Search results for "Oxide"

showing 10 items of 6424 documents

Fractional exhaled nitric oxide is associated with more severe asthma

2018

Fractional exhaled nitric oxide (FeNO) levels are used as a marker of airway inflammation. The aim of the present work was to evaluate a possible relationship between FeNO and parameters of asthma control and severity in different asthma phenotypes. FeNO was evaluated in 200 asthma patients (37% male, mean age ± SD 54±15 years, 19% controlled (GINA), 30% treated with oral corticosteroids (OCS), median FEV1 (interquartile range) 2,05 L (1,49-2,70), 74% pred. (56-90%)), together with other asthma characteristics (lung function, asthma control, allergies, serum IgE, serum ECP, and blood eosinophils). Patients with poorly controlled asthma had significantly higher FeNO values (ACQ-5≥1.5 vs. 70%…

medicine.medical_specialtyAllergybiologybusiness.industrySevere asthmaAirway inflammationrespiratory systemImmunoglobulin Emedicine.diseaseGastroenterologySerum igerespiratory tract diseases03 medical and health sciences0302 clinical medicine030228 respiratory systemInterquartile rangeInternal medicineExhaled nitric oxidemedicinebiology.protein030212 general & internal medicinebusinessAsthmaMonitoring Airway Disease
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Estradiol or genistein prevent Alzheimer's disease-associated inflammation correlating with an increase PPAR gamma expression in cultured astrocytes.

2009

Inflammation has been implicated in neurodegenerative disorders such as Alzheimer's disease (AD). The main inflammatory players in AD are the glial cells which initiate the inflammatory response. One of the earliest neuropathological changes in AD is the accumulation of astrocytes at sites of A beta deposition. It is desirable to find methods of tipping the balance towards anti-inflammatory state. Estrogenic compounds have shown anti-inflammatory and also antioxidant activity. Astrocytes were pretreated with 17-beta estradiol or with genistein, and 48 h later treated with 5 microM amyloid beta (A beta) for 24 h. We found that A beta induces inflammatory mediators, such as cyclooxygenase 2 (…

medicine.medical_specialtyAmyloid betaInterleukin-1betaGenisteinPeroxisome proliferator-activated receptorNitric Oxide Synthase Type IIInflammationEnzyme-Linked Immunosorbent Assaychemistry.chemical_compoundInternal medicinemedicineAnimalsDrug InteractionsMolecular BiologyProtein Kinase InhibitorsCells Culturedchemistry.chemical_classificationCerebral CortexAmyloid beta-PeptidesbiologyDose-Response Relationship DrugEstradiolTumor Necrosis Factor-alphaGeneral NeuroscienceInterleukinEstrogensGenisteinPeptide FragmentsRatsPPAR gammaEndocrinologymedicine.anatomical_structurechemistryGene Expression RegulationCyclooxygenase 2Astrocytesbiology.proteinNeurogliaTumor necrosis factor alphaNeurology (clinical)medicine.symptomDevelopmental BiologyAstrocyteBrain research
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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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Oxidative stress and endothelial dysfunction: therapeutic implications.

2011

In a previous issue of Annals of Medicine, we presented evidence in support of the concept that an abnormally increased production of reactive oxygen species plays a central role in the genesis and progression of cardiovascular disease. While a number of preclinical lines of evidence support this concept, and despite the results of many studies suggesting a beneficial impact of antioxidant drugs on endothelial function, large clinical trials have failed to demonstrate a benefit of antioxidants on cardiovascular outcomes. Studies exploring the possibility that classical antioxidants such as vitamin C, vitamin E, selenium, or folic acid may improve the prognosis of patients with cardiac disea…

medicine.medical_specialtyAntioxidantEndotheliummedicine.medical_treatmentAdrenergic beta-AntagonistsAngiotensin-Converting Enzyme InhibitorsDiseaseBioinformaticsmedicine.disease_causeNitric OxideAntioxidantsInternal medicinemedicineHumansEndothelial dysfunctionVitamin Cbusiness.industryVitamin EGeneral Medicinemedicine.diseaseClinical trialOxidative StressEndocrinologymedicine.anatomical_structureCardiovascular DiseasesEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessReactive Oxygen SpeciesAngiotensin II Type 1 Receptor BlockersOxidative stressAnnals of medicine
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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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Pentaerithrityl tetranitrate improves angiotensin II induced vascular dysfunction via induction of heme oxygenase-1

2010

The organic nitrate pentaerythritol tetranitrate is devoid of nitrate tolerance, which has been attributed to the induction of the antioxidant enzyme heme oxygenase (HO)-1. With the present study, we tested whether chronic treatment with pentaerythritol tetranitrate can improve angiotensin II–induced vascular oxidative stress and dysfunction. In contrast to isosorbide-5 mononitrate (75 mg/kg per day for 7 days), treatment with pentaerythritol tetranitrate (15 mg/kg per day for 7 days) improved the impaired endothelial and smooth muscle function and normalized vascular and cardiac reactive oxygen species production (mitochondria, NADPH oxidase activity, and uncoupled endothelial NO synthase)…

medicine.medical_specialtyAntioxidantNitric Oxide Synthase Type IIImedicine.medical_treatmentVasodilator AgentsBlotting WesternFluorescent Antibody TechniquePentaerythritol tetranitratemedicine.disease_causePentaerythritolArticlechemistry.chemical_compoundInternal medicineRats Inbred SHRInternal MedicinemedicineAnimalsPentaerythritol TetranitrateEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesAnalysis of VarianceAngiotensin IImedicine.diseaseAngiotensin IIMitochondriaRatsHeme oxygenaseOxidative StressEndocrinologychemistryHeminEndothelium VascularReactive Oxygen SpeciesOxidative stressHeme Oxygenase-1
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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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