Search results for "REACTIVE OXYGEN SPECIES"

showing 10 items of 879 documents

As2O3-induced oxidative stress and cycle progression in a human intestinal epithelial cell line (Caco-2)

2007

Foods and drinking water are the main routes for human exposure to inorganic arsenic, the intestinal epithelium being the first barrier against such exogenous toxicants. The present study evaluates the effect of As(III) (0.5-25 microM) upon Caco-2 cells as an intestinal epithelia model. Cell viability, intracellular formation of reactive oxygen species (ROS), mitochondrial membrane potential (Deltapsim) changes, and cell cycle distribution in exposed cultures were evaluated. The intracellular production of ROS was seen to increase in a non-dose dependent manner at all concentrations tested, with impairment of cell mitochondrial enzyme function secondary to a loss of Deltapsim. Concentration…

G2 PhaseCell SurvivalCellTetrazolium SaltsOxidative phosphorylationBiologyToxicologymedicine.disease_causeArsenicalsMembrane PotentialsArsenic TrioxidemedicineHumansViability assaychemistry.chemical_classificationReactive oxygen speciesCell CycleG1 PhaseOxidesGeneral MedicineCell cycleIntestinal epitheliumMitochondriaCell biologyOxidative StressThiazolesmedicine.anatomical_structurechemistryMitochondrial MembranesCaco-2 CellsReactive Oxygen SpeciesOxidative stressIntracellularToxicology in Vitro
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Beauvericin-induced cytotoxicity via ROS production and mitochondrial damage in Caco-2 cells.

2013

The cytotoxicity of beauvericin (BEA) on human colon adenocarcinoma (Caco-2) cells was studied as a function of time. Moreover, the oxidative damage and cell death endpoints were monitored after 24, 48 and 72 h. After BEA exposure, the IC₅₀ values ranged from 1.9 ± 0.7 to 20.6 ± 6.9 μM. A decrease in reduced glutathione (GSH; 31%) levels, as well as an increase in oxidized glutathione (GSSG, 20%) was observed. In the presence of BEA, reactive oxygen species (ROS) level was highly increased at an early stage with the highest production of 2.0-fold higher than the control that was observed at 120 min. BEA induced cell death by mitochondria-dependent apoptotic process with loss of the mitochon…

G2 PhaseProgrammed cell deathDNA damageCell SurvivalApoptosisBiologyToxicologymedicine.disease_causechemistry.chemical_compoundInhibitory Concentration 50NecrosisDepsipeptidesmedicineHumansIntestinal Mucosachemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesIonophoresCell growthGeneral MedicineGlutathioneMycotoxinsMolecular biologyGlutathioneBeauvericinCell biologyMitochondriaKineticsOxidative StresschemistryApoptosisLipid PeroxidationCaco-2 CellsReactive Oxygen SpeciesOxidation-ReductionOxidative stressDNA DamageToxicology letters
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Glutathione peroxidase-1 in health and disease: from molecular mechanisms to therapeutic opportunities.

2011

Reactive oxygen species, such as superoxide and hydrogen peroxide, are generated in all cells by mitochondrial and enzymatic sources. Left unchecked, these reactive species can cause oxidative damage to DNA, proteins, and membrane lipids. Glutathione peroxidase-1 (GPx-1) is an intracellular antioxidant enzyme that enzymatically reduces hydrogen peroxide to water to limit its harmful effects. Certain reactive oxygen species, such as hydrogen peroxide, are also essential for growth factor-mediated signal transduction, mitochondrial function, and maintenance of normal thiol redox-balance. Thus, by limiting hydrogen peroxide accumulation, GPx-1 also modulates these processes. This review explor…

GPX1AntioxidantPhysiologyProtein Conformationmedicine.medical_treatmentClinical BiochemistryMolecular Sequence DataGene ExpressionBiologymedicine.disease_causeBiochemistryDiabetes mellitus geneticschemistry.chemical_compoundGlutathione Peroxidase GPX1Risk FactorsComprehensive Invited ReviewNeoplasmsmedicineDiabetes MellitusAnimalsHumansGenetic Predisposition to DiseaseAmino Acid SequenceEnzyme InhibitorsHydrogen peroxideMolecular BiologyGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasePolymorphism GeneticCell DeathSuperoxideCell BiologyGlutathioneSelenocysteineOxidative StresschemistryBiochemistryGene Expression RegulationCardiovascular DiseasesGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidation-ReductionOxidative stressAntioxidantsredox signaling
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γ-Glutamylcysteine detoxifies reactive oxygen species by acting as glutathione peroxidase-1 cofactor

2012

This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 3.0 Unported License.

GPX1Antioxidantmedicine.medical_treatmentGlutathione reductaseCoenzymesGeneral Physics and AstronomyApoptosisBiologymedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyArticleCell Linechemistry.chemical_compoundMiceGlutathione Peroxidase GPX1SuperoxidesmedicineAnimalsHumansRNA Small InterferingRats Wistarchemistry.chemical_classificationNeuronsReactive oxygen speciesGlutathione PeroxidaseMultidisciplinarySuperoxideGlutathione peroxidaseGeneral ChemistryGlutathione3T3 CellsDipeptidesHydrogen PeroxideGlutathioneMitochondriaRatsOxidative StressGlutathione ReductaseHEK293 CellsBiochemistrychemistryInactivation MetabolicRNA InterferenceReactive Oxygen SpeciesOxidative stress
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Living with stress: regulation of antioxidant defense genes in the subterranean, hypoxia-tolerant mole rat, Spalax.

2011

Lack of oxygen is life threatening for most mammals. It is therefore of biomedical interest to investigate the adaptive mechanisms which enable mammalian species to tolerate extremely hypoxic conditions. The subterranean mole rat Spalax survives substantially longer periods of hypoxia than the laboratory rat. We hypothesized that genes of the antioxidant defense, detoxifying harmful reactive oxygen species generated during hypoxia and hyperoxia, are involved in Spalax underground adaptation. Using quantitative RT-PCR, we analyzed the mRNA expression levels of seven antioxidant defense genes (catalase, glutathione peroxidase 1, glutathione-S-transferase Pi1, heme oxygenase 1, superoxide dism…

GPX1SpalaxNF-E2-Related Factor 2Molecular Sequence DataHyperoxiamedicine.disease_causeAntioxidantsSuperoxide dismutaseSpecies SpecificityGeneticsmedicineAnimalsAmino Acid SequenceHypoxiaHyperoxiachemistry.chemical_classificationReactive oxygen speciesbiologyEcologyBrainHeartGeneral Medicinebiology.organism_classificationAdaptation PhysiologicalCell biologyRatsHeme oxygenaseOxygenOxidative StresschemistryGene Expression RegulationLiverCatalaseOrgan Specificitybiology.proteinSpalaxmedicine.symptomReactive Oxygen SpeciesSequence AlignmentOxidative stressTranscription FactorsGene
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Glutathione peroxidase 1 activity dictates the sensitivity of glioblastoma cells to oxidative stress.

2012

The high intratumoral and intertumoral heterogeneity of glioblastoma (GBM) leads to resistance to different therapies, and hence, selecting an effective therapy is very challenging. We hypothesized that the antioxidant enzyme status is a significant feature of GBM heterogeneity. The most important reactive oxygen/nitrogen species (ROS/RNS) detoxification mechanisms include superoxide dismutase (SOD), catalase, and glutathione peroxidase (GPx). Expression and activity of these enzymes and the cellular response to induced oxidative stress were systematically analyzed and compared between GBM cells and nontransformed glial cells of both human and murine origin. Regardless of cell type or speci…

GPX1medicine.disease_causeSuperoxide dismutaseCellular and Molecular NeuroscienceMiceCell Line TumormedicineAnimalsHumanschemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologyMicrogliaBrain NeoplasmsSuperoxide DismutaseGlutathione peroxidaseCatalaseMolecular biologyOxidative Stressmedicine.anatomical_structureNeurologychemistryCell culturebiology.proteinCancer researchNeurogliaGlioblastomaReactive Oxygen SpeciesNeurogliaOxidative stressGlia
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Mitochondrial DNA mutations in cancer--from bench to bedside.

2009

Mitochondria are cell organelles mostly known for their production of ATP through oxidative phosphorylation. As suggested over 70 years ago by O. Warburg and recently confirmed with molecular techniques, alterations in respiratory activity and mitochondrial DNA appear to be a common feature of malignant cells. Somatic mtDNA mutations have been reported in many types of cancer cells. MtDNA mutation pattern may enhance the specificity of cancer diagnostics, detection and prediction of tumor growth rate and patients' outcome. Therefore it may be used as a molecular cancer bio-marker. Nevertheless recently published papers list a large number of mitochondrial DNA mutations in many different can…

GeneticsMutationMitochondrial DNASettore BIO/16 - Anatomia UmanaSomatic cellRespiratory chainCancerContext (language use)ApoptosisMitochondrionBiologymedicine.disease_causemedicine.diseaseDNA MitochondrialModels BiologicalTranslational Research BiomedicalCell Transformation NeoplasticNeoplasmsCancer cellMutationmedicineHumansCancer Mitochondria Molecular Marker Mutation OXPHOS ReviewReactive Oxygen SpeciesCell ProliferationFrontiers in bioscience (Landmark edition)
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Human cytochrome P450 reductase can act as a source of endogenous oxidative DNA damage and genetic instability.

2005

Studies with repair-deficient mice and other experiments suggest that oxidative DNA modifications are generated in all types of cells even under physiological conditions and that this type of endogenous DNA damage contributes to spontaneous cancer incidence. However, the cellular sources of reactive oxygen species that are relevant for nuclear oxidative DNA damage are largely unknown. Here, we report that expression of human NADPH-cytochrome P450 reductase (hOR) in cultured V79 Chinese hamster cells gives rise to elevated basal levels of oxidative purine modifications after depletion of glutathione. Also, the basal levels of micronuclei are increased in the hOR-expressing cells, and again t…

Genome instabilityAntioxidantDNA damagemedicine.medical_treatmentGlutathione reductaseEndogenyOxidative phosphorylationCHO CellsBiologyBiochemistryGenomic Instabilitychemistry.chemical_compoundPhysiology (medical)CricetinaemedicineAnimalsHumansMicronuclei Chromosome-DefectiveNADPH-Ferrihemoprotein Reductasechemistry.chemical_classificationReactive oxygen speciesGlutathioneMolecular biologyGlutathionechemistryPurinesReactive Oxygen SpeciesOxidation-ReductionDNA DamageFree radical biologymedicine
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Redox regulation of genome stability by effects on gene expression, epigenetic pathways and DNA damage/repair

2015

Reactive oxygen and nitrogen species (e.g. H2O2, nitric oxide) confer redox regulation of essential cellular signaling pathways such as cell differentiation, proliferation, migration and apoptosis. In addition, classical regulation of gene expression or activity, including gene transcription to RNA followed by translation to the protein level, by transcription factors (e.g. NF-κB, HIF-1α) and mRNA binding proteins (e.g. GAPDH, HuR) is subject to redox regulation. This review will give an update of recent discoveries in this field, and specifically highlight the impact of reactive oxygen and nitrogen species on DNA repair systems that contribute to genomic stability. Emphasis will be placed …

Genome instabilityRedox signalingRNA UntranslatedEpigenetic regulation of neurogenesisDNA RepairHuR mRNA-binding protein in the 3′-untranslated regionClinical BiochemistryHDAC histone deacetylaseReview ArticleAP-1 activator protein 1BiochemistryApe-1 apurinic/apyrimidinic endonuclease 1GPx-1 glutathione peroxidase-1Epigenesis GeneticHistonesTrx thioredoxinPHD prolylhydroxylaseBER base excision repairlcsh:QH301-705.5HO-1 heme oxygenase-1EpigenomicsGeneticsRegulation of gene expressionNox member of the NADPH oxidase familylcsh:R5-920JmjC Jumonji C domain-containing histone demethylasesHIF-1α hypoxia inducible factor-1α5-hmC 5-hydroxymethylcytosineddc:Cell biologyMMP matrix metalloproteinaseGrx glutaredoxinGAPDH glyceraldehyde-3-phosphate dehydrogenaseNrf2 nuclear factor erythroid related factor 2DNA methylationEpigeneticslcsh:Medicine (General)Oxidation-ReductionSignal Transduction5-mC 5-methylcytosineDNA repairDNA damageNF-κB nuclear factor-κBBiologyGenomic InstabilityRNS reactive nitrogen speciesROS reactive oxygen speciesNER nucleotide excision repairSOD superoxide dismutaseOxyR transcription factor (hydrogen peroxide-inducible genes activator)HumansEpigeneticsOrganic ChemistryPETN pentaerithrityl tetranitrateGene regulationOxidative StressDNMT DNA methyltransferaseGene Expression Regulationlcsh:Biology (General)AREs AU-rich elementsHAT histone acetyltransferaseKeap1 kelch-like ECH-associated protein 1BiomarkersCOPD chronic obstructive pulmonary disorderDNA DamageRedox Biology
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Long-Lasting Genomic Instability Following Arsenite Exposure inMammalian Cells: The Role of Reactive Oxygen Species

2011

Previously, we reported that the progeny of mammalian cells, which has been exposed to sodium arsenite for two cell cycles, exhibited chromosomal instability and concurrent DNA hypomethylation, when they were subsequently investigated after two months of subculturing (about 120 cell generations) in arsenite-free medium. In this work, we continued our investigations of the long-lasting arsenite-induced genomic instability by analyzing additional endpoints at several time points during the cell expanded growth. In addition to the progressive increase of aneuploid cells, we also noted micronucleated and multinucleated cells that continued to accumulate up to the 50th cell generation, as well a…

Genome instabilitySodium arseniteEpidemiologyArsenitesHealth Toxicology and MutagenesisPopulationCellarsenite; genomic instability; reactive oxygen speciesCHO CellsBiologyGenomic Instabilitychemistry.chemical_compoundMultinucleateCricetulusChromosome instabilityCricetinaemedicineAnimalseducationGenetics (clinical)Arseniteeducation.field_of_studyCell cycleDNA MethylationFlow CytometryMolecular biologyarseniteSettore BIO/18 - Geneticamedicine.anatomical_structurechemistryEnvironmental PollutantsReactive Oxygen Species
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