Search results for "Active oxygen"

showing 10 items of 884 documents

Critical limb ischaemia is characterised by an increased production of whole blood reactive oxygen species and expression of TREM-1 on neutrophils

2013

Atherosclerosis is a chronic inflammatory process involving polymorphonuclear neutrophils (PMN) and formation of reactive oxygen species (ROS). The aim of the present study was to investigate the phenotype of inflammatory cells in regard to the expression of triggering receptor expressed on myeloid cells (TREM)-1 and its soluble form (sTREM-1) as well as its relationship with oxidative stress in peripheral artery disease (PAD) patients.In total 90 patients with PAD (N = 30 intermittent claudication (IC)300 m absolute walking distance, N = 30 IC300 m absolute walking distance, N = 30 critical limb ischaemia (CLI)) and 30 control persons were included. ROS formation was measured at basal or s…

Malemedicine.medical_specialtyNeutrophilsWalkingmedicine.disease_causeMonocytesFlow cytometryPeripheral Arterial DiseaseBasal (phylogenetics)IschemiaRisk FactorsInternal medicinePrevalencemedicineHumansReceptors ImmunologicReceptorAgedWhole bloodchemistry.chemical_classificationReactive oxygen speciesMembrane Glycoproteinsmedicine.diagnostic_testbusiness.industryMiddle AgedAtherosclerosisFlow CytometryPhenotypeTriggering Receptor Expressed on Myeloid Cells-1Intermittent claudicationOxidative StressEndocrinologychemistryImmunologyDisease ProgressionFemaleEndothelium Vascularmedicine.symptomReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessBiomarkersOxidative stressAtherosclerosis
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Resveratrol Reverses Endothelial Nitric-Oxide Synthase Uncoupling in Apolipoprotein E Knockout Mice

2010

A crucial cause of the decreased bioactivity of nitric oxide (NO) in cardiovascular diseases is the uncoupling of the endothelial NO synthase (eNOS) caused by the oxidative stress-mediated deficiency of the NOS cofactor tetrahydrobiopterin (BH(4)). The reversal of eNOS uncoupling might represent a novel therapeutic approach. The treatment of apolipoprotein E knockout (ApoE-KO) mice with resveratrol resulted in the up-regulation of superoxide dismutase (SOD) isoforms (SOD1-SOD3), glutathione peroxidase 1 (GPx1), and catalase and the down-regulation of NADPH oxidases NOX2 and NOX4 in the hearts of ApoE-KO mice. This was associated with reductions in superoxide, 3-nitrotyrosine, and malondiald…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIISOD3SOD2ResveratrolAntioxidantsSuperoxide dismutaseMicechemistry.chemical_compoundApolipoproteins ESuperoxidesEnosMalondialdehydeInternal medicineStilbenesmedicineAnimalsGTP CyclohydrolaseMice KnockoutPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyReverse Transcriptase Polymerase Chain ReactionSuperoxide DismutaseChemistrySuperoxideMyocardiumTetrahydrobiopterinbiology.organism_classificationBiopterinIsoenzymesOxidative StressEndocrinologyBiochemistryResveratrolbiology.proteinRNATyrosineMolecular Medicinemedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Human leukocyte/endothelial cell interactions and mitochondrial dysfunction in type 2 diabetic patients and their association with silent myocardial …

2013

OBJECTIVE Diabetes is associated with oxidative stress and increased mortality, but a possible correlation between leukocyte-endothelium interactions, oxidative stress, and silent myocardial ischemia (SMI) is yet to be confirmed. RESEARCH DESIGN AND METHODS Mitochondrial dysfunction and interactions between leukocytes and human umbilical vein endothelial cells were evaluated in 200 type 2 diabetic patients (25 with SMI) and 60 body composition– and age-matched control subjects. A possible correlation between these parameters and the onset of SMI was explored, and anthropometric and metabolic parameters were also analyzed. RESULTS Waist, levels of triglycerides, proinflammatory cytokines (i…

Malemedicine.medical_specialtyUmbilical VeinsCardiovascular and Metabolic RiskEndocrinology Diabetes and Metabolismmedicine.medical_treatmentMyocardial IschemiaVascular Cell Adhesion Molecule-1Type 2 diabetesmedicine.disease_causeProinflammatory cytokineInsulin resistanceDiabetes mellitusInternal medicineInternal MedicinemedicineLeukocytesHumansOriginal ResearchAdvanced and Specialized NursingbiologyGlutathione Disulfidebusiness.industryInsulinC-reactive proteinEndothelial CellsMiddle Agedmedicine.diseaseOxidative StressEndocrinologyC-Reactive ProteinDiabetes Mellitus Type 2biology.proteinFemalebusinessReactive Oxygen SpeciesHomeostasisOxidative stress
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Dexamethasone upregulates Nox1 expression in vascular smooth muscle cells.

2014

<b><i>Background/Aim:</i></b> It has been demonstrated that dexamethasone-induced hypertension can be prevented by the NADPH oxidase inhibitor apocynin. The effect of dexamethasone on NADPH oxidase, however, is unknown. The present study was conducted to investigate the effect of dexamethasone on the gene expression of Nox1, the major NADPH oxidase isoform in vascular smooth muscle cells. <b><i>Results:</i></b> Oral treatment of Wistar-Kyoto rats with dexamethasone (0.03 mg/kg/day) for 12 days led to an upregulation of Nox1 mRNA expression in the aorta. In cultured A7r5 rat aortic smooth muscle cells, dexamethasone increased Nox1 mRNA expressi…

Malemedicine.medical_specialtyVascular smooth muscleTime FactorsMyocytes Smooth Musclemedicine.disease_causeRats Inbred WKYDexamethasoneHistone DeacetylasesMuscle Smooth Vascularchemistry.chemical_compoundReceptors GlucocorticoidInternal medicinemedicineAnimalsNADH NADPH Oxidoreductasescardiovascular diseasesRNA MessengerGlucocorticoidsDexamethasoneAortaPharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyDose-Response Relationship DrugChemistryfungifood and beveragesGeneral MedicineRatsUp-RegulationEndocrinologyNOX1Gene Knockdown TechniquesApocynincardiovascular systembiology.proteinNADPH Oxidase 1Oxidative stresscirculatory and respiratory physiologymedicine.drugPharmacology
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The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
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Betulinic Acid Protects from Ischemia-Reperfusion Injury in the Mouse Retina

2021

Ischemia/reperfusion (I/R) events are involved in the pathophysiology of numerous ocular diseases. The purpose of this study was to test the hypothesis that betulinic acid protects from I/R injury in the mouse retina. Ocular ischemia was induced in mice by increasing intraocular pressure (IOP) to 110 mm Hg for 45 min, while the fellow eye served as a control. One group of mice received betulinic acid (50 mg/kg/day p.o. once daily) and the other group received the vehicle solution only. Eight days after the I/R event, the animals were killed and the retinal wholemounts and optic nerve cross-sections were prepared and stained with cresyl blue or toluidine blue, respectively, to count cells in…

Malemedicine.medical_specialtyretinagenetic structuresQH301-705.5ischemia-reperfusion injuryarteriolesVideo microscopyProtective AgentsArticlechemistry.chemical_compoundMicebetulinic acidInternal medicineBetulinic acidmedicineAnimalsBiology (General)AxonGanglion cell layerreactive oxygen speciesRetinaAnti-Inflammatory Agents Non-SteroidalRetinalGeneral Medicinemedicine.diseaseeye diseasesMice Inbred C57BLmedicine.anatomical_structureEndocrinologychemistryReperfusion InjuryOptic nervesense organsPentacyclic TriterpenesReperfusion injuryCells
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Abnormalities of mitochondrial functioning can partly explain the metabolic disorders encountered in sarcopenic gastrocnemius.

2007

International audience; Aging triggers several abnormalities in muscle glycolytic fibers including increased proteolysis, reactive oxygen species (ROS) production and apoptosis. Since the mitochondria are the main site of substrate oxidation, ROS production and programmed cell death, we tried to know whether the cellular disorders encountered in sarcopenia are due to abnormal mitochondrial functioning. Gastrocnemius mitochondria were extracted from adult (6 months) and aged (21 months) male Wistar rats. Respiration parameters, opening of the permeability transition pore and ROS production, with either glutamate (amino acid metabolism) or pyruvate (glucose metabolism) as a respiration substr…

Malemuscle atrophyMESH : Cell Aging[SDV]Life Sciences [q-bio]MESH : Reactive Oxygen SpeciesMitochondrion0302 clinical medicineGlycolysisMESH: AnimalsMESH : Muscle SkeletalMESH : Fatty AcidsCellular SenescencePhospholipidsMESH: Superoxide Dismutasereactive oxygen speciesMESH : Free Radicals0303 health sciencesMESH: Muscle SkeletalMESH : RatsFatty Acidsfatty acid profile of mitochondrial lipidsMESH: Reactive Oxygen SpeciesPyruvate dehydrogenase complexMESH: Fatty Acidsmitochondria[SDV] Life Sciences [q-bio]BiochemistryMESH: Cell AgingMESH: CalciumMESH : MitochondriaCell agingPyruvate decarboxylationmedicine.medical_specialtyFree RadicalsMESH: RatsCellular respirationMESH: MitochondriaMESH : MaleCell Respirationchemistry.chemical_elementOxidative phosphorylationBiologyCalciumMESH : Rats WistarMESH : Phospholipids03 medical and health sciencesMESH: Free RadicalsInternal medicinemedicineAnimalsMESH : Superoxide DismutaseRats WistarMuscle SkeletalMESH : Calcium030304 developmental biologyMESH: Phospholipidscalciumpermeability transition poreSuperoxide Dismutaseagingaging;calcium;fatty acid profile of mitochondrial lipids;mitochondria;muscle atrophy;permeability transition pore;reactive oxygen species;Animals;Calcium;Cell Aging;Cell Respiration;Fatty Acids;Free Radicals;Male;Mitochondria;Muscle;Skeletal;Phospholipids;Rats;Wistar;Reactive Oxygen Species;Superoxide DismutaseCell BiologyMESH: Rats WistarMESH: MaleRatsEndocrinologychemistryMESH : Cell RespirationMESH : AnimalsMESH: Cell Respiration030217 neurology & neurosurgery
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ALLOPURINOL BLOCKS AORTIC ANEURYSM IN A MOUSE MODEL OF MARFAN SYNDROME VIA REDUCING AORTIC OXIDATIVE STRESS

2022

ABSTRACTBackgroundIncreasing evidence indicates that redox stress participates in MFS aortopathy, though its mechanistic contribution is little known. We reported elevated reactive oxygen species (ROS) formation and NADPH oxidase NOX4 upregulation in MFS patients and mouse aortae. Here we address the contribution of xanthine oxidoreductase (XOR), which catabolizes purines into uric acid and ROS in MFS aortopathy.Methods and ResultsIn aortic samples from MFS patients, XOR protein expression, revealed by immunohistochemistry, increased in both the tunicae intima and media of the dilated zone. In MFS mice (Fbn1C1041G/+), aortic XOR mRNA transcripts and enzymatic activity of the oxidase form (X…

Marfan syndromemedicine.medical_specialtyEstrès oxidatiuAortic aneurysmsAllopurinolAllopurinolBiochemistryMarfan SyndromeMicechemistry.chemical_compoundAortic aneurysmMetal·loproteïnasesPhysiology (medical)medicine.arteryInternal medicinemedicineAnimalsAortaAortaNADPH oxidasebiologybusiness.industryConnective tissues diseasesNOX4Enzyme inhibitorsHydrogen Peroxidemedicine.diseaseMetalloproteinasesAortic AneurysmÀcid úricDisease Models AnimalOxidative StressEndocrinologyInhibidors enzimàticschemistryXanthine dehydrogenaseOxidative stressbiology.proteinUric acidMalalties del teixit connectiuAneurismes aòrticsReactive Oxygen SpeciesbusinessOxidation-ReductionUric acidmedicine.drug
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Response of human endothelial cells to oxidative stress on Ti6Al4V alloy.

2007

Titanium and its alloys are amongst the most frequently used materials in bone and dental implantology. The good biocompatibility of titanium(-alloys) is attributed to the formation of a titanium oxide layer on the implant surface. However, implant failures do occur and this appears to be due to titanium corrosion. Thus, cells participating in the wound healing processes around an implanted material, among them endothelial cells, might be subjected to reactive oxygen species (ROS) formed by electrochemical processes during titanium corrosion. Therefore, we studied the response of endothelial cells grown on Ti6Al4V alloy to H(2)O(2) and compared this with the response of endothelial cells gr…

Materials scienceBiophysicsCell Culture Techniqueschemistry.chemical_elementBioengineeringInflammationmedicine.disease_causeAntioxidantsBiomaterialsSuperoxide dismutasechemistry.chemical_compoundCoated Materials BiocompatibleMaterials TestingmedicineAlloysHumansCells Culturedchemistry.chemical_classificationInflammationTitaniumReactive oxygen speciesbiologySuperoxide DismutaseMetallurgytechnology industry and agricultureEndothelial CellsGlutathioneHydrogen PeroxideProstheses and Implantsequipment and suppliesGlutathioneOxidative StresschemistryMechanics of MaterialsCell cultureCeramics and Compositesbiology.proteinBiophysicsmedicine.symptomWound healingReactive Oxygen SpeciesOxidative stressTitaniumBiomaterials
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The effect of electrochemically simulated titanium cathodic corrosion products on ROS production and metabolic activity of osteoblasts and monocytes/…

2006

Nowadays aseptic loosening is the most common cause of orthopaedic implant failure. Some of its reasons have already been described up to now; however, others remain still hypothetical. Besides the inflammatory response to wear particles originating at different sources, the role of reactive oxygen species as products of cellular reactions and/or as a result of the process of corrosion of an implant leading to implant failure has recently been discussed too. In the present study, we used a galvanostatic polarization to simulate the cathodic partial reaction of the corrosion process at a titanium alloy surface. With respect to cells occurring at the interface of a metal implant, the behaviou…

Materials scienceBiophysicschemistry.chemical_elementBioengineeringBiocompatible Materialsmedicine.disease_causeMonocytesCorrosionBiomaterialschemistry.chemical_compoundMiceCell Line TumormedicineAlloysElectrochemistryAnimalsHumansPolarization (electrochemistry)Hydrogen peroxideElectrodeschemistry.chemical_classificationTitaniumReactive oxygen speciesOsteoblastsMonocyteMacrophagesMetallurgyOsteoblastCorrosionOxidative Stressmedicine.anatomical_structurechemistryMechanics of MaterialsCeramics and CompositesBiophysicsReactive Oxygen SpeciesOxidative stressTitaniumBiomaterials
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