Search results for "Superoxide"

showing 10 items of 462 documents

Multi-step metabolic activation of benzene. Effect of superoxide dismutase on covalent binding to microsomal macromolecules, and identification of gl…

1980

Abstract Incubation of [ 14 C]benzene or [ 14 C]phenol with liver microsomes from untreated rats, in the presence of a NADPH-generating system, gave rise to irreversible binding of metabolites to microsomal macromolecules. For both substrates this binding was inhibited by more than 50% by addition of superoxide dismutase to the incubation mixtures. The decrease in binding was compensated for by accumulation of [ 14 C]hydroquinone, indicating superoxide-mediated oxidation of hydroquinone as one step in the activation of benzene to metabolites binding to microsomal macromolecules. Since our previous work had shown that binding occurred mainly with protein rather than ribonucleic acid and was …

MaleMacromolecular SubstancesMetaboliteIn Vitro TechniquesToxicologyMass SpectrometryAdductchemistry.chemical_compoundPhenolsAnimalsPhenolBenzeneBiotransformationChromatography High Pressure LiquidCatecholChromatographyHydroquinoneSuperoxide DismutaseChemistryBenzeneGeneral MedicineGlutathioneGlutathioneBenzoquinoneRatsMicrosomes LiverChemico-Biological Interactions
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Estimation of the prevalence and incidence of motor neuron diseases in two Spanish regions: Catalonia and Valencia

2021

AbstractAccording to the degree of upper and lower motor neuron degeneration, motor neuron diseases (MND) can be categorized into amyotrophic lateral sclerosis (ALS), primary lateral sclerosis (PLS) or progressive muscular atrophy (PMA). Although several studies have addressed the prevalence and incidence of ALS, there is a high heterogeneity in their results. Besides this, neither concept has been previously studied in PLS or PMA. Thus, the objective of this study was to estimate the prevalence and incidence of MND, (distinguishing ALS, PLS and PMA), in the Spanish regions of Catalonia and Valencia in the period 2011–2019. Two population-based Spanish cohorts were used, one from Catalonia …

MaleMalalties neuromuscularsGene ExpressionSuperoxide Dismutase-10302 clinical medicinePrevalence030212 general & internal medicineAmyotrophic lateral sclerosisEstimation theoryPrimary Lateral Sclerosismedia_commonMotor neuronsMotor Neuronseducation.field_of_studyMultidisciplinaryIncidenceIncidence (epidemiology)QRMiddle AgedProgressive muscular atrophyNeuromuscular diseasesmedicine.anatomical_structureNeurones motoresNeurologyMedicineFemaleRiskSciencemedia_common.quotation_subjectPopulationBiologyArticleMuscular Atrophy Spinal03 medical and health sciencesmedicineHumansMotor Neuron DiseaseEspanyaEstimació Teoria de l'educationAgedEstimationSelection biasMotor neurons -- DiseasesModels StatisticalC9orf72 ProteinAmyotrophic Lateral SclerosisMotor neuronmedicine.diseaseRisk factorsSpainNeurones motores -- MalaltiesMutationBiomarkers030217 neurology & neurosurgeryDemography
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Part of the Series: From Dietary Antioxidants to Regulators in Cellular Signalling and Gene ExpressionRole of reactive oxygen species and (phyto)oest…

2006

There is increasing evidence that reactive oxygen species (ROS) are not only toxic but play an important role in cellular signalling and in the regulation of gene expression. We, here, discuss two examples of improved adaptive response to an altered cellular redox state. First, differences in longevity between males and females may be explained by a higher expression of antioxidant enzymes in females resulting in a lower yield of mitochondrial ROS. Oestrogens are made responsible for these phenomena. Oestradiol induces glutathione peroxidase-1 and MnSOD by processes requiring the cell surface oestrogen receptor (ER) and the activation of pathways usually involved in oxidative stress respons…

MaleMitochondrial ROSAgingAntioxidantmedicine.medical_treatmentGene ExpressionPhytoestrogensmedicine.disease_causeBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundGlutathione Peroxidase GPX1medicineAnimalsHumansRegulation of gene expressionchemistry.chemical_classificationGlutathione PeroxidaseReactive oxygen speciesEstradiolbiologySuperoxide DismutaseGeneral MedicineGlutathioneCatalaseRatsOxidative StressReceptors EstrogenBiochemistrychemistryCatalaseDietary Supplementsbiology.proteinFemaleReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionFree Radical Research
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Mitochondrial reactive oxygen species are obligatory signals for glucose-induced insulin secretion.

2009

OBJECTIVE—Insulin secretion involves complex events in which the mitochondria play a pivotal role in the generation of signals that couple glucose detection to insulin secretion. Studies on the mitochondrial generation of reactive oxygen species (ROS) generally focus on chronic nutrient exposure. Here, we investigate whether transient mitochondrial ROS production linked to glucose-induced increased respiration might act as a signal for monitoring insulin secretion. RESEARCH DESIGN AND METHODS—ROS production in response to glucose was investigated in freshly isolated rat islets. ROS effects were studied using a pharmacological approach and calcium imaging. RESULTS—Transient glucose increase …

MaleMitochondrial ROSmedicine.medical_specialtyEndocrinology Diabetes and Metabolismmedicine.medical_treatment[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionchemistry.chemical_elementCalciumMitochondrionBiologySuperoxide dismutaseIslets of Langerhans03 medical and health scienceschemistry.chemical_compoundAdenosine Triphosphate0302 clinical medicineSuperoxidesInternal medicineInsulin SecretionInternal MedicinemedicineAnimalsInsulinSecretionChromansRats Wistar030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesSuperoxide DismutaseSuperoxideInsulinNADMitochondriaRatsKinetics[SDV.AEN] Life Sciences [q-bio]/Food and NutritionGlucoseEndocrinologyIslet Studieschemistrybiology.proteinThapsigarginCalciumReactive Oxygen Species[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgerySignal Transduction
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Novel Small Molecule Inhibitor of C1s Exerts Cardioprotective Effects in Ischemia-Reperfusion Injury in Rabbits

2001

Abstract Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic agents, adhesion molecule expression, release of cytokines and oxygen-derived free radicals, and subsequent neutrophil accumulation. In the present study the cardioprotective effects of a novel highly selective small molecule C1s inhibitor (C1s-INH-248, Knoll) were examined in a rabbit model of myocardial ischemia (I) and reperfusion (R; i.e., 60 min I + 180 min R). In in vitro tests (enzyme activity and SRBC lysis) C1s-INH-248 demonstrated profound inhibitory potency. In vivo C1s-INH-248 (1 mg/kg body weight) administered 5 min before reperfusion significantly attenuated m…

MaleNecrosisEndotheliumNeutrophilsG proteinImmunologyMyocardial IschemiaIschemiaMyocardial Reperfusion InjuryComplement C1 Inactivator ProteinsPharmacologyHemolysisLeukocyte CountClassical complement pathwaySuperoxidesIn vivomedicineAnimalsImmunology and AllergyComplement Activationbusiness.industryHemodynamicsmedicine.diseaseComplement systemmedicine.anatomical_structureAnesthesiaEndothelium VascularRabbitsmedicine.symptombusinessReperfusion injuryThe Journal of Immunology
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Pharmacological activity of PF-904 in guinea pig in vivo, and on human bronchus and neutrophils in vitro.

1997

The effects of PF-904 (4-amino-1-ethyl-6-methylpyrazino[2,3-c][1,2,6]thiadiazine 2,2-dioxide), a pyrazinothiadiazine derivative, were examined in guinea-pig airways in vivo, in human isolated bronchus and human polymorphonuclear leukocytes. PF-904 (12.5-200 mg/kg, intraduodenal) reduced bronchoconstriction in response to histamine, arachidonic acid, platelet-activating factor (PAF) and methacholine. PF-904 (50-200 mg/kg) prevented PAF-induced airways hyperreactivity and inhibited antigen-induced bronchoconstriction, airway microvascular leakage and eosinophil lung accumulation, but antigen-induced airways hyperresponsiveness was not reduced. PF-904 (1 microM-1 mM) produced complete inhibiti…

MaleNeutrophilsPhosphodiesterase InhibitorsGuinea PigsBronchiPharmacologyIn Vitro TechniquesBronchial Provocation TestsCapillary Permeabilitychemistry.chemical_compoundIn vivoSuperoxidesmedicineAnimalsHumansAnti-Asthmatic AgentsPlatelet Activating FactorRolipramPharmacologyBronchusThiadiazinesAnti-Inflammatory Agents Non-SteroidalPhosphodiesteraseBiological activityrespiratory systemBronchodilator AgentsN-Formylmethionine Leucyl-Phenylalaninemedicine.anatomical_structurechemistryBiochemistryPyrazinesBronchoconstrictionMethacholinemedicine.symptomBronchial HyperreactivityHistaminemedicine.drugEuropean journal of pharmacology
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Redox Regulation of Dihydrofolate Reductase: Friend or Troublemaker?

2015

Oxidative stress is a hallmark of cardiovascular diseases1 and a major contributor to vascular dysfunction.2 On the basis on recent concepts, vascular oxidative stress is caused mainly by infiltrating inflammatory cells such as monocytes/macrophages or leucocytes,3,4 producing so-called kindling radicals that lead to the activation of secondary, vascular enzymatic sources of reactive oxygen species (mainly superoxide).2,5 A prominent example is the uncoupled nitric oxide (NO) synthase, which means that an NO-producing antiatherosclerotic enzyme is getting switched to a superoxide-producing proatherosclerotic enzyme.2 Molecular mechanisms causing endothelial NO synthase (eNOS) uncoupling or …

MaleNitric Oxide Synthase Type IIIAorta ThoracicOxidative phosphorylationBiologymedicine.disease_causeNitric OxideArticleNitric oxidechemistry.chemical_compoundEnosmedicineAnimalschemistry.chemical_classificationReactive oxygen speciesSuperoxideNitric Oxide Synthase Type IIIEndothelial CellsTetrahydrobiopterinbiology.organism_classificationTetrahydrofolate DehydrogenasechemistryBiochemistryCardiology and Cardiovascular MedicineOxidative stressmedicine.drugArteriosclerosis, thrombosis, and vascular biology
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Diminished neurogenic femoral artery vasoconstrictor response in a Zucker obese rat model: differential regulation of NOS and COX derivatives.

2014

Objective: Peripheral arterial disease is one of the macrovascular complications of type 2 diabetes mellitus. This study addresses femoral artery regulation in a prediabetic model of obese Zucker rats (OZR) by examining cross-talk between endothelial and neural factors. Methods and Results: Arterial preparations from lean (LZR) and OZR were subjected to electrical field stimulation (EFS) on basal tone. Nitric oxide synthase (NOS) and cyclooxygenase (COX) isoform expression patterns were determined by immunohistochemical labelling and Western blotting. Results indicate significantly reduced noradrenergic contractions in preparations from OZR compared with those of LZR. Functional inhibition …

MalePotassium ChannelsPhysiologylcsh:MedicineFemoral arteryCardiovascular PhysiologyBioinformaticsVascular Medicinechemistry.chemical_compoundSuperoxidesEnosMedicine and Health SciencesEndothelial dysfunctionlcsh:ScienceNeuronsDiabetisMultidisciplinarybiologyFemoral ArteryIsoenzymesVasodilationNitric oxide synthasemedicine.anatomical_structuremedicine.symptomResearch Articlemedicine.medical_specialtyEndotheliumMedicinaCardiologyEndothelial NOSCardiovascular PharmacologyNitric oxidemedicine.arteryInternal medicinemedicineAnimalsObesityVascular DiseasesPharmacologybusiness.industrylcsh:RBiology and Life Sciencesmedicine.diseasebiology.organism_classificationElectric StimulationRats ZuckerDisease Models AnimalEndocrinologychemistryProstaglandin-Endoperoxide SynthasesVasoconstrictionbiology.proteinFisiologia humanalcsh:QEndothelium VascularNitric Oxide SynthasebusinessVasoconstrictionPLoS ONE
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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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Cell death and oxidative stress in gliomas.

1999

In gliomas, apoptosis and necrosis are determined by a number of promoting and inhibiting factors including oxidative cell stress mediated by nitric oxide synthases (NOS) and reduced by superoxide dismutases. Therefore, in 46 gliomas (including astrocytomas, oligodendrogliomas, oligo-astrocytomas, and glioblastomas), the relationship of apoptosis and necrosis and the expression of apoptosis-promoting (p53, bax, Fas, Fas-L) and inhibiting (bcl-2) factors as well as of different isoforms of NOS (NOSb, NOSe, NOSi) and manganese superoxide dismutase (MnSOD) were studied. Apoptosis was measured in situ by the TUNEL method while expression profiles of apoptosis-related and oxidative stress-associ…

MaleProgrammed cell deathHistologyNecrosisTissue FixationOligodendrogliomaDNA FragmentationBiologyAstrocytomamedicine.disease_causePathology and Forensic MedicineSuperoxide dismutaseDownregulation and upregulationPhysiology (medical)GliomamedicineIn Situ Nick-End LabelingHumansAgedParaffin EmbeddingCell DeathBrain NeoplasmsCarcinomaGliomaMiddle Agedmedicine.diseaseImmunohistochemistrynervous system diseasesOxidative StressNeurologyApoptosisbiology.proteinCancer researchFemaleNeurology (clinical)Oligodendrogliomamedicine.symptomGlioblastomaOxidative stressNeuropathology and applied neurobiology
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