Search results for "Smut"

showing 10 items of 493 documents

Significant in vivo anti-inflammatory activity of Pytren4Q-Mn a superoxide dismutase 2 (SOD2) mimetic scorpiand-like Mn (II) complex.

2015

Background The clinical use of purified SOD enzymes has strong limitations due to their large molecular size, high production cost and immunogenicity. These limitations could be compensated by using instead synthetic SOD mimetic compounds of low molecular weight. Background/Methodology We have recently reported that two SOD mimetic compounds, the MnII complexes of the polyamines Pytren2Q and Pytren4Q, displayed high antioxidant activity in bacteria and yeast. Since frequently molecules with antioxidant properties or free-radical scavengers also have anti-inflammatory properties we have assessed the anti-inflammatory potential of Pytren2Q and Pytren4Q MnII complexes, in cultured macrophages …

MaleMAP Kinase Signaling Systemmedicine.drug_classAnti-Inflammatory AgentsSOD2lcsh:MedicineBiologymedicine.disease_causeAnti-inflammatoryCell LineSuperoxide dismutaseMicechemistry.chemical_compoundIn vivoChlorocebus aethiopsmedicineAnimalsHumanslcsh:ScienceVero Cellschemistry.chemical_classificationManganeseMultidisciplinarySuperoxide DismutaseSuperoxideImmunogenicityMolecular Mimicrylcsh:RMolecular mimicryEnzymechemistryBiochemistrybiology.proteinlcsh:QResearch ArticlePLoS ONE
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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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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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Beneficial effect of dipyridyl, a liposoluble iron chelator against focal cerebral ischemia: In vivo and in vitro evidence of protection of cerebral …

2007

Whereas iron chelators were shown to induce neuroprotection against brain injury, the effect of iron chelators on ischemia-induced damage of cerebral endothelium is largely unknown. Our objective was to explore the endothelioprotective effect of the lipophilic iron chelator dipyridyl (DP) (i) in vitro on the death of cerebral endothelial cells (CECs) subjected to intracellular iron loading and (ii) in vivo on the ischemia-induced blood-brain barrier (BBB) disruption. When given shortly after iron exposure or brain ischemia, DP prevented the death of CECs and diminished BBB disruption, respectively, whereas a delayed administration of DP was associated with a lower CECs protection. Interesti…

MaleProgrammed cell deathTime FactorsIronIschemiaPharmacologymedicine.disease_causeBlood–brain barrierIron Chelating AgentsTransfectionNeuroprotectionStatistics NonparametricBrain IschemiaBrain ischemiaMice22'-DipyridylIn vivoIschemiamedicineAnimalsPROTECTIONMolecular BiologyCells CulturedtherapyCell DeathDose-Response Relationship DrugChemistrySuperoxide DismutaseGeneral NeuroscienceLEDEndothelial CellsBrainProteinscellmedicine.diseaseEndothelial stem cellIn VitroDisease Models Animalmedicine.anatomical_structureGene Expression RegulationBlood-Brain BarrierBrain InjuriesImmunologyCELLScardiovascular systemNeurology (clinical)Oxidative stressHeme Oxygenase-1Developmental Biology
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Bcl-2 and Mn-SOD antisense oligodeoxynucleotides and a glutamine-enriched diet facilitate elimination of highly resistant B16 melanoma cells by tumor…

2005

Mitochondrial glutathione (mtGSH) depletion increases sensitivity of Bcl-2-overexpressing B16 melanoma (B16M)-F10 cells (high metastatic potential) to tumor necrosis factor-alpha (TNF-alpha)-induced oxidative stress and death in vitro. In vivo, mtGSH depletion in B16M-F10 cells was achieved by feeding mice (where the B16M-F10 grew as a solid tumor in the footpad) with an L-glutamine (L-Gln)-enriched diet, which promoted in the tumor cells an increase in glutaminase activity, accumulation of cytosolic L-glutamate, and competitive inhibition of GSH transport into mitochondria. L-Gln-adapted B16M-F10 cells, isolated using anti-Met-72 monoclonal antibodies and flow cytometry-coupled cell sortin…

MaleProgrammed cell deathgovernment.form_of_governmentGlutamineSOD2Antineoplastic AgentsSoft Tissue NeoplasmsMitochondrionBiologyBiochemistryGlutaminase activitySuperoxide dismutaseMiceAnimalsMolecular BiologyMelanomaAntisense therapySuperoxide DismutaseTumor Necrosis Factor-alphaCell BiologyGenetic TherapyOligonucleotides AntisenseMolecular biologyAnimal FeedCombined Modality TherapyGlutathioneMitochondriaMice Inbred C57BLDisease Models AnimalOxidative StressMitochondrial permeability transition poreProto-Oncogene Proteins c-bcl-2Drug Resistance Neoplasmgovernmentbiology.proteinTumor necrosis factor alphaNeoplasm TransplantationThe Journal of biological chemistry
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Proteome analysis of myocardial tissue following ischemia and reperfusion--effects of complement inhibition.

2006

Myocardial ischemia-reperfusion injury can be related to complement activation with generation of chemotactic mediators, release of cytokines, leukocyte accumulation, and subsequent severe tissue injury. In this regard, activation of transcription factors (i.e., NFkappaB) and de novo protein synthesis or inflammatory protein degradation seems to play an important role. In the present study, we analyzed the cardiac protein expression following myocardial ischemia (60 min) and reperfusion (180 min) in a rabbit model utilizing two-dimensional electrophoresis and nanoHPLC/ESI-MS/MS for biochemical protein identification. To achieve cardioprotective effects, we used a novel highly selective smal…

MaleProteomeG proteinNeutrophilsMolecular Sequence DataBiophysicsIschemiaMyocardial IschemiaMyocardial Reperfusion InjuryProtein degradationComplement C1 Inactivator ProteinsBiochemistryAnalytical ChemistrySuperoxide dismutaseClassical complement pathwayElectrocardiographyNecrosismedicineProtein biosynthesisAnimalsAmino Acid SequenceMolecular BiologyCreatine KinasebiologySuperoxide DismutaseMyocardiumalpha-Crystallin B ChainComplement System Proteinsmedicine.diseaseMolecular biologyComplement systembiology.proteinCreatine kinaseRabbitsMicrotubule-Associated ProteinsBiomarkersBiochimica et biophysica acta
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Reduction of mdx mouse muscle degeneration by low-intensity endurance exercise: a proteomic analysis in quadriceps muscle of exercised versus sedenta…

2015

By proteomic analysis we found an up-regulation of four carbonic anhydrase-3 (CA3) isoforms and a down-regulation of superoxide dismutase [Cu-Zn] (SODC) in quadriceps of sedentary X-linked muscular dystrophy (mdx) mice as compared with wild–type (WT) mice and the levels were significantly restored to WT values following low-intensity endurance exercise.

MaleProteomicsmuscular dystrophymdx mousemedicine.medical_specialtycarbonic anhydrase exercise mdx muscle oxidative stress muscle proteomic muscular dystrophyBlotting Westerncarbonic anhydraseBiophysicsMuscle Proteinsmedicine.disease_causeBiochemistryQuadriceps Musclemuscle proteomicSuperoxide dismutaseWestern blotEndurance trainingInternal medicinemedicineAnimalsoxidative stressElectrophoresis Gel Two-DimensionalMuscular dystrophyMolecular BiologyOriginal Paperexercisebiologymedicine.diagnostic_testSuperoxide Dismutasebusiness.industryReproducibility of ResultsSkeletal muscleCell Biologymedicine.diseaseOriginal PapersCarbonic Anhydrase IIIMice Inbred C57BLMuscular Dystrophy Duchennemedicine.anatomical_structureEndocrinologyX-linked muscular dystrophy (mdx)carbonic anhydrase; oxidative stress; muscle proteomicMice Inbred mdxPhysical Endurancebiology.proteinCarbonic anhydrase 3businessmuscle oxidative stressOxidative stress
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