderly [1]. Noticeably, it has been increasingly demonstrated thatserum uric acid (UA) is associated with AF [2–9]. In a recent meta-analysis performed by Tamariz and coworkers, the authors concludedthat high levels of UA and AF are clearly associated [10]. Interestingly,serum UA has been linked to AF in obstructive sleep apnea patients[11], whereas it has been also associated with thromboembolic risk inpatients with nonvalvular AF [12].The treatment of gout, a metabolic disorder caused by chronic hyper-uricemia, is based on administration of colchicine, xanthine oxidase (XO)competitive inhibitors such as allopurinol, and…

medicine.medical_specialtyAnti-gout; atrial fibrillation; allopurinolAllopurinolSaludallopurinolGout Suppressantschemistry.chemical_compoundInternal medicineAtrial FibrillationMedicineColchicineHumansEducación físicaXanthine oxidaseCondición físicabusiness.industryMetabolic disorderAtrial fibrillationmedicine.diseaseEjercicio físicoGoutBlood pressurechemistryAnesthesiaAnti-goutCardiologyUric acidCardiology and Cardiovascular Medicinebusinessmedicine.drugInternational journal of cardiology
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Exercise as a Model to Study Oxidative Stress

2011

Physical exercise generates free radicals. The major source of radicals in exercise appears to be extracellular. Our experiments show that xanthine oxidase is a key player in the generation of superoxide during exercise. Mitochondrial contribution appears to be less important: during high oxygen utilization by mitochondria in state 3, the proportion of oxygen that is converted to superoxide is on an order of magnitude lower than in resting, state 4 conditions. Exercise-induced radicals constitute a double-edged sword: high intensity ­exercise causes the generation of relatively high concentrations of radicals that cause oxidative stress and eventually damage. On the other hand, low intensit…

medicine.medical_specialtyAntioxidantChemistrySuperoxideRadicalmedicine.medical_treatmentPhysical exerciseMitochondrionmedicine.disease_causechemistry.chemical_compoundEndocrinologyInternal medicinemedicineExtracellularXanthine oxidaseOxidative stress
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The Activation Pattern of the Antioxidant Enzymes in the Right Ventricle of Rat in Response to Pressure Overload is of Heart Failure Type

2003

In the left ventricle subjected to pressure overload activity, the antioxidant enzymes increased at the hyperfunctional stage. During the transition to heart failure, these enzymes are down-regulated, oxidative stress increases, and apoptosis progresses. Maladaptative activation of the antioxidant enzymes at an early stage may contribute to the intrinsic vulnerability of right ventricle to pressure overload. The authors studied changes in expression and activity of the enzymes manganese and copper-zinc superoxide dismutases, glutathione peroxidase, and catalase in the right ventricle of rat following induction of pulmonary hypertension by injection of monocrotaline. Increase in the manganes…

medicine.medical_specialtyAntioxidantHeart Ventriclesmedicine.medical_treatmentmedicine.disease_causeAntioxidantsSuperoxide dismutaseInternal medicinePressuremedicineAnimalsRats WistarHeart Failurechemistry.chemical_classificationPressure overloadGlutathione PeroxidaseBase SequenceHypertrophy Right VentricularbiologySequence Analysis RNASuperoxide Dismutasebusiness.industryGlutathione peroxidaseCatalasemedicine.diseasePulmonary hypertensionRatsOxidative Stressmedicine.anatomical_structureEndocrinologychemistryVentricleHeart failureModels Animalbiology.proteinCardiologyReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessOxidative stressHeart Disease
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Janus-faced role of endothelial NO synthase in vascular disease: uncoupling of oxygen reduction from NO synthesis and its pharmacological reversal

2006

Endothelial NO synthase (eNOS) is the predominant enzyme responsible for vascular NO synthesis. A functional eNOS transfers electrons from NADPH to its heme center, where L-arginine is oxidized to L-citrulline and NO. Common conditions predisposing to atherosclerosis, such as hypertension, hypercholesterolemia, diabetes mellitus and smoking, are associated with enhanced production of reactive oxygen species (ROS) and reduced amounts of bioactive NO in the vessel wall. NADPH oxidases represent major sources of ROS in cardiovascular pathophysiology. NADPH oxidase-derived superoxide avidly interacts with eNOS-derived NO to form peroxynitrite (ONOO(-)), which oxidizes the essential NOS cofactor…

medicine.medical_specialtyAntioxidantNitric Oxide Synthase Type IIImedicine.medical_treatmentClinical BiochemistryNitric Oxidemedicine.disease_causeBiochemistrychemistry.chemical_compoundEnosInternal medicinemedicineAnimalsHumansVascular DiseasesEnzyme InhibitorsMolecular BiologyHemeJanus Kinaseschemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxidebiology.organism_classificationOxygenEndocrinologychemistrybiology.proteinPeroxynitriteOxidative stressBiological Chemistry
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Effect of a Diet Supplemented with alpha-Tocopherol and beta-Carotene on ATP and Antioxidant Levels after Hepatic Ischemia-Reperfusion.

2008

Ischemia-reperfusion injury associated with liver transplantation remains a serious complication in clinical practice. In the present study the effect of intake of alpha-tocopherol or beta-carotene to limit liver injury by oxidative stress in ischemia and reperfusion was explored. Wistar rats were fed with diets enriched with alpha-tocopherol (20 mg/day) or beta-carotene (3 mg/day) for 21 days. After 21 days, their livers were subjected to 15 and 30 min of ischemia and afterwards were reperfused for 60 min. The recovery of levels of ATP during reperfusion was better in the group of rats whose diets were supplemented with alpha-tocopherol or beta-carotene than in the group control. The suppl…

medicine.medical_specialtyAntioxidantmedicine.medical_treatmentClinical BiochemistryIschemiaMedicine (miscellaneous)medicine.disease_causeSuperoxide dismutasechemistry.chemical_compoundInternal medicineβ-carotenemedicineGSHoxidative stresschemistry.chemical_classificationLiver injuryNutrition and Dieteticsα-tocopherolbiologybusiness.industryGlutathione peroxidaseGlutathionemedicine.diseaseischemia/reperfusionEndocrinologychemistryBiochemistrybiology.proteinOriginal ArticlebusinessReperfusion injuryOxidative stressJournal of clinical biochemistry and nutrition
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Redox modulation of mitochondriogenesis in exercise. Does antioxidant supplementation blunt the benefits of exercise training?

2015

Physical exercise increases the cellular production of reactive oxygen species (ROS) in muscle, liver, and other organs. This is unlikely due to increased mitochondrial production but rather to extramitochondrial sources such as NADPH oxidase or xanthine oxidase. We have reported a xanthine oxidase-mediated increase in ROS production in many experimental models from isolated cells to humans. Originally, ROS were considered as detrimental and thus as a likely cause of cell damage associated with exhaustion. In the past decade, evidence showing that ROS act as signals has been gathered and thus the idea that antioxidant supplementation in exercise is always recommendable has proved incorrect.…

medicine.medical_specialtyAntioxidantmedicine.medical_treatmentPhysical exerciseBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMuscle SkeletalXanthine oxidaseExercisechemistry.chemical_classificationReactive oxygen speciesOrganelle BiogenesisNADPH oxidasebiologyMuscle adaptationGlutathione peroxidaseAdaptation PhysiologicalMitochondria MuscleOxidative StressEndocrinologychemistryDietary Supplementsbiology.proteinOxidation-ReductionFree Radical Biology and Medicine
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Oxidative stress in vascular disease and its pharmacological prevention

2013

Cardiovascular risk factors lead to enhanced production of reactive oxygen species (ROS) generated by NADPH oxidase, xanthine oxidase (XO), the mitochondrial electron-transport chain (ETC), and dysfunctional endothelial nitric oxide synthase (eNOS). When the capacity of antioxidant defense systems [e.g., superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx), heme oxygenase (HO), paraoxonase (PON)] is exceeded, this results in oxidative stress, which can promote atherogenesis. Therefore, pharmacological means to prevent oxidative stress are of major therapeutic interest. Some established drugs and novel therapeutic approaches can prevent oxidative stress and, presumably, vascula…

medicine.medical_specialtyAntioxidantmedicine.medical_treatmentToxicologymedicine.disease_causeAntioxidantsSuperoxide dismutasechemistry.chemical_compoundInternal medicinemedicineAnimalsHumansVascular DiseasesXanthine oxidasePharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyGlutathione peroxidaseHeme oxygenaseOxidative StressEndocrinologychemistrybiology.proteinOxidative stressTrends in Pharmacological Sciences
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Chelation of synaptic zinc induces overexcitation in the hilar mossy cells of the rat hippocampus.

2004

Complete removal of synaptic zinc by the chelator dietyldithiocarbamate (DEDTC; 500 mg/kg i.p.) in rat was followed by convulsive behaviour including wet dog shakes alternating immobility. Histological analysis 1 day after DEDTC administration detected expression of heat shock protein in the hippocampus restricted to hilar cells. These cells colocalize the marker for neurons and the glutamate receptor GluR2/3 showing that they are excitatory neurons. Additionally, they projected to the contralateral dentate gyrus. Therefore, they correspond to hilar mossy cells. These data show that the synaptic zinc has a role in normal hippocampus avoiding overexcitation, that would impair functionality e…

medicine.medical_specialtyCentral nervous systemPresynaptic TerminalsWheat Germ Agglutinin-Horseradish Peroxidase ConjugateHippocampusAction PotentialsHSP72 Heat-Shock Proteinsc-FosHippocampusSynaptic TransmissionSeizuresInternal medicineNeural PathwaysmedicineAnimalsReceptors AMPAHeat-Shock ProteinsChelating AgentsbiologyGeneral NeuroscienceDentate gyrusGlutamate receptorColocalizationImmunohistochemistryRatsZincEndocrinologymedicine.anatomical_structurenervous systemDentate GyrusMossy Fibers Hippocampalbiology.proteinExcitatory postsynaptic potentialDitiocarbImmediate early geneProto-Oncogene Proteins c-fosNeuroscience letters
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