Search results for "Reactive"

showing 10 items of 1469 documents

Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species

2010

This review highlights the important role of redox signaling between mitochondria and NADPH oxidases. Besides the definition and general importance of redox signaling, the cross-talk between mitochondrial and Nox-derived reactive oxygen species (ROS) is discussed on the basis of 4 different examples. In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. This concept was supported by observations that ethidium bromide-induced mitochondrial d…

Mitochondrial ROSAgingPotassium ChannelsMyocytes Smooth MuscleBiophysicsIn Vitro TechniquesMitochondrionmedicine.disease_causeMitochondrial Membrane Transport ProteinsModels BiologicalMitochondrial apoptosis-induced channelBiochemistryPeroxynitritechemistry.chemical_compoundmedicineAnimalsHumansMitochondrionFeedback PhysiologicalNADPH oxidasebiologyNADPH oxidaseMitochondrial Permeability Transition PoreSuperoxideAngiotensin IINADPH OxidasesSuperoxideNitric oxideCell BiologyReactive Nitrogen SpeciesMitochondriaCell biologyOxidative StressOxidative protein modificationchemistryMitochondrial permeability transition poreRedox regulationNOX1Hypertensionbiology.proteinReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionBiochimica et Biophysica Acta (BBA) - Bioenergetics
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Oxidant antioxidants and adaptive responses to exercise.

2015

The extensive damage produced by unaccustomed (acute) exercise and the health benefits of regular physical activity are well-known phenomena as well as the role played in them by reactive oxygen species (ROS). The present issue reports some interesting studies showing that the Janus faced effects of exercise-induced ROS in skeletal muscle. Most studies dealing with ROS contribution to acute exercise-induced tissue damage determine the levels of markers of oxidative damage to specific substances but they do not take into account total redox status of an individual before and after exercise. In their research article D. Stagos et al. used markers measuring plasma static (sORP) and capacity (c…

Mitochondrial ROSAgingmedicine.medical_specialtyArticle SubjectPhysical exerciseOxidative phosphorylationBiologymedicine.disease_causeBiochemistryAntioxidantsLipid peroxidationchemistry.chemical_compoundInternal medicinemedicineHumanslcsh:QH573-671Exercisechemistry.chemical_classificationReactive oxygen specieslcsh:CytologyCell BiologyGeneral MedicineOxidantsGlutathioneMitochondrial respiratory chainEndocrinologyEditorialchemistryBiochemistryExercise intensityReactive Oxygen SpeciesOxidative stressOxidative medicine and cellular longevity
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ALDH-2 deficiency increases cardiovascular oxidative stress--evidence for indirect antioxidative properties.

2007

Abstract Mitochondrial aldehyde dehydrogenase (ALDH-2) reduces reactive oxygen species (ROS) formation related to toxic aldehydes; additionally, it provides a bioactivating pathway for nitroglycerin. Since acetaldehyde, nitroglycerin, and doxorubicin treatment provoke mitochondrial oxidative stress, we used ALDH-2−/− mice and purified recombinant human ALDH-2 to test the hypothesis that ALDH-2 has an indirect antioxidant function in mitochondria. Antioxidant capacity of purified ALDH-2 was comparable to equimolar doses of glutathione, cysteine, and dithiothreitol; mitochondrial oxidative stress was comparable in C57Bl6 and ALDH-2−/− mice after acute challenges with nitroglycerin or doxorubi…

Mitochondrial ROSAntioxidantmedicine.medical_treatmentBiophysicsAldehyde dehydrogenaseAcetaldehydeMitochondrionPharmacologymedicine.disease_causeBiochemistryCardiovascular SystemModels BiologicalAntioxidantschemistry.chemical_compoundMiceNitroglycerinmedicineAnimalsHumansCysteineMolecular Biologychemistry.chemical_classificationReactive oxygen speciesbiologyDose-Response Relationship DrugAldehyde Dehydrogenase MitochondrialAcetaldehydeCell BiologyGlutathioneAldehyde DehydrogenaseGlutathioneMitochondriaMice Inbred C57BLDithiothreitolOxidative StresschemistryBiochemistryDoxorubicincardiovascular systembiology.proteinReactive Oxygen SpeciesOxidative stressBiochemical and biophysical research communications
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Reactive oxygen species derived from the mitochondrial respiratory chain are not responsible for the basal levels of oxidative base modifications obs…

2004

The mitochondrial electron transport chain (ETC) is the most important source of reactive oxygen species (ROS) in mammalian cells. To assess its relevance to the endogenous generation of oxidative DNA damage in the nucleus, we have compared the background (steady-state) levels of oxidative DNA base modifications sensitive to the repair glycosylase Fpg (mostly 7,8-dihydro-8-oxoguanine) in wild-type HeLa cells and HeLa rho0 cells. The latter are depleted of mitochondrial DNA and therefore are unable to produce ROS in the ETC. Although the levels of ROS measured by flow cytometry and redox-sensitive probes in rho0 cells were only 10-15% those of wild-type cells, steady-state levels of oxidativ…

Mitochondrial ROSCarbonyl Cyanide m-Chlorophenyl HydrazoneMitochondrial DNADNA damageCells[SDV]Life Sciences [q-bio]Oxidative phosphorylationMitochondrionBiologyBiochemistryElectron Transport03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsHumansComputingMilieux_MISCELLANEOUS030304 developmental biologyCell Nucleus0303 health sciencesGuanosineNucleotidesEscherichia coli ProteinsDNAFlow CytometryMitochondriaNuclear DNAMitochondrial respiratory chainDNA-Formamidopyrimidine GlycosylaseBiochemistryDNA glycosylaseMacrolidesReactive Oxygen SpeciesOxidation-Reduction030217 neurology & neurosurgeryDNA DamageHeLa Cells
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Heterozygous deficiency of manganese superoxide dismutase in mice (Mn-SOD+/-): a novel approach to assess the role of oxidative stress for the develo…

2005

Nitroglycerin (GTN)-induced tolerance was reported to be associated with increased levels of reactive oxygen species (ROS) in mitochondria. In the present study, we further investigated the role of ROS for the development of nitrate tolerance by using heterozygous manganese superoxide dismutase knock-out mice (Mn-SOD+/-). Mn-SOD is acknowledged as a major sink for mitochondrial superoxide. Vasodilator potency of mouse aorta in response to acetylcholine and GTN was assessed by isometric tension studies. Mitochondrial ROS formation was detected by 8-amino-5-chloro-7-phenylpyrido[3,4-d]pyridazine-1,4-(2H,3H)dione sodium salt (L-012)-enhanced chemiluminescence and mitochondrial aldehyde dehydro…

Mitochondrial ROSHeterozygoteAldehyde dehydrogenaseMitochondrionPharmacologymedicine.disease_causeMitochondria HeartSuperoxide dismutaseMiceNitroglycerinDrug tolerancemedicineAnimalsEndothelial dysfunctionAortaPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologySuperoxide DismutaseDrug ToleranceAldehyde Dehydrogenasemedicine.diseaseEnzyme ActivationMice Inbred C57BLOxidative StresschemistryBiochemistrycardiovascular systembiology.proteinMolecular MedicineOxidative stresscirculatory and respiratory physiologyMolecular pharmacology
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Manganese superoxide dismutase and aldehyde dehydrogenase deficiency increase mitochondrial oxidative stress and aggravate age-dependent vascular dys…

2008

AimsImbalance between pro- and antioxidant species (e.g. during aging) plays a crucial role for vascular function and is associated with oxidative gene regulation and modification. Vascular aging is associated with progressive deterioration of vascular homeostasis leading to reduced relaxation, hypertrophy, and a higher risk of thrombotic events. These effects can be explained by a reduction in free bioavailable nitric oxide that is inactivated by an age-dependent increase in superoxide formation. In the present study, mitochondria as a source of reactive oxygen species (ROS) and the contribution of manganese superoxide dismutase (MnSOD, SOD-2) and aldehyde dehydrogenase (ALDH-2) were inves…

Mitochondrial ROSMaleAgingPhysiologyVasodilator AgentsMitochondrionVascular dysfunctionmedicine.disease_causeMitochondria HeartMuscle Smooth Vascularchemistry.chemical_compoundMiceEndothelial dysfunctionAortachemistry.chemical_classificationMice KnockoutbiologySuperoxideAldehyde Dehydrogenase MitochondrialAge FactorsVasodilationBiochemistryCardiology and Cardiovascular MedicineMitochondrial aldehyde dehydrogenasemedicine.medical_specialty8-oxodGOxidative phosphorylationDNA MitochondrialSuperoxide dismutaseManganese superoxide dismutaseddc:570Physiology (medical)Internal medicinemedicineAnimalsReactive oxygen speciesDose-Response Relationship DrugSuperoxide DismutaseMitochondrial oxidative stressOriginal ArticlesAldehyde Dehydrogenasemedicine.diseaseMice Inbred C57BLOxidative StressEndocrinologychemistrybiology.proteinEndothelium VascularReactive Oxygen SpeciesOxidative stressDNA DamageCardiovascular research
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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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