Search results for "RATS"

showing 10 items of 3537 documents

Osseous reaction to implantation of two endodontic cements : mineral trioxide aggregate (MTA) and calcium enriched mixture (CEM)

2012

Aim: The aim of the present in vivo study was to determine bone tissue reaction to calcium enriched mixture (CEM) and mineral trioxide aggregate (MTA) using a rat femur model. Study Design: Sixty-three rats were selected and randomly divided into three groups of 21 each [experimental groups (n=15), control (n=6)]. Implantation cavities were prepared in each femoral bone and randomly filled with the biomaterials only in the experimental groups. The animals in three groups were sacrificed 1, 4, and 8 weeks postoperatively. Histologic evaluations comprising inflammation severity and new bone formation were blindly made on H&E-stained decalcified 6-µm sections. Results: At 1, 4, and 8 weeks aft…

Mineral trioxide aggregateBiocompatibilityDental CementsDentistrychemistry.chemical_elementCalciumBone tissueBone and BonesEndodonticsRoot Canal Filling MaterialsDental cementIn vivomedicineAnimalsFemurRats WistarAluminum CompoundsGeneral DentistryChemistrybusiness.industrySilicatesBiomaterialOxidesCalcium Compounds:CIENCIAS MÉDICAS [UNESCO]RatsDrug Combinationsmedicine.anatomical_structureOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASResearch-ArticleCalciumSurgerybusiness
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Evidence for a relationship between mitochondrial Complex I activity and mitochondrial aldehyde dehydrogenase during nitroglycerin tolerance: effects…

2012

The medical use of nitroglycerin (GTN) is limited by patient tolerance. The present study evaluated the role of mitochondrial Complex I in GIN biotransformation and the therapeutic effect of mitochondrial antioxidants. The development of GIN tolerance (in rat and human vessels) produced a decrease in mitochondrial 02 consumption. Co-incubation with the mitochondria-targeted antioxidant mitoquinone (MQ 10(-6) mol/L) or with glutathione ester (GEE, 10(-4) mol/L) blocked GTN tolerance and the effects of GTN on mitochondrial respiration and aldehyde dehydrogenase 2 (ALDH-2) activity. Biotransformation of GTN depended on the mitochondria being functionally active, particularly mitochondrial Comp…

Mitochondrial ROSMaleAntioxidantmedicine.medical_treatmentAldehyde dehydrogenaseMitochondrionmedicine.disease_causeBiochemistryAntioxidantsRats Sprague-Dawleychemistry.chemical_compoundMiceNitroglycerinCyclic GMPAortaBiotransformationbiologyDrug ToleranceGlutathioneMitochondriaVasodilationBiochemistrycardiovascular systemAntioxidantcirculatory and respiratory physiologyBiophysicsIn Vitro TechniquesALDH-2Nitric oxideCell LineOxygen ConsumptionRotenoneRespirationmedicineHuman Umbilical Vein Endothelial CellsAnimalsHumansElectron Transport Complex IDose-Response Relationship DrugNitric oxideGlutathioneCell BiologyAldehyde DehydrogenaseRatschemistryOxidative stressMutationbiology.proteinReactive Oxygen SpeciesOxidative stressBiochimica et biophysica acta
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Mitochondrial oxidative stress and nitrate tolerance – comparison of nitroglycerin and pentaerithrityl tetranitrate in Mn-SOD+/- mice

2006

Abstract Background Chronic therapy with nitroglycerin (GTN) results in a rapid development of nitrate tolerance which is associated with an increased production of reactive oxygen species (ROS). According to recent studies, mitochondrial ROS formation and oxidative inactivation of the organic nitrate bioactivating enzyme mitochondrial aldehyde dehydrogenase (ALDH-2) play an important role for the development of nitrate and cross-tolerance. Methods Tolerance was induced by infusion of wild type (WT) and heterozygous manganese superoxide dismutase mice (Mn-SOD+/-) with ethanolic solution of GTN (12.5 μg/min/kg for 4 d). For comparison, the tolerance-free pentaerithrityl tetranitrate (PETN, 1…

Mitochondrial ROSMaleHeterozygotelcsh:Diseases of the circulatory (Cardiovascular) systemVasodilator AgentsAldehyde dehydrogenaseOxidative phosphorylationMitochondrionPharmacologyIn Vitro Techniquesmedicine.disease_causeDrug Administration ScheduleMitochondria HeartCell LineSuperoxide dismutaseMiceNitroglycerinmedicineAnimalsHumansPentaerythritol TetranitrateRNA MessengerRats WistarHeart metabolismAortachemistry.chemical_classificationReactive oxygen speciesbiologybusiness.industrySuperoxide DismutaseAldehyde Dehydrogenase MitochondrialBilirubinDrug ToleranceFree Radical ScavengersAldehyde DehydrogenaseAcetylcholineRatsVasodilationOxidative Stresschemistrylcsh:RC666-701Anesthesiabiology.proteinCardiology and Cardiovascular MedicinebusinessReactive Oxygen SpeciesOxidative stressHeme Oxygenase-1Research ArticleBMC Cardiovascular Disorders
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Effects of a high-fat diet on energy metabolism and ROS production in rat liver.

2011

International audience; BACKGROUND & AIMS: A high-fat diet affects liver metabolism, leading to steatosis, a complex disorder related to insulin resistance and mitochondrial alterations. Steatosis is still poorly understood since diverse effects have been reported, depending on the different experimental models used. METHODS: We hereby report the effects of an 8 week high-fat diet on liver energy metabolism in a rat model, investigated in both isolated mitochondria and hepatocytes. RESULTS: Liver mass was unchanged but lipid content and composition were markedly affected. State-3 mitochondrial oxidative phosphorylation was inhibited, contrasting with unaffected cytochrome content. Oxidative…

Mitochondrial ROSMaleTranscription GeneticMESH : Reactive Oxygen SpeciesMitochondria LiverMESH : HepatocytesMitochondrionOxidative PhosphorylationMESH: Hepatocytes0302 clinical medicineMESH: Membrane Potential MitochondrialCitrate synthaseMESH: AnimalsBeta oxidationMESH : Electron Transport2. Zero hungerMembrane Potential Mitochondrial0303 health sciencesMESH : RatsAdenine nucleotide translocatorMESH: Energy MetabolismMESH: Reactive Oxygen SpeciesLipidsBiochemistryLiverMESH: Dietary FatsMitochondrial matrix030220 oncology & carcinogenesisBody CompositionMESH : Oxidative PhosphorylationATP–ADP translocaseMESH: Mitochondria LiverMESH: RatsMESH : Body CompositionMESH : MaleOxidative phosphorylationBiologyMESH : Rats WistarElectron Transport03 medical and health sciencesMESH: Oxidative Phosphorylation[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRats WistarMESH: Electron Transport[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyHepatologyMESH: Transcription GeneticMESH : Transcription GeneticMESH : LiverMESH : LipidsMESH: Body CompositionMESH: Rats WistarMESH: LipidsDietary FatsMESH: MaleRatsMESH : Energy MetabolismMESH : Membrane Potential MitochondrialMESH : Mitochondria Liverbiology.proteinHepatocytesMESH : AnimalsEnergy MetabolismReactive Oxygen SpeciesMESH : Dietary FatsMESH: Liver
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Nitroglycerine causes mitochondrial reactive oxygen species production: In vitro mechanistic insights

2007

Background Nitroglycerine (GTN) is an organic nitrate that has been used for more than 100 years. Despite its widespread clinical use, several aspects of the pharmacology of GTN remain elusive. In a recent study, the authors of the present study showed that GTN causes opening of the mitochondrial permeability transition pore (mPTP) and mitochondrial production of reactive oxygen species (ROS). Objective In the present study, it was tested whether GTN-induced ROS production depends on mitochondrial potassium ATP-dependent channel or mPTP opening, and/or GTN biotransformation. Methods and results Isolated rat heart mitochondria were incubated with succinate (a substrate for complex II) and GT…

Mitochondrial ROSPotassium ChannelsVasodilator AgentsRespiratory chainIn Vitro TechniquesPharmacologyMitochondrionMitochondrial Membrane Transport ProteinsMitochondria HeartToxicologyNitroglycerinchemistry.chemical_compoundMitochondrial membrane transport proteinKATP ChannelsAnimalsMedicineRats WistarBiotransformationchemistry.chemical_classificationReactive oxygen speciesbiologyMitochondrial Permeability Transition Porebusiness.industryMPTPPotassium channelRatsBasic ResearchchemistryMitochondrial permeability transition poreModels Animalcardiovascular systembiology.proteinReactive Oxygen SpeciesCardiology and Cardiovascular Medicinebusinesscirculatory and respiratory physiologyCanadian Journal of Cardiology
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Synthesis, cytotoxicity, and inhibitory effects on tubulin polymerization of a new 3-heterocyclo substituted 2-styrylquinazolinones

2004

In order to study the influence of 3-substitution on the cytotoxic activity of 2-styrylquinazolinones, new 6-chloro-2-styryl-3-(heteroaryl)-4(3H)-quinazolinones were synthesized by refluxing equimolar amounts of 6-chloro-2-methyl-3-(heteroaryl)-4(3H)-quinazolinones and benzaldehyde in glacial acetic acid. At 1 microg ml(-1) concentration, almost all 2-styrylquinazolinones showed some cytotoxic activity against the L1210 and K562 leukemia cell lines. However, only 6-chloro-2-styryl-3-(pyrimidin-2yl)-4(3H)-quinazolinone inhibited the growth of these cells by over 50%. This last compound was also the only member of the series that inhibited tubulin polymerization, with an IC(50) value of 5.8 v…

Mitotic indexCell SurvivalPolymersAntineoplastic AgentsSettore BIO/19 - Microbiologia GeneraleMicrotubuleschemistry.chemical_compoundAcetic acidHeterocyclic CompoundsTubulinMicrotubuleDrug DiscoveryTumor Cells CulturedmedicineColchicineAnimalsHumansCytotoxic T cellCytotoxicityPharmacologyMolecular StructureChemistryTubulin ModulatorsOrganic ChemistryBiological activityGeneral MedicineMolecular biologySettore CHIM/08 - Chimica FarmaceuticaTubulin ModulatorsRatsMechanism of actionBiochemistryCell cultureQuinazolinesDrug Screening Assays Antitumormedicine.symptomK562 cells2-Styrylquinazolinones Antimitotic agents Cytotoxic activity MicrotubulesEuropean Journal of Medicinal Chemistry
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Astrocytes Protect Neurons from Aβ1-42 Peptide-Induced Neurotoxicity Increasing TFAM and PGC-1 and Decreasing PPAR-γ and SIRT-1

2015

One of the earliest neuropathological events in Alzheimer's disease is accumulation of astrocytes at sites of Aβ1-42 depositions. Our results indicate that Aβ1-42 toxic peptide increases lipid peroxidation, apoptosis and cell death in neurons but not in astrocytes in primary culture. Aβ1-42-induced deleterious neuronal effects are not present when neurons and astrocytes are mixed cultured. Stimulation of astrocytes with toxic Aβ1-42 peptide increased p-65 and decreased IκB resulting in inflammatory process. In astrocytes Aβ1-42 decreases protein expressions of sirtuin 1 (SIRT-1) and peroxisome proliferator-activated receptor γ (PPAR-γ) and over-expresses peroxisome proliferator-activated re…

MnSODProgrammed cell deathPPAR-γPeroxisome proliferator-activated receptorMitochondrionBiologyBioinformaticsmedicine.disease_causeAlzheimer's DiseaseNeurologiaPGC-1Sirtuin 1medicineAnimalsTFAMCells Culturedchemistry.chemical_classificationNeuronsAmyloid beta-PeptidesCell DeathSirtuin 1Caspase 3Superoxide DismutaseNeurotoxicityTranscription Factor RelAGeneral MedicineTFAMmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaCoculture TechniquesPeptide FragmentsCell biologyMitochondriaPeroxidesRatsPPAR gammachemistryMitochondrial biogenesisNF-κB.Astrocytesbiology.proteinFisiologia humanaLipid PeroxidationOxidative stressResearch PaperTranscription FactorsInternational Journal of Medical Sciences
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A novel rat CVB1-VP1 monoclonal antibody 3A6 detects a broad range of enteroviruses

2018

AbstractEnteroviruses (EVs) are common RNA viruses that cause diseases ranging from rash to paralytic poliomyelitis. For example, EV-A and EV-C viruses cause hand-foot and mouth disease and EV-B viruses cause encephalitis and myocarditis, which can result in severe morbidity and mortality. While new vaccines and treatments for EVs are under development, methods for studying and diagnosing EV infections are still limited and therefore new diagnostic tools are required. Our aim was to produce and characterize new antibodies that work in multiple applications and detect EVs in tissues and in vitro. Rats were immunized with Coxsackievirus B1 capsid protein VP1 and hybridomas were produced. Hybr…

Models Molecular0301 basic medicineBiolääketieteet - BiomedicineProtein Conformationmedicine.drug_classImmunoelectron microscopylcsh:MedicineEnzyme-Linked Immunosorbent AssayCoxsackievirusmedicine.disease_causeMonoclonal antibodyenterovirusesArticleEpitopeEpitopesMice03 medical and health sciencesProtein DomainsEnterovirus InfectionsmedicineantibodiesAnimalsHumanslcsh:ScienceMultidisciplinary030102 biochemistry & molecular biologybiologyPolioviruslcsh:Rvasta-aineetAntibodies Monoclonalbiology.organism_classificationAntibodies NeutralizingImmunohistochemistryVirologyEnterovirus B HumanRats3. Good healthenterovirukset030104 developmental biologyKasvibiologia mikrobiologia virologia - Plant biology microbiology virologybiology.proteinImmunohistochemistrylcsh:QCapsid ProteinsAntibodyClone (B-cell biology)Protein BindingScientific Reports
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2,3,9- and 2,3,11-Trisubstituted tetrahydroprotoberberines as D2 dopaminergic ligands

2013

Dopamine-mediated neurotransmission plays an important role in relevant psychiatric and neurological disorders. Nowadays, there is an enormous interest in the development of new dopamine receptors (DR) acting drugs as potential new targets for the treatment of schizophrenia or Parkinson's disease. Previous studies have revealed that isoquinoline compounds such as tetrahydroisoquinolines (THIQs) and tetrahydroprotoberberines (THPBs) can behave as selective D-2 dopaminergic alkaloids since they share structural similarities with dopamine. In the present study we have synthesized eleven 2,3,9- and 2,3,11-trisubstituted THPB compounds (six of them are described for the first time) and evaluated…

Models MolecularBerberineStereochemistryCell SurvivalMTT and cytofluorometric analysisTheoretical calculationsMolecular Dynamics SimulationLigandsCiencias BiológicasCompostos orgànics SíntesiDrug DiscoveryAlcaloidesDopamina ReceptorsAnimalsHumansTetrahydroprotoberberinesDopamine receptorsStructure-activity relationships cytotoxicityPharmacologyMolecular StructureChemistryReceptors Dopamine D2Organic ChemistryDopaminergicGeneral MedicineBioquímica y Biología MolecularRatsDopamine receptorStructureeactivity relationships cytotoxicityQuímica orgànicaCIENCIAS NATURALES Y EXACTAS
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Asp333, Asp495, and His52.3 Form the Catalytic Triad of Rat Soluble Epoxide Hydrolase

1996

On the basis of the sequence similarity between mammalian epoxide hydrolases and bacterial haloalkane dehalogenase reported earlier (Arand, M., Grant, D. F., Beetham, J. K., Friedberg, T., Oesch, F., and Hammock, B. D. (1994) FEBS Lett. 338, 251-256; Beetham, J. K., Grant, D., Arand, M., Garbarino, J., Kiyosue, T., Pinot, F., Oesch, F., Belknap, W. R., Shinozaki, K., and hammock, B. D. (1995) DNA Cell. Biol. 14, 61-71) we selected candidate amino acid residues for the putative catalytic triad of the rat soluble epoxide hydrolase. The predicted amino acid residues were exchanged by site-directed mutagenesis of the epoxide hydrolase cDNA, followed by the expression of the respective mutant en…

Models MolecularEpoxide hydrolase 2StereochemistryMolecular Sequence DataRestriction MappingPolymerase Chain ReactionBiochemistryCatalysisProtein Structure SecondaryCatalytic triadEscherichia coliAnimalsHumansPoint MutationHistidineAmino Acid SequenceCloning MolecularEpoxide hydrolaseMolecular BiologyPeptide sequenceDNA PrimersEpoxide Hydrolaseschemistry.chemical_classificationAspartic AcidBinding SitesSequence Homology Amino AcidChemistryCell BiologyRecombinant ProteinsRatsAmino acidEpoxide hydrolase activityKineticsBiochemistryEpoxide HydrolasesMutagenesis Site-DirectedHaloalkane dehalogenaseJournal of Biological Chemistry
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