Search results for "REACTIVE OXYGEN SPECIES"

showing 10 items of 879 documents

Nitrogen Dioxide-induced Reactive Oxygen Intermediates Production by Human Alveolar Macrophages and Peripheral Blood Mononuclear Cells

1994

Alveolar macrophages located on the alveolar surface have contact with air pollutants. We evaluated the dose-dependent effect of nitrogen dioxide exposure on the oxidative metabolism of alveolar macrophages and peripheral blood mononuclear cells by measuring the spontaneous and stimulated reactive oxygen intermediates production. Alveolar macrophages or peripheral blood mononuclear cells were placed on a polycarbonate membrane, which was in direct contact with the surface of a nutrient reservoir. The cells were exposed to nitrogen dioxide during different periods of time, varying between 30 and 120 min at concentrations ranging from 0.1 to 0.5 ppm. Exposure of alveolar macrophages to nitrog…

MaleNitrogen Dioxidechemistry.chemical_elementPeripheral blood mononuclear cellOxygenchemistry.chemical_compoundMacrophages AlveolarmedicineHumansEnvironmental ChemistryMacrophageNitrogen dioxideAgedGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship DrugPublic Health Environmental and Occupational HealthIn vitromedicine.anatomical_structurechemistryBiochemistryToxicityLeukocytes MononuclearBiophysicsFemalePulmonary alveolusReactive Oxygen SpeciesArchives of Environmental Health: An International Journal
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Oxidative and nitrosative stress in acute pancreatitis. Modulation by pentoxifylline and oxypurinol

2011

Item does not contain fulltext Reactive oxygen species are considered mediators of the inflammatory response and tissue damage in acute pancreatitis. We previously found that the combined treatment with oxypurinol - as inhibitor of xanthine oxidase- and pentoxifylline - as inhibitor of TNF-alpha production-restrained local and systemic inflammatory response and decreased mortality in experimental acute pancreatitis. Our aims were (1) to determine the time-course of glutathione depletion and oxidation in necrotizing pancreatitis in rats and its modulation by oxypurinol and pentoxifylline; (2) to determine whether TNF-alpha is responsible for glutathione depletion in acute pancreatitis; and (…

MaleNitrosationOxypurinolPharmacologymedicine.disease_causeBiochemistryPentoxifyllineMicechemistry.chemical_compoundCell Line TumorAnimalsMedicinePentoxifyllineRats WistarXanthine oxidasePharmacologychemistry.chemical_classificationReactive oxygen speciesPancreatitis Acute Necrotizingbusiness.industryPathogenesis and modulation of inflammation Infection and autoimmunity [N4i 1]GlutathioneNitro Compoundsmedicine.diseaseRatsOxidative StresschemistryBiochemistryAcute pancreatitisPancreatitisDrug Therapy CombinationTumor necrosis factor alphabusinessOxidative stressmedicine.drugBiochemical Pharmacology
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Consequences on offspring of abnormal function in ageing gametes.

2000

The present review aims to analyse (i) the molecular, biochemical and cellular changes that accompany oocyte and sperm ageing in any of the internal or external environments where they can reside, and (ii) the consequences of the abnormal function in ageing gametes on pre- and post-implantation development and later life of offspring. This review also aims to propose and discuss cellular/molecular mechanisms framed within the 'free radical theory of ageing'. It appears that the ageing of gametes prior to fertilization may affect many molecular, biochemical and cellular pathways that may jeopardize not only pre- and post-implantation embryo/fetal development but also later life of offspring.…

MaleOffspringmedia_common.quotation_subjectBiologyAntioxidantsAndrologyPregnancymedicineAnimalsHumansCellular Senescencemedia_commonGeneticsPregnancyReproductive successLongevityPregnancy OutcomeObstetrics and GynecologyEmbryomedicine.diseaseSpermSpermatozoaOxidative Stressmedicine.anatomical_structureReproductive MedicineAgeingOocytesGameteFemaleReactive Oxygen SpeciesHuman reproduction update
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Lymphocytic Mitochondrial Aconitase Activity is Reduced in Alzheimer's Disease and Mild Cognitive Impairment

2015

Background: Specific mechanisms behind the role of oxidative/nitrosative stress and mitochondrial dysfunction in Alzheimer's disease (AD) pathogenesis remain elusive. Mitochondrial aconitase (ACO2) is a Krebs cycle enzyme sensitive to free radicalmediated damage. Objective: We assessed activity and expression of ACO2 extracted from blood lymphocytes of subjects with AD, mild cognitive impairment (MCI), older adults with normal cognition (OCN, age >= 65 years), and younger adults with normal cognition (YCN, age < 65 years). Plasma levels and activities of antioxidants were also measured. Methods: Blood samples were collected from 28 subjects with AD, 22 with MCI, 21 OCN, and 19 YCN. ACO2 act…

MalePathologyantioxidantAntioxidantmedicine.medical_treatmentLymphocyteMitochondrionmedicine.disease_causePolymerase Chain ReactionPathogenesisVitamin Eoxidative stressLymphocytesaconitase (aconitate hydratase)Aconitate Hydratasereactive oxygen speciesGeneral NeuroscienceACO2General MedicineAlzheimer's diseasemitochondriaPsychiatry and Mental healthClinical Psychologyantioxidantsmedicine.anatomical_structureDisease ProgressionSettore MED/26 - NeurologiaFemaleAlzheimer diseaseAlzheimer's diseaseAzheimer diseasereactive nitrogen speciemedicine.medical_specialtyaconitase (aconitate hydratase); Alzheimer disease; antioxidants; free radicals; lymphocyte; mild cognitive impairment; mitochondria; oxidative stress; reactive nitrogen species; reactive oxygen speciesBlotting Westernfree radicalslymphocytemild cognitive impairmentInternal medicinemedicineHumansCognitive DysfunctionRNA MessengerAgedfree radicaloxidative strebusiness.industryVitamin EAconitasimedicine.diseasereactive nitrogen speciesEndocrinologyGeriatrics and GerontologyAlzheimer's disease; Aconitasi; oxidative stress; Aconitase (aconitate hydratase) Azheimer disease antioxidants free radicals lymphocyte mild cognitive impairment mitochondria oxidative stress reactive nitrogen species reactive oxygen speciesMental Status SchedulebusinessBiomarkersOxidative stressJournal of Alzheimer's Disease
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First Evidence for a Crosstalk Between Mitochondrial and NADPH Oxidase-Derived Reactive Oxygen Species in Nitroglycerin-Triggered Vascular Dysfunction

2008

Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revea…

MalePhysiologyVasodilator AgentsClinical BiochemistryMitochondrionPharmacologymedicine.disease_causeBiochemistryMitochondria HeartMiceNitroglycerinchemistry.chemical_compoundEthidiumAortaChromatography High Pressure LiquidHeart metabolismGeneral Environmental Sciencechemistry.chemical_classificationNADPH oxidasebiologyReverse Transcriptase Polymerase Chain ReactionReactive Nitrogen SpeciesBiochemistryCyclosporinecardiovascular systemcirculatory and respiratory physiologyBlotting WesternIn Vitro TechniquesTransfectionCell LineRotenonemedicineAnimalsHumansRNA MessengerRats WistarMolecular BiologyReactive oxygen speciesNADPH OxidasesCell BiologyRotenoneRatsMice Inbred C57BLchemistryMitochondrial permeability transition poreVasoconstrictionApocyninbiology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidants &amp; Redox Signaling
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Increased Hypoxic Tolerance by Chemical Inhibition of Oxidative Phosphorylation: “Chemical Preconditioning”

1997

A short ischemic episode preceding sustained ischemia is known to increase tolerance against ischemic cell death. We report early-onset long-lasting neuroprotection against in vitro hypoxia by preceding selective chemical inhibition of oxidative phosphorylation: “chemical preconditioning.” The amplitude of CA1population spikes (psap) in hippocampal slices prepared from control animals (control slices) was 31 ± 27% (mean ± SD) upon 45-min recovery from 15-min in vitro hypoxia. In slices prepared from animals treated in vivo with 20 mg/kg 3-nitropropionate (3-np) 1–24 h prior to slice preparation (preconditioned slices), psap improved to 90 ± 15% (p &lt; 0.01). Posthypoxic oxygen free radical…

MalePotassium ChannelsFree RadicalsPopulationIschemiaNerve Tissue ProteinsBiologyPharmacologyHippocampusNeuroprotectionOxidative PhosphorylationBrain Ischemia030218 nuclear medicine & medical imagingGlibenclamide03 medical and health sciencesAdenosine Triphosphate0302 clinical medicineSlice preparationIn vivoGlyburidemedicineAnimalsEnzyme InhibitorsRats WistarHypoxia BraineducationNeuronseducation.field_of_studyAntagonistHypoxia (medical)NADNitro Compoundsmedicine.diseaseCell HypoxiaRatsSuccinate DehydrogenaseNeuroprotective AgentsNeurologyAnesthesiaNeurology (clinical)Propionatesmedicine.symptomReactive Oxygen SpeciesCardiology and Cardiovascular Medicine030217 neurology & neurosurgerymedicine.drugJournal of Cerebral Blood Flow &amp; Metabolism
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Sodium metabisulfite as a cytotoxic food additive induces apoptosis in HFFF2 cells

2021

Sodium metabisulfite (SMB), an antioxidant agent, is extensively used as a preservative in food industry. The current study was aimed to clarify its potential toxic effects on human fetal foreskin fibroblasts (HFFF2) cells, in vitro. Subsequently, MTT results illustrated that exposure to SMB significantly (p  0.0001) decreased HFFF2 cell viability in a dose-dependent manner, and the concentration of 25 μM reduced cell survival rates to 50% as the half-maximal inhibitory concentration of SMB. It was further shown that SMB exerted this cytotoxic effect on HFFF2 cells through apoptosis induction. qRT-PCR and western blotting results showed that treatment of HFFF2 cells with this food additive …

MalePreservativeAntioxidantfood.ingredientCell Survivalmedicine.medical_treatmentForeskinApoptosisPharmacology01 natural sciencesAnalytical Chemistrychemistry.chemical_compound0404 agricultural biotechnologyfoodAutophagymedicineHumansSulfitesCytotoxic T cellCytotoxicityCells Culturedbcl-2-Associated X ProteinCaspase 8Dose-Response Relationship DrugCaspase 3Food additive010401 analytical chemistry04 agricultural and veterinary sciencesGeneral MedicineSodium metabisulfiteFibroblasts040401 food scienceCaspase 9In vitro0104 chemical sciencesGene Expression RegulationchemistryApoptosisFood AdditivesReactive Oxygen SpeciesFood ScienceFood Chemistry
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Glutamine potentiates TNF-α-induced tumor cytotoxicity

2001

L-glutamine (Gln) sensitizes tumor cells to tumor necrosis factor (TNF)-alpha-induced cytotoxicity. The type and mechanism of cell death induced by TNF-alpha was studied in Ehrlich ascites tumor (EAT)-bearing mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln). A high rate of Gln oxidation promotes a selective depletion of mitochondrial glutathione (mtGSH) content to approximately 58% of the level found in tumor mitochondria of mice fed a nutritionally complete elemental diet (standard diet, SD). The mechanism of mtGSH depletion involves a glutamate-induced inhibition of GSH transport from the cytosol into mitochondria. The increase in reactive oxygen in…

MaleProgrammed cell deathFree RadicalsCell SurvivalGlutamineApoptosisCytochrome c GroupMitochondrionBiologyBiochemistryMembrane PotentialsMiceNecrosischemistry.chemical_compoundAdenosine TriphosphateSuperoxidesPhysiology (medical)Tumor Cells CulturedAnimalsButhionine sulfoximineCaspase 3Tumor Necrosis Factor-alphaDrug SynergismHydrogen PeroxideGlutathioneGlutathioneMolecular biologyDietMitochondriaCell biologyOxygenGlutamineOxidative StressCytosolProto-Oncogene Proteins c-bcl-2chemistryApoptosisCaspasesReactive Oxygen SpeciesOxidation-ReductionCell DivisionIntracellularFree Radical Biology and Medicine
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Catchup: a mouse model for imaging-based tracking and modulation of neutrophil granulocytes

2015

Neutrophil granulocyte biology is a central issue of immunological research, but the lack of animal models that allow for neutrophil-selective genetic manipulation has delayed progress. By modulating the neutrophil-specific locus Ly6G with a knock-in allele expressing Cre recombinase and the fluorescent protein tdTomato, we generated a mouse model termed Catchup that exhibits strong neutrophil specificity. Transgene activity was found only in very few eosinophils and basophils and was undetectable in bone marrow precursors, including granulomonocytic progenitors (GMPs). Cre-mediated reporter-gene activation allowed for intravital two-photon microscopy of neutrophils without adoptive transfe…

MaleProgrammed cell deathGenotypeNeutrophilsTransgeneMedizinCre recombinaseMice TransgenicPeritonitisBiologyBiochemistryMiceCell MovementAnimalsAntigens LyTransgenesMolecular BiologyMice KnockoutCell DeathGene Transfer TechniquesCell BiologyCell movementMolecular biologyMice Inbred C57BLGene Expression RegulationFemaleReactive Oxygen SpeciesBiotechnologyNature Methods
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Cigarette smoke exposure up-regulates endothelin receptor B in human pulmonary artery endothelial cells: molecular and functional consequences

2010

BACKGROUND AND PURPOSEPulmonary arteries from smokers and chronic obstructive pulmonary disease patients show abnormal endothelium-dependent vascular reactivity. We studied the effect of cigarette smoke extract (CSE) on endothelin receptor B (ETB) expression in human pulmonary artery endothelial cells (HPAECs) and its role in endothelial dysfunction.EXPERIMENTAL APPROACHETB receptor expression was measured by real time RT-PCR, Western blot and immunofluorescence. Cell contraction, intracellular Ca2+, F/G-actin, RhoA activity, myosin light chain phosphorylation, ET, NO, thromboxane (Tx)A2 and reactive oxygen species (ROS) were measured by traction microscopy, fluorescence microscopy, phalloi…

MalePulmonary ArteryNitric OxideTransfectionMuscle Smooth Vascularendothelial dysfunctionendothelin receptor Bpulmonary artery endothelial cellsSmokeTobaccoHumansRNA Small InterferingCells CulturedAgedSulfonamidesrho-Associated KinasesEndothelin-1bosentancigarette smokeEndothelial CellsResearch PapersReceptor Endothelin BUp-RegulationThromboxane B2FemaleEndothelium VascularReactive Oxygen Species
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