Search results for "Dative"

showing 10 items of 2381 documents

Differential effects of cysteine and methionine residues in the antioxidant activity of human serum albumin

2005

Antioxidant properties of human serum albumin (HSA) may explain part of its beneficial role in various diseases related to free radical attack. In the present study, the antioxidant role of Cys and Met was studied by copper-mediated oxidation of human low density lipoproteins and by free radical-induced blood hemolysis which essentially assessed metal-chelating and free radical scavenging activities, respectively. Mild conditions were set up to specifically modify Cys and Met residues by N-ethylmaleimide (NEM) and chloramine T treatments, respectively. We found that Met and Cys accounted for 40-80% of total antioxidant activity of HSA. Copper binding to HSA was decreased by about 50% with c…

Time FactorsAntioxidantFree Radicalsmedicine.medical_treatmentDithionitrobenzoic AcidHemolysisBiochemistryAntioxidantsTosyl Compoundschemistry.chemical_compoundMethioninemedicineHumansChelationCysteineSerum AlbuminMethionineDose-Response Relationship DrugChloraminesFree Radical ScavengersGeneral MedicineFree radical scavengerHuman serum albuminmedicine.diseaseHemolysisLipoproteins LDLOxygenOxidative StresschemistryBiochemistryEthylmaleimideChloramine-TOxidation-ReductionCopperPhenanthrolinesProtein Bindingmedicine.drugCysteineFree Radical Research
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Gold Nanoparticles Supported on Nanoparticulate Ceria as a Powerful Agent against Intracellular Oxidative Stress

2012

Ceria-supported gold nanoparticles are prepared exhibiting peroxidase activity and acting as radical traps. Au/CeO2 shows a remarkable biocompatibility as demonstrated by measuring cellular viability, proliferation, and lack of apoptosis for two human cell lines (Hep3B and HeLa). The antioxidant activity of Au/CeO2 against reactive oxygen species (ROS) is demonstrated by studying the cellular behavior of Hep3B and HeLa in a model of cellular oxidative stress. It is determined that Au/CeO2 exhibits higher antioxidant activity than glutathione, the main cytosolic antioxidant compound, and its CeO2 carrier. Overall the result presented here shows the potential of implementing well-established …

Time FactorsAntioxidantMaterials scienceBiocompatibilityCell SurvivalPolymersPeroxidase activitymedicine.medical_treatmentMetal NanoparticlesApoptosisBiocompatible MaterialsIntracellular oxidative stressmedicine.disease_causeAntioxidantsCatalysisCell LineBiomaterialsHeLachemistry.chemical_compoundCeriaQUIMICA ORGANICAmedicineHumansNanotechnologyGold nanoparticlesGeneral Materials ScienceCell Proliferationchemistry.chemical_classificationReactive oxygen speciesbiologyGeneral ChemistryGlutathionebiology.organism_classificationOxidative StressNanomedicinePeroxidasesBiochemistrychemistryColloidal goldNanoparticlesGoldReactive Oxygen SpeciesIntracellularOxidative stressHeLa CellsBiotechnologySmall
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Cardiovascular effects of air pollution

2017

Air pollution is composed of particulate matter (PM) and gaseous pollutants, such as nitrogen dioxide and ozone. PM is classified according to size into coarse particles (PM 10), fine particles (PM 2.5) and ultrafine particles. We aim to provide an original review of the scientific evidence from epidemiological and experimental studies examining the cardiovascular effects of outdoor air pollution. Pooled epidemiological studies reported that a 10 μg/m 3 increase in long-term exposure to PM 2.5 was associated with an 11% increase in cardiovascular mortality. Increased cardiovascular mortality was also related to long-term and short-term exposure to nitrogen dioxide. Exposure to air pollution…

Time FactorsCardiovascular mortalityOzoneair pollutionAir pollution030204 cardiovascular system & hematology010501 environmental sciencesmedicine.disease_causeCardiovascular SystemRisk Assessment01 natural sciencesArticleToxicology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRisk FactorsEnvironmental healthUltrafine particleAnimalsHumansoxidative stressMedicineNitrogen dioxidePlatelet activationBlood CoagulationAir quality index0105 earth and related environmental sciencesparticulate matterPollutantAir Pollutantsbusiness.industryEnvironmental ExposureGeneral MedicineParticulatesPrognosisPlaque Atheroscleroticmyocardial infarctionchemistryCardiovascular DiseasesReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessArchives of Cardiovascular Diseases
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Does low concentration mycotoxin exposure induce toxicity in HepG2 cells through oxidative stress?

2020

The purpose of this study was to determine whether exposure to low concentrations of deoxynivalenol (DON), T-2 toxin (T-2) and patulin (PAT) in a human hepatocellular carcinoma cell line (HepG2) exerts toxic effects through mechanisms related to oxidative stress, and how cells deal with such exposure. Cell viability was determined by the MTT and protein content (PC) assays over 24, 48 and 72 h. The IC

Time FactorsCell SurvivalHealth Toxicology and MutagenesisMitochondria LiverHepatic carcinoma010501 environmental sciencesToxicologymedicine.disease_cause01 natural sciencesPatulinInhibitory Concentration 5003 medical and health scienceschemistry.chemical_compoundmedicineHumansMycotoxinVolume concentration0105 earth and related environmental sciencesMembrane Potential Mitochondrial0303 health sciencesDose-Response Relationship DrugToxinChemistry030302 biochemistry & molecular biologyfood and beveragesHep G2 CellsMycotoxinsMolecular biologydigestive system diseasesOxidative StressT-2 ToxinPatulinHepg2 cellsToxicityHepatocytesLipid PeroxidationReactive Oxygen SpeciesTrichothecenesOxidative stressToxicology Mechanisms and Methods
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pRb suppresses camptothecin-induced apoptosis in human osteosarcoma Saos-2 cells by inhibiting c-Jun N-terminal kinase

2001

AbstractThis paper studies the cytotoxic effect induced by the topoisomerase I inhibitor camptothecin in human osteosarcoma Saos-2 cells, which lack p53 and contain a non-functional form of the product of the retinoblastoma gene, pRb. Cytotoxicity induced by camptothecin was dose- and time-dependent; the treatment with 100 nM camptothecin reduced cell viability by 50% at 32 h and by 75% at 72 h of exposure. The cytotoxic effect was caused by apoptosis, as ascertained by morphological evidence, acridine orange-ethidium bromide staining and flow cytometric analysis. Apoptosis was accompanied by both the activation of caspase-3 and the fragmentation of poly(ADP-ribose) polymerase. Treatment wi…

Time FactorsCell SurvivalProto-Oncogene Proteins c-junBlotting WesternBiophysicsApoptosisBiologyTransfectionRetinoblastoma ProteinBiochemistryStructural BiologyTumor Cells CulturedpRb JNK topoisomerase I inhibitors osteosarcomaGeneticsmedicineHumansCytotoxic T cellViability assayPhosphorylationFragmentation (cell biology)neoplasmsMolecular BiologySaos-2 cellsc-Jun N-terminal kinaseCell SizeDose-Response Relationship DrugCaspase 3Cell growthCell Cyclec-junJNK Mitogen-Activated Protein KinasesHydrogen PeroxideCell BiologyFlow CytometryGlutathioneMolecular biologyEnzyme ActivationOxidative StresspRbDNA Topoisomerases Type IApoptosisCaspasesCamptothecinMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesTopoisomerase I InhibitorsCamptothecinmedicine.drugFEBS Letters
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Cadmium regulation of apoptotic and stress response genes in tumoral and immortalized epithelial cells of the human breast

2008

Cadmium (Cd) is a widely-disseminated metal which can be imported and accumulated in living cells thereby drastically interfering with their biological mechanisms. Increasing interest has been recently focused on the elucidation of the cellular and molecular aspects of Cd-dependent regulation of gene expression and signal transduction pathways in different model system. Concerning breast cancer, very limited studies have been produced so far on the role played by Cd on estrogen receptor-negative human breast cancer cells, that are expected to be insensitive to the already-proven metallo-estrogenic effect exerted by Cd on the estrogen receptor-positive cell counterparts. Here, we have examin…

Time FactorsCellApoptosisBiologyBiochemistryHsp27Cell Line TumorHeat shock proteincadmium apoptosis stress response tumor cells human breastmedicineAnimalsHumansBreastSettore BIO/06 - Anatomia Comparata E CitologiaRegulation of gene expressionDose-Response Relationship DrugEpithelial CellsGeneral MedicineMolecular biologyCell biologyGene Expression Regulation NeoplasticOxidative StressSettore BIO/18 - Geneticamedicine.anatomical_structureReceptors EstrogenApoptosisCell cultureCancer cellbiology.proteinCattleEnvironmental PollutantsSignal transductionCadmium
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''Deferoxamine blocks death induced by glutathione depletion in PC 12 cells''

2013

Chouraqui, E. | Leon, A. | Repesse, Y. | Prigent-Tessier, A. | Bouhallab, S. | Bougle, D. | Marie, C. | Duval, D.; International audience; ''The purpose of the present work was to investigate the mechanisms by which glutathione depletion induced by treatment with buthionine sulfoximine (BSO) led within 24-30 h to PC 12 cells apoptosis. Our results showed that treatment by relatively low concentrations (10-30 mu M) of deferoxamine (DFx), a natural iron-specific chelator, almost completely shielded the cells from BSO-induced toxicity and that DFx still remained protective when added up to 9-12 h after BSO treatment. On the other hand, phosphopeptides derived from milk casein and known to carr…

Time FactorsIronApoptosisDeferoxaminePharmacologyIron Chelating AgentsToxicologymedicine.disease_causePC12 Cellschemistry.chemical_compoundOXIDATIVE-STRESSPARKINSONS-DISEASECaseinmedicineAnimalsHomeostasisButhionine sulfoximineButhionine SulfoximineNeuronsCELLULAR IRONDose-Response Relationship DrugbiologyChemistryGeneral NeuroscienceGlutathioneGlutathioneIRON CHELATORRatsDeferoxamineFerritinSYMPATHETIC NEURONSISCHEMIC-STROKEBiochemistryBRAIN IRONCELLULAR IRON''CytoprotectionApoptosisToxicity[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinSERUM DEPRIVATIONHEME OXYGENASE-1NEURODEGENERATIVE DISORDERSOxidative stress''OXIDATIVE-STRESSmedicine.drug
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Comprehensive transcriptional analysis of the oxidative response in yeast

2008

The oxidative stress response in Saccharomyces cerevisiae has been analyzed by parallel determination of mRNA levels and transcription rates for the entire genome. A mathematical algorithm has been adapted for a dynamic situation such as the response to stress, to calculate theoretical mRNA decay rates from the experimental data. Yeast genes have been grouped into 25 clusters according to mRNA level and transcription rate kinetics, and average mRNA decay rates have been calculated for each cluster. In most of the genes, changes in one or both experimentally determined parameters occur during the stress response. 24% of the genes are transcriptionally induced without an increase inmRNAlevels…

Time FactorsTranscription GeneticSaccharomyces cerevisiaeResponse elementSaccharomyces cerevisiaeBiochemistryModels BiologicalEvolution MolecularFungal ProteinsTranscription (biology)Gene Expression Regulation FungalP-bodiesProtein biosynthesisCluster AnalysisRNA MessengerRRNA processingMolecular BiologyGeneMessenger RNAbiologyCell Biologybiology.organism_classificationMolecular biologyCell biologyOxygenKineticsOxidative StressModels ChemicalRNARibosomes
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Oxidative stress responses and lipid peroxidation damage are induced during dehydration in the production of dry active wine yeasts.

2009

The tolerance of the yeast Saccharomyces cerevisiae to desiccation is important for the use of this microorganism in the wine industry, since active dry wine yeast is routinely used as starter for must fermentations. Many studies have shown the complexity of the cellular effects caused by water loss, including oxidative injuries on macromolecular components. However the technological interest of yeast drying was not addressed in those studies, and the dehydration conditions were far from the industrial practice. In the present study a molecular approach was used to characterize the relevant injuring conditions during pilot plant dehydrations under two different drying temperatures (i.e., 35…

Time FactorsWineSaccharomyces cerevisiaeBiologymedicine.disease_causeMicrobiologyLipid peroxidationchemistry.chemical_compoundIndustrial MicrobiologyGlutaredoxinGene Expression Regulation FungalmedicineBiomassDesiccationWinemakingWinefood and beveragesGeneral MedicineGlutathioneYeastYeast in winemakingOxidative StressBiochemistrychemistryFermentationLipid PeroxidationOxidation-ReductionOxidative stressFood ScienceInternational journal of food microbiology
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Transcriptional activation of apurinic/apyrimidinic endonuclease (Ape, Ref-1) by oxidative stress requires CREB.

1999

Abstract Apurinic/apyrimidinic endonuclease (APE alias Ref-1) is a multifunctional enzyme involved in DNA repair and redox regulation of transcription factors (e.g., AP-1). It also acts as a repressor of its own and other genes. Recently, it was shown that the level of APE mRNA and protein is enhanced upon treatment of cells with oxidative agents, such as hydrogen peroxide (H 2 O 2 ), which gives rise to an adaptive response of cells to oxidative stress. Induction of APE is due to APE promoter activation. To elucidate the mechanism of transcriptional activation of APE by oxidative agents, we introduced mutations into the cloned human APE promoter and checked its activity in transient transf…

Transcription GeneticDNA repairProto-Oncogene Proteins c-junvirusesCarbon-Oxygen LyasesBiophysicsRepressorContext (language use)CHO CellsCREBTransfectionBiochemistryPolymerase Chain ReactionEndonucleasestomatognathic systemCricetinaeDNA-(Apurinic or Apyrimidinic Site) LyaseAnimalsHumansAP siteBinding siteCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticMolecular BiologyTranscription factorBinding SitesbiologyActivating Transcription Factor 2social sciencesCell BiologyHydrogen PeroxideOxidantsMolecular biologybody regionsOxidative Stressbiology.proteinMutagenesis Site-DirectedTranscription FactorsBiochemical and biophysical research communications
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