Search results for "REACTIVE OXYGEN SPECIES"

showing 10 items of 879 documents

Females Live Longer than Males: Role of Oxidative Stress

2011

One of the most significant achievements of the twentieth century is the increase in human lifespan. In any period studied, females live longer than males. We showed that mitochondrial oxidative stress is higher in males than females and that the higher levels of estrogens in females protect them against ageing, by up-regulating the expression of antioxidant, longevity-related genes. The chemical structure of estradiol confers antioxidant properties to the molecule. However, the low concentration of estrogens in females makes it unlikely that they exhibit significant antioxidant capacity in the organism. Therefore we studied the mechanisms enabling estradiol to be antioxidant at physiologic…

MaleMAPK/ERK pathwayAgingmedicine.medical_specialtyAntioxidantCell Survivalmedicine.medical_treatmentEstrogen receptorGenisteinPhytoestrogensBiologymedicine.disease_causeAntioxidantschemistry.chemical_compoundLife ExpectancyCell Line TumorInternal medicineDrug DiscoverymedicineAnimalsHumansReceptorPharmacologySex CharacteristicsMolecular StructureEstrogensMitochondriaOxidative StressEndocrinologyReceptors EstrogenchemistryAgeingFemalePhytoestrogensReactive Oxygen Specieshormones hormone substitutes and hormone antagonistsOxidative stressProtein BindingCurrent Pharmaceutical Design
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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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Preconditioning by Mitochondrial Reactive Oxygen Species Improves the Proangiogenic Potential of Adipose-Derived Cells-Based Therapy

2009

Objective— Transplantation of adipose-derived stroma cells (ADSCs) stimulates neovascularization after experimental ischemic injury. ADSC proangiogenic potential is likely mediated by their ability to differentiate into endothelial cells and produce a wide array of angiogenic and antiapoptotic factors. Mitochondrial reactive oxygen species (ROS) have been shown to control ADSC differentiation. We therefore hypothesized that mitochondrial ROS production may change the ADSC proangiogenic properties. Methods and Results— The use of pharmacological strategies (mitochondrial inhibitors, antimycin, and rotenone, with or without antioxidants) allowed us to specifically and precisely modulate mito…

MaleMitochondrial ROSProgrammed cell deathStromal Cells/cytology/metabolismAngiogenesisCellsReactive Oxygen Species/*metabolismNeovascularization PhysiologicBiologyMitochondrionmedicine.disease_causeMice03 medical and health sciences0302 clinical medicineAdipocytesmedicineAnimalsEndothelial Cells/*cytology/*physiologyCells CulturedNeovascularization030304 developmental biologyMitochondria/*metabolismchemistry.chemical_classificationReperfusion Injury/physiopathology0303 health sciencesReactive oxygen speciesCulturedEndothelial CellsCell DifferentiationMitochondriaCell biologyCell Differentiation/*physiologyTransplantationPhysiologic/*physiologychemistryReperfusion Injury030220 oncology & carcinogenesisImmunologyStromal CellsStem cellReactive Oxygen SpeciesCardiology and Cardiovascular MedicineOxidative stressArteriosclerosis, Thrombosis, and Vascular Biology
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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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TBC1D24-TLDc-related epilepsy exercise-induced dystonia: rescue by antioxidants in a disease model

2019

Genetic mutations in TBC1D24 have been associated with multiple phenotypes, with epilepsy being the main clinical manifestation. The TBC1D24 protein consists of the unique association of a Tre2/Bub2/Cdc16 (TBC) domain and a TBC/lysin motif domain/catalytic (TLDc) domain. More than 50 missense and loss-of-function mutations have been described and are spread over the entire protein. Through whole genome/exome sequencing we identified compound heterozygous mutations, R360H and G501R, within the TLDc domain, in an index family with a Rolandic epilepsy exercise-induced dystonia phenotype (http://omim.org/entry/608105). A 20-year long clinical follow-up revealed that epilepsy was self-limited in…

MaleModels Molecular0301 basic medicineProtein ConformationAmino Acid Motifsalpha-TocopherolMutantCrystallography X-RayPHENOTYPECompound heterozygosityAntioxidantsAnimals Genetically ModifiedEpilepsy0302 clinical medicineCatalytic DomainDrosophila ProteinsMissense mutationoxidative stressChildTLDC DOMAINVITAMIN-EExome sequencingSequence DeletionNeuronsDystoniaGeneticsexercise-induced dystoniaTBC1D24GTPase-Activating ProteinsANNOTATIONSEpilepsy RolandicPhenotypeRecombinant ProteinsPedigree3. Good healthRolandic epilepsyDystoniaDrosophila melanogasterChild PreschoolFemaleSettore MED/26 - NeurologiaSynaptic VesiclesDrosophila melanogasterPROTEIN STABILITYLife Sciences & BiomedicineLocomotionAdolescentPhysical ExertionMutation MissenseClinical NeurologyPREDICTIONSBiology03 medical and health sciencesmedicineAnimalsHumansAmino Acid SequenceCOMPARTMENToxidative streScience & TechnologySequence Homology Amino AcidMUTATIONSNeurosciencesInfantBiological TransportDEGRADATIONmedicine.diseasebiology.organism_classificationAcetylcysteineDisease Models AnimalOxidative Stress030104 developmental biologyrab GTP-Binding ProteinsSEIZURESNeurosciences & NeurologyNeurology (clinical)Reactive Oxygen SpeciesSequence Alignment030217 neurology & neurosurgery
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Antiatherosclerotic Effects of Small-Molecular-Weight Compounds Enhancing Endothelial Nitric-Oxide Synthase (eNOS) Expression and Preventing eNOS Unc…

2008

Many cardiovascular diseases are associated with reduced levels of bioactive nitric oxide (NO) and an uncoupling of oxygen reduction from NO synthesis in endothelial NO synthase (eNOS uncoupling). In human endothelial EA.hy 926 cells, two small-molecular-weight compounds with related structures, 4-fluoro-N-indan-2-yl-benzamide (CAS no. 291756-32-6; empirical formula C16H14FNO; AVE9488) and 2,2-difluoro-benzo[1,3]dioxole-5-carboxylic acid indan-2-ylamide (CAS no. 450348-85-3; empirical formula C17H13F2NO3; AVE3085), enhanced eNOS promoter activity in a concentration-dependent manner; with the responsible cis-element localized within the proximal 263 base pairs of the promoter region. RNA int…

MaleNeointimamedicine.medical_specialtyNitric Oxide Synthase Type IIINitric Oxide Synthase Type IINitric OxideProtective AgentsUmbilical veinCell LineNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosInternal medicinemedicineAnimalsHumansBenzodioxolesRNA MessengerAortaMice KnockoutPharmacologychemistry.chemical_classificationSp1 transcription factorReactive oxygen speciesGene knockdownbiologyEndothelial CellsAtherosclerosisbiology.organism_classificationVasoprotectiveMice Inbred C57BLMolecular WeightEndocrinologychemistryBenzamidesIndansMolecular MedicineJournal of Pharmacology and Experimental Therapeutics
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Identification of Patulin from

2019

The identification and characterization of fungal commensals of the human gut (the mycobiota) is ongoing, and the effects of their various secondary metabolites on the health and disease of the host is a matter of current research. While the neurons of the central nervous system might be affected indirectly by compounds from gut microorganisms, the largest peripheral neuronal network (the enteric nervous system) is located within the gut and is exposed directly to such metabolites. We analyzed 320 fungal extracts and their effect on the viability of a human neuronal cell line (SH-SY5Y), as well as their effects on the viability and functionality of the most effective compound on primary ent…

MaleNeuronsCell SurvivalPrimary Cell CulturePenicilliummicrobiomeComplex MixturesMycotoxinsEnteric Nervous SystemArticleMice Inbred C57BLMicePatulinCell Line TumorAnimalsHumansgastrointestinal systemFemaleCalcium SignalingfungiReactive Oxygen SpeciesfusariumMolecules (Basel, Switzerland)
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Inhibitors of poly (ADP-ribose) synthetase reduce renal ischemia-reperfusion injury in the anesthetized rat in vivo.

2000

The activation of poly (ADP-ribose) synthetase (PARS) subsequent to DNA damage caused by reactive oxygen or nitrogen species has been implicated in several pathophysiological conditions, including ischemia-reperfusion injury and shock. The aim of this study was to investigate whether PARS inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo. Male Wistar rats were subjected to 45 min bilateral clamping of the renal pedicles, followed by 6 h reperfusion (control animals). Animals were administered the PARS inhibitors 3-aminobenzamide, 1, 5-dihydroxyisoquinoline, or nicotinamide during the reperfusion period. Ischemia, followed by reperfusion, produc…

MaleNiacinamideIschemiaRenal functionNatriuresisKidney; Poly (ADP-ribose) synthetase inhibitors; Proximal tubule; Reactive oxygen species; Reperfusion injuryPharmacologyPoly(ADP-ribose) Polymerase InhibitorsKidneyBiochemistryExcretionchemistry.chemical_compoundIn vivoGeneticsmedicineAnimalsUreaAnesthesiaEnzyme InhibitorsRats WistarMolecular BiologyKidneyCreatinineNicotinamidemedicine.diseaseIsoquinolinesRatsOxidative Stressmedicine.anatomical_structurechemistryCreatinineReperfusion InjuryBenzamidesReactive Oxygen SpeciesReperfusion injuryBiotechnologyGlomerular Filtration RateFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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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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Nitroglycerin-induced endothelial dysfunction and tolerance involve adverse phosphorylation and S-glutathionylation of endothelial nitric oxide synth…

2011

Continuous administration of nitroglycerin (GTN) causes tolerance and endothelial dysfunction by inducing reactive oxygen species (ROS) production from various enzymatic sources, such as mitochondria, NADPH oxidase, and an uncoupled endothelial nitric oxide synthase (eNOS). In the present study, we tested the effects of type 1 angiotensin (AT(1))-receptor blockade with telmisartan on GTN-induced endothelial dysfunction in particular on eNOS phosphorylation and S-glutathionylation sites and the eNOS cofactor synthesizing enzyme GTP-cyclohydrolase I.Wistar rats were treated with telmisartan (2.7 or 8 mg/kg per day PO for 10 days) and with GTN (50 mg/kg per day SC for 3 days). Aortic eNOS phos…

MaleNitric Oxide Synthase Type IIIPhysiologyVasodilator AgentsPharmacologyBenzoatesCell LineNitroglycerinmedicineAnimalsHumansTelmisartanEnzyme InhibitorsPhosphorylationRats WistarS-GlutathionylationEndothelial dysfunctionGTP CyclohydrolaseBeneficial effectsNitroglycerinPharmacologyAngiotensin II receptor type 1Dose-Response Relationship DrugEndothelial nitric oxide synthaseChemistryEndothelial CellsDrug ToleranceAldehyde Dehydrogenasemedicine.diseaseGlutathioneMitochondriaRatsVasodilationOxidative StressTetrahydrofolate DehydrogenaseMolecular MedicinePhosphorylationBenzimidazolesEndothelium VascularTelmisartanReactive Oxygen SpeciesAngiotensin II Type 1 Receptor BlockersProtein Processing Post-Translationalmedicine.drugVascular Pharmacology
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