Search results for "REACTIVE OXYGEN SPECIES"

showing 10 items of 879 documents

Enhanced oxidative stress and increased mitochondrial mass during Efavirenz-induced apoptosis in human hepatic cells

2010

BACKGROUND AND PURPOSE Efavirenz (EFV) is widely used in the treatment of HIV-1 infection. Though highly efficient, there is growing concern about EFV-related side effects, the molecular basis of which remains elusive. EXPERIMENTAL APPROACH In vitro studies were performed to address the effect of clinically relevant concentrations of EFV (10, 25 and 50 mu M) on human hepatic cells. KEY RESULTS Cellular proliferation and viability were reduced in a concentration-dependent manner. Analyses of the cell cycle and several cell death parameters (chromatin condensation, phosphatidylserine exteriorization, mitochondrial proapoptotic protein translocation and caspase activation) revealed that EFV tr…

CyclopropanesMalehepatotoxicityCarcinoma HepatocellularTime FactorsAnti-HIV AgentsCell SurvivalApoptosisMitochondria LiverPhosphatidylserinesAntioxidantsSuperoxidesHumansChromansantiretroviral drugsCell Proliferationreactive oxygen speciesDose-Response Relationship DrugCell CycleLiver NeoplasmsChromatin Assembly and DisassemblyResearch PapersGlutathioneBenzoxazinesmitochondriaOxidative Stressside effectscell deathLiverAlkynesFemaleEfavirenzApoptosis Regulatory ProteinsHeLa Cells
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Roflumilast inhibits respiratory syncytial virus infection in human differentiated bronchial epithelial cells.

2013

Respiratory syncytial virus (RSV) causes acute exacerbations in COPD and asthma. RSV infects bronchial epithelial cells (HBE) that trigger RSV associated lung pathology. This study explores whether the phosphodiesterase 4 (PDE4) inhibitor Roflumilast N-oxide (RNO), alters RSV infection of well-differentiated HBE (WD-HBE) in vitro. WD-HBE were RSV infected in the presence or absence of RNO (0.1-100 nM). Viral infection (staining of F and G proteins, nucleoprotein RNA level), mRNA of ICAM-1, ciliated cell markers (digital high speed videomicroscopy, β-tubulin immunofluorescence, Foxj1 and Dnai2 mRNA), Goblet cells (PAS), mRNA of MUC5AC and CLCA1, mRNA and protein level of IL-13, IL-6, IL-8, T…

CyclopropanesScienceAminopyridinesBronchiCell CountRespiratory Syncytial Virus InfectionsBiologyMucin 5ACImmunofluorescenceVirus ReplicationVirusAntioxidantsChloride ChannelsTubulinGene expressionmedicineHumansCiliaRNA MessengerRespiratory systemRoflumilastMessenger RNAMetaplasiaMultidisciplinarymedicine.diagnostic_testQRvirus diseasesCell DifferentiationEpithelial CellsForkhead Transcription FactorsAxonemal Dyneinsrespiratory systemViral LoadVirologyMolecular biologyRespiratory Syncytial VirusesOxidative StressViral replicationBenzamidesMedicineCytokinesTumor necrosis factor alphaGoblet CellsReactive Oxygen SpeciesBiomarkersmedicine.drugResearch ArticlePloS one
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Dynamic changes in the subcellular distribution of the tobacco ROS-producing enzyme RBOHD in response to the oomycete elicitor cryptogein.

2014

Highlight text The oomycete elicitor cryptogein triggers the relocation of RBOHD from intracellular compartments to the plasma membrane in tobacco cells. This suggests that intracellular trafficking is a potential determinant of RBOHD activity.

DETERGENT-RESISTANT MEMBRANESPhysiologyNicotiana tabacum[SDV]Life Sciences [q-bio]BY-2 cellsPlant SciencecryptogeinCell membranechemistry.chemical_compoundAPOPLASTIC OXIDATIVE BURSTCELL-SURFACEDISEASE RESISTANCE[MATH]Mathematics [math]Plant Proteinsreactive oxygen speciesFungal proteinNADPH oxidaseMicroscopy Confocalbiologyfood and beveragesElicitorCell biologymedicine.anatomical_structureBiochemistryprotein trafficking.[SDE]Environmental SciencessymbolsNADPH OXIDASE RBOHDprotein traffickingResearch PaperPhytophthoraCycloheximiderespiratory burst oxidase homolog D (RBOHD)Real-Time Polymerase Chain ReactionFungal Proteinssymbols.namesakeNICOTIANA-BENTHAMIANAMicroscopy Electron TransmissionTobaccomedicine[SDV.BV]Life Sciences [q-bio]/Vegetal Biology[INFO]Computer Science [cs]NITRIC-OXIDENicotiana tabacumCell MembraneNADPH OxidasesGolgi apparatusbiology.organism_classificationSubcellular localizationLIPID RAFTSchemistryPLASMA-MEMBRANEbiology.proteinPLANT DEFENSE
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A loop involving NRF2, miR‐29b‐1‐5p and AKT, regulates cell fate of MDA‐MB‐231 triple‐negative breast cancer cells

2019

The present study shows that nuclear factor erythroid 2-related factor 2 (NRF2) and miR-29b-1-5p are two opposite forces which could regulate the fate of MDA-MB-231 cells, the most studied triple-negative breast cancer (TNBC) cell line. We show that NRF2 activation stimulates cell growth and markedly reduces reactive oxygen species (ROS) generation, whereas miR-29b-1-5p overexpression increases ROS generation and reduces cell proliferation. Moreover, NRF2 downregulates miR-29b-1-5p expression, whereas miR-29b-1-5p overexpression decreases p-AKT and p-NRF2. Furthermore, miR-29b-1-5p overexpression induces both inhibition of DNA N-methyltransferases (DNMT1, DNMT3A, and DNMT3B) expression and …

DNA (Cytosine-5-)-Methyltransferase 10301 basic medicineNF-E2-Related Factor 2PhysiologyClinical BiochemistryTriple Negative Breast NeoplasmsAKT DNMTs miR‐29b‐1‐5p NRF2 parthenolide tumor suppressor genesCell fate determinationenvironment and public healthDNA Methyltransferase 3A03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSettore BIO/10 - BiochimicaCell Line TumorCyclin D2HumansParthenolideDNA (Cytosine-5-)-MethyltransferasesProtein kinase BTriple-negative breast cancerCell Proliferationchemistry.chemical_classificationReactive oxygen speciesCell growthTumor Suppressor ProteinsCell BiologyDNA Methylationrespiratory systemCell biologyGene Expression Regulation NeoplasticMicroRNAs030104 developmental biologychemistryCell culture030220 oncology & carcinogenesisDNMT1FemaleReactive Oxygen SpeciesProto-Oncogene Proteins c-aktSesquiterpenesSignal TransductionJournal of Cellular Physiology
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Oxidative stress impairs the repair of oxidative DNA base modifications in human skin fibroblasts and melanoma cells.

2008

Irradiation of mammalian cells with solar light is associated with the generation of reactive oxygen species (ROS) and oxidative stress, which is mediated in part by endogenous photosensitizers absorbing in the visible range of the solar spectrum. Accordingly, oxidative DNA base modifications such as 7,8-dihydro-8-oxoguanine (8-oxoG) are the predominant types of DNA damage in cells irradiated at wavelengths >400 nm. We have analysed the repair of oxidative purine modifications in human skin fibroblasts and melanoma cells using an alkaline elution technique, both under normal conditions and after depletion of glutathione. Similar repair rates were observed in fibroblasts and melanoma cells f…

DNA RepairLightDNA damageUltraviolet RaysPyrimidine dimerOxidative phosphorylationBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundmedicineHumansMolecular BiologyMelanomaAgedSkinchemistry.chemical_classificationReactive oxygen speciesGuanosineCell BiologyBase excision repairGlutathioneMolecular biologyGlutathioneOxidative StresschemistryBiochemistryFemaleOxidative stressNucleotide excision repairDNA repair
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UVA irradiation induces relocalisation of the DNA repair protein hOGG1 to nuclear speckles

2006

The DNA glycosylase hOGG1 initiates base excision repair (BER) of oxidised purines in cellular DNA. Using confocal microscopy and biochemical cell fractionation experiments we show that, upon UVA irradiation of human cells, hOGG1 is recruited from a soluble nucleoplasmic localisation to the nuclear matrix. More specifically, after irradiation, hOGG1 forms foci colocalising with the nuclear speckles, organelles that are interspersed between chromatin domains and that have been associated with transcription and RNA-splicing processes. The use of mutant forms of hOGG1 unable to bind the substrate showed that relocalisation of hOGG1 does not depend on the recognition of the DNA lesion by the en…

DNA RepairTranscription GeneticUltraviolet RaysDNA repairRecombinant Fusion ProteinsGreen Fluorescent ProteinsFluorescent Antibody TechniqueBiologyDNA GlycosylasesSubstrate Specificitychemistry.chemical_compoundDNA Repair ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseHumansCell NucleusGuanosineBiological TransportCell BiologyBase excision repairNuclear matrixMolecular biologyChromatinCell biologychemistryDNA glycosylaseCell fractionationReactive Oxygen SpeciesDNAHeLa CellsJournal of Cell Science
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Role of Endogenous Oxidative DNA Damage in Carcinogenesis: What Can We Learn from Repair-Deficient Mice?

2002

Basal steady-state levels of oxidative DNA base modifications such as 7,8-dihydro-8-oxo-2'-deoxyguanosine (8-oxoG) are observed in all types of cells, most probably due to a continuous generation of reactive oxygen species (ROS) in the cellular oxygen metabolism, and it has long been suspected that they might play an important role in the initiation of carcinogenesis. Experimental evidence for this assumption can be obtained by studying the effects of a modulation of the steady-state levels, either by in- or decreasing the generation of oxidative DNA damage, on spontaneous mutation rates and cancer incidence. However, clear answers have not yet been obtained by these strategies. It is still…

DNA RepairTransgeneClinical BiochemistryEndogenyOxidative phosphorylationBiologymedicine.disease_causeBiochemistryMiceNeoplasmsmedicineAnimalsHumansEpigeneticsMolecular BiologyMice Knockoutchemistry.chemical_classificationReactive oxygen speciesNeoplasms ExperimentalCell biologychemistryBiochemistryTumor promotionReactive Oxygen SpeciesCarcinogenesisOxidation-ReductionOxidative stressDNA DamageBiological Chemistry
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Lovastatin protects human endothelial cells from the genotoxic and cytotoxic effects of the anticancer drugs doxorubicin and etoposide

2006

Background and purpose: 3-Hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors (statins) are frequently used lipid-lowering drugs. Moreover, they exert pleiotropic effects on cellular stress responses and death. Here, we analysed whether lovastatin affects the sensitivity of primary human endothelial cells (HUVEC) to the anticancer drug doxorubicin. Experimental approach: We investigated whether pretreatment of HUVEC with low dose of lovastatin influences the cellular sensitivity to doxorubicin. To this end, cell viability, proliferation and apoptosis as well as DNA damage-triggered stress response were analysed. Key results: Lovastatin reduced the cytotoxic potency of doxorub…

DNA ReplicationCell SurvivalDNA damageApoptosisBiologyPharmacologypolycyclic compoundsmedicineHumansTopoisomerase II InhibitorsDoxorubicinLovastatinEtoposideEtoposideFluorescent DyesPharmacologyAntibiotics AntineoplasticReverse Transcriptase Polymerase Chain ReactionTopoisomeraseCell CycleEndothelial Cellsnutritional and metabolic diseasesAntimutagenic AgentsFibroblastsCell cycleResearch PapersAntineoplastic Agents PhytogenicDoxorubicinDrug Resistance NeoplasmHMG-CoA reductasebiology.proteinlipids (amino acids peptides and proteins)LovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsTopoisomerase-II InhibitorReactive Oxygen SpeciesFluorescein-5-isothiocyanateDNA Damagemedicine.drugBritish Journal of Pharmacology
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Oxidative damage to mitochondrial DNA and glutathione oxidation in apoptosis: studiesin vivoandin vitro

1999

Free radicals may be involved in apoptosis although this is the subject of some controversy. Furthermore, the source of free radicals in apoptotic cells is not certain. The aim of this study was to elucidate the role of oxidative stress in the induction of apoptosis in serum-deprived fibroblast cultures and in weaned lactating mammary glands as in vitro and in vivo experimental models, respectively. Oxidative damage to mtDNA is higher in apoptotic cells than in controls. Oxidized glutathione (GSSG) levels in mitochondria from lactating mammary gland are also higher in apoptosis. There is a direct relationship between mtDNA damage and the GSSG/reduced glutathione (GSH) ratio. Furthermore, wh…

DNA damageApoptosisWeaningMitochondrionmedicine.disease_causeDNA MitochondrialBiochemistryCulture Media Serum-FreeMembrane Potentialschemistry.chemical_compoundCytosolMammary Glands AnimalIn vivoGeneticsmedicineAnimalsLactationAnaerobiosisRats WistarFragmentation (cell biology)Molecular BiologyCells CulturedGlutathione DisulfideGlutathioneFibroblastsGlutathioneIn vitroPeroxidesRatsCell biologyOxidative StresschemistryApoptosisFemaleReactive Oxygen SpeciesOxidative stressDNA DamageBiotechnologyThe FASEB Journal
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Differences between cysteine and homocysteine in the induction of deoxyribose degradation and DNA damage.

2001

The effect of two naturally occurring thiols, such as cysteine and homocysteine, has been examined for their ability to induce deoxyribose degradation and DNA damage. Copper(II) ions have been added to incubation mixtures and oxygen consumption measurements have been performed in order to correlate the observed damaging effects with the rate of metal catalyzed thiol oxidation. Ascorbic acid plus copper has been used as a positive control of deoxyribose and DNA oxidation due to reactive oxygen species. Cysteine or homocysteine in the presence of copper ions induce the degradation of deoxyribose and the yield of 8-hydroxy-2'-deoxyguanosine (8-OHdG), although important differences are observed…

DNA damageAscorbic AcidThymus GlandBiochemistrySuperoxide dismutasechemistry.chemical_compoundOxygen ConsumptionPhysiology (medical)DeoxyguanosineAnimalsCysteineHomocysteineElectrophoresis Agar GelbiologyDeoxyriboseSuperoxide DismutaseThiourea8-Hydroxy-2'-deoxyguanosineDeoxyguanosineDNA oxidationAscorbic acidCatalasechemistryDeoxyriboseBiochemistry8-Hydroxy-2'-DeoxyguanosineSpectrophotometrybiology.proteinCattleReactive Oxygen SpeciesOxidation-ReductionCopperCysteineDNA DamageFree radical biologymedicine
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