Search results for "REACTIVE OXYGEN SPECIES"

showing 10 items of 879 documents

Synthesis and In Vitro Evaluation of a Photosensitizer-BODIPY Derivative for Potential Photodynamic Therapy Applications

2015

A new photosensitizer (1) based on the 4,4-difluoro-4-bora-3a,4a-diaza-s-indacene (BODIPY) scaffold has been synthesized. 1 is water soluble and showed an intense absorption band at 490 nm (e=77600 cm-1M-1) and an emission at 514 nm. In vitro toxicity of 1 in the presence of light and in darkness has been studied with HeLa, HaCaT, MCF-7, and SCC-13 cell lines. Moreover, internalization studies of 1 in these cell lines were also performed. These results suggested that 1 is more toxic for SCC-13 and HeLa carcinoma cells than for the HaCaT noncancerous immortal human keratinocytes. Toxicity upon light irradiation was due to the formation of singlet oxygen and reactive oxygen species (ROS). Cel…

Boron CompoundsLightmedicine.medical_treatmentBodipyPhotodynamic therapyPhotochemistrysensorsBiochemistryHeLachemistry.chemical_compoundQUIMICA ORGANICACell Line TumormedicineBIOQUIMICA Y BIOLOGIA MOLECULARHumansPhotosensitizerchemistry.chemical_classificationReactive oxygen speciesPhotosensitizing AgentsphotochemistryMolecular StructureSinglet OxygenbiologySinglet oxygenEndoplasmic reticulumOrganic ChemistryQUIMICA INORGANICAGeneral Chemistrybiology.organism_classificationHaCaTPhotochemotherapychemistryphotodynamic therapyfluorescenceBODIPYReactive Oxygen Species
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Regulation and role of nitric oxide production in Arabidopsis thaliana defense responses induced by oligogalacturonides

2014

SPEIPM; International audience

Botrytis cinereaArabidopsis thalianaPlant defense[SDV.BV]Life Sciences [q-bio]/Vegetal BiologyNitric oxideCalcium[SDV.BV] Life Sciences [q-bio]/Vegetal BiologyOligogalacturonidesReactive oxygen speciesNitrate reductase
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Effects of cadmium chloride on some mitochondria-related activity and gene expression of human MDA-MB231 breast tumor cells.

2007

It was reported that cadmium is able to exert a cytotoxic effect on tumor MDA-MB231 cells, which shows signs of "non-classical" apoptosis and is characterized by drastic changes in gene expression pattern. In this study, we have extended our knowledge of metal-breast cancer cell interactions by analyzing some mitochondria-related aspects of the stress response to CdCl(2) at either 5 or 50 microM 24- or 96-h exposure, by cytochemical, conventional PCR and Northern/Western blot techniques. We demonstrated that (i) no modification of the mitochondrial mass was detectable due to CdCl(2) exposure; (ii) the respiration activity appeared to be increased after 96-h exposures, while the production o…

Breast cancer Cadmium MitochondriaAntineoplastic AgentsApoptosisBreast NeoplasmsMitochondrionCadmium chlorideBiochemistryElectron Transport Complex IVMitochondrial Proteinscadmium mitochondria breast tumor cellsInorganic Chemistrychemistry.chemical_compoundCadmium ChlorideWestern blotCell Line TumorGene expressionmedicineHumansCytochrome c oxidaseSettore BIO/06 - Anatomia Comparata E CitologiaHeat-Shock Proteinsbiologymedicine.diagnostic_testChemistryMolecular biologyMitochondriaOxidative StressGene Expression RegulationApoptosisbiology.proteinHSP60Reactive Oxygen SpeciesIntracellular
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Multiple in vitro and in vivo regulatory effects of budesonide in CD4+ T lymphocyte subpopulations of allergic asthmatics.

2012

Abstract BACKGROUND: Increased activation and increased survival of T lymphocytes characterise bronchial asthma. OBJECTIVES: In this study the effect of budesonide on T cell survival, on inducible co-stimulator T cells (ICOS), on Foxp3 and on IL-10 molecules in T lymphocyte sub-populations was assessed. METHODS: Cell survival (by annexin V binding) and ICOS in total lymphocytes, in CD4+/CD25+ and in CD4+/CD25- and Foxp3 and IL-10 in CD4+/CD25+ and in CD4+/CD25-cells was evaluated, by cytofluorimetric analysis, in mild intermittent asthmatics (n = 19) and in controls (n = 15). Allergen induced T lymphocyte proliferation and the in vivo effects of budesonide in mild persistent asthmatics (n =…

BudesonideCD4-Positive T-LymphocytesMalePulmonologylcsh:Medicineimmune system diseasesT-Lymphocyte SubsetsMolecular Cell Biologylcsh:ScienceBudesonidecigarette smoke airway epithelial cells reactive oxygen species.MultidisciplinaryT CellsAllergy and HypersensitivityClinical Pharmacologyhemic and immune systemsForkhead Transcription Factorsrespiratory systemMiddle AgedFlow CytometryBronchodilator AgentsInterleukin-10Interleukin 10MedicineFemalemedicine.drugResearch ArticleAdultDrugs and DevicesAdolescentCell SurvivalImmune CellsImmunologychemical and pharmacologic phenomenaInducible T-Cell Co-Stimulator ProteinImmunomodulationIn vivomedicineHumansInducible T-Cell Co-Stimulator ProteinBiologyAsthmaCell Proliferationbusiness.industrylcsh:RT lymphocytemedicine.diseaseIn vitroAsthmarespiratory tract diseasesApoptosisImmunologylcsh:QClinical ImmunologybusinessCytometryPloS one
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Cyclic AMP-mediated upregulation of the expression of neuronal NO synthase in human A673 neuroepithelioma cells results in a decrease in the level of…

2004

The expression level of neuronal nitric oxide synthase (nNOS) can vary depending on the (patho)physiological conditions. Here we document a marked induction of nNOS mRNA, protein, and total NO production in response to dibutyryl cyclic AMP (db-cAMP) in human A673 neuroepithelial cells. However, the upregulation of nNOS was associated with a decreased level of production of bioactive NO and by an increase in the level of generation of reactive oxygen species (ROS). ROS production could be prevented by the NOS inhibitor L-NAME, suggesting nNOS itself is involved in ROS generation. Sepiapterin supplementation of db-cAMP-treated A673 cells could restore full bioactive NO production, most likely…

CAMP-Responsive Element ModulatorNitric Oxide Synthase Type IBiologyCREBNitric OxideBiochemistryAdenylyl cyclaseCyclic AMP Response Element Modulatorchemistry.chemical_compoundMiceNeuroblastomaCoactivatorComplement C3b Inactivator ProteinsCyclic AMPAnimalsHumansNeuroectodermal Tumors Primitive PeripheralCREB-binding proteinEnzyme InhibitorsProtein kinase AeducationCyclic AMP Response Element-Binding ProteinGTP CyclohydrolaseCAMP response element bindingHomeodomain ProteinsNeuronseducation.field_of_studyForskolinPhosphoric Diester HydrolasesIntracellular Signaling Peptides and ProteinsBlood ProteinsLIM Domain ProteinsMolecular biologyCyclic AMP-Dependent Protein KinasesPterinsUp-RegulationDNA-Binding ProteinsRepressor ProteinsAntisense Elements (Genetics)NG-Nitroarginine Methyl EsterchemistryBucladesineGene Expression RegulationComplement Factor Hbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesSignal TransductionBiochemistry
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Histone deacetylase inhibition modulates deoxyribonucleotide pools and enhances the antitumor effects of the ribonucleotide reductase inhibitor 3’-C-…

2011

Histone deacetylase (HDAC) inhibitors are a new class of epigenetic agents that were reported to enhance the cytotoxic effects of classical anticancer drugs through multiple mechanisms. However, which of the possible drug combinations would be the most effective and clinically useful are to be determined. We treated the HL60 and NB4 promyelocytic leukaemia cells with a combination of the ribonucleotide reductase (RR) inhibitor 3'-C-methyladenosine (3'-Me-Ado) and several hydroxamic acid-derived HDAC inhibitors, including two recently synthesized molecules, MC1864 and MC1879, and the reference compound trichostatin A (TSA). The results showed significant growth inhibitory and apoptotic syner…

Cancer ResearchAdenosineHL60CellDeoxyribonucleotidesAntineoplastic AgentsApoptosisHL-60 CellsRibonucleotide reductase inhibitorBiologyHydroxamic AcidsHDAC inhibitors RR inhibitors Apoptosis Leukaemia ROSchemistry.chemical_compoundRibonucleotide ReductasesmedicineHumansCell ProliferationLeukemiaG1 PhaseCell cycleHistone Deacetylase InhibitorsRibonucleotide reductasemedicine.anatomical_structureTrichostatin AOncologychemistryApoptosisCancer researchSettore BIO/14 - FarmacologiaHistone deacetylaseReactive Oxygen Speciesmedicine.drug
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Role of glutathione in the induction of apoptosis and c-fos and c-jun mRNAs by oxidative stress in tumor cells.

2003

We have used two tumor cell clones (B9 and G2), derived from the methylcholanthrene-induced murine fibrosarcoma GR9 and normal BALB/c3T3 fibroblasts, to study the ability of t-BOOH derived reactive oxygen radicals to induce oxidative stress, apoptosis and c-fos and c-jun mRNA transcription. These clones differ in terms of their major histocompatibility complex (MHC) (H-2) class I genes expression, their tumor induction and metastatic potential and their reduced glutathione (GSH) levels. Incubation of both cell clones in the presence of t-BOOH results in the increase of 8-oxo-2'-deoxyguanosine (8-oxo-dG) and malondialdehyde and the decrease of GSH. The xenobiotic also induces the transcripti…

Cancer ResearchBALB 3T3 CellsTranscription GeneticProto-Oncogene Proteins c-junFibrosarcomaCellApoptosisBiologymedicine.disease_causeAntioxidantsSuperoxide dismutasechemistry.chemical_compoundMicetert-ButylhydroperoxideCell CloneMalondialdehydemedicineTumor Cells CulturedAnimalsRNA MessengerDNA Primerschemistry.chemical_classificationReactive oxygen speciesReverse Transcriptase Polymerase Chain Reactionc-junHistocompatibility Antigens Class IDeoxyguanosineGlutathioneFibroblastsMolecular biologyGlutathioneOxidative Stressmedicine.anatomical_structureOncologychemistryGene Expression RegulationApoptosis8-Hydroxy-2'-Deoxyguanosinebiology.proteinReactive Oxygen SpeciesProto-Oncogene Proteins c-fosOxidative stressCancer letters
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The novel NF-κB inhibitor DHMEQ synergizes with celecoxib to exert antitumor effects on human liver cancer cells by a ROS-dependent mechanism

2012

In a previous work of ours dehydroxymethyl-epoxyquinomicin (DHMEQ), an inhibitor of NF-κB, was shown to induce apoptosis through Reactive Oxygen Species (ROS) production in hepatoma cells. The present study demonstrated that DHMEQ cooperates with Celecoxib (CLX) to decrease NF-κB DNA binding and to inhibit cell growth and proliferation more effectively than treatment with these single agents alone in the hepatoma cell lines HA22T/VGH and Huh-6. ROS production induced by the DHMEQ-CLX combination in turn generated the expression of genes involved in endoplasmic reticulum (ER) stress and silencing TRB3 mRNA significantly decreased DHMEQ-CLX-induced cell growth inhibition. Moreover, the DHMEQ-…

Cancer ResearchCarcinoma HepatocellularAntineoplastic AgentsApoptosisCell Cycle ProteinsProtein Serine-Threonine KinasesBiologyDHMEQ Celecoxib NF-jB CD95/CD95L Liver cancer cellsCell Line TumorSurvivinHumansGene silencingfas ReceptorProtein kinase BCell ProliferationSulfonamidesGene knockdownCyclooxygenase 2 InhibitorsCyclohexanonesCell growthEndoplasmic reticulumLiver NeoplasmsNF-kappa BDrug SynergismEndoplasmic Reticulum StressMolecular biologyAcetylcysteineRepressor ProteinsOncologyCelecoxibCell cultureApoptosisBenzamidesCancer researchPyrazolesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesCancer Letters
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In human retinoblastoma Y79 cells okadaic acid-parthenolide co-treatment induces synergistic apoptotic effects, with PTEN as a key player.

2013

Retinoblastoma is the most common intraocular malignancy of childhood. In developing countries, treatment is limited, long-term survival rates are low and current chemotherapy causes significant morbidity to pediatric patients and significantly limits dosing. Therefore there is an urgent need to identify new therapeutic strategies to improve the clinical outcome of patients with retinoblastoma. here, we investigated the effects of two natural compounds okadaic acid (OKa) and parthenolide (PN) on human retinoblastoma Y79 cells. For the first time we showed that OKa/PN combination at subtoxic doses induces potent synergistic apoptotic effects accompanied by lowering in p-akt levels, increasin…

Cancer ResearchCell SurvivalGene ExpressionAntineoplastic AgentsApoptosisBiologychemistry.chemical_compoundSettore BIO/10 - BiochimicaCell Line TumorOkadaic AcidmedicinePTENCytotoxic T cellHumansParthenolideViability assayProtein kinase BCell ShapePharmacologyRetinoblastomaPTEN PhosphohydrolaseRetinoblastomaDrug SynergismProto-Oncogene Proteins c-mdm2Okadaic acidmedicine.diseaseGlutathioneOxidative StressOncologychemistryApoptosisCancer researchbiology.proteinMolecular Medicineretinoblastoma Y79 cells synergistic apoptotic effects oxidative stress natural drugs PTEN/Akt/Mdm2/p53 pathway parthenolide okadaic acid.Drug Screening Assays AntitumorTumor Suppressor Protein p53Reactive Oxygen SpeciesProtein Processing Post-TranslationalProto-Oncogene Proteins c-aktSesquiterpenesResearch PaperCancer biologytherapy
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Autophagy and mitochondrial alterations in human retinal pigment epithelial cells induced by ethanol: implications of 4-hydroxy-nonenal

2014

Retinal pigment epithelium has a crucial role in the physiology and pathophysiology of the retina due to its location and metabolism. Oxidative damage has been demonstrated as a pathogenic mechanism in several retinal diseases, and reactive oxygen species are certainly important by-products of ethanol (EtOH) metabolism. Autophagy has been shown to exert a protective effect in different cellular and animal models. Thus, in our model, EtOH treatment increases autophagy flux, in a concentration-dependent manner. Mitochondrial morphology seems to be clearly altered under EtOH exposure, leading to an apparent increase in mitochondrial fission. An increase in 2′,7′-dichlorofluorescein fluorescenc…

Cancer ResearchImmunologyApoptosisRetinal Pigment EpitheliumMitochondrionBiologymedicine.disease_causeCell LineLipid peroxidationCellular and Molecular Neurosciencechemistry.chemical_compoundRetinal DiseasesmedicineAutophagyHumanschemistry.chemical_classificationReactive oxygen speciesAldehydesRetinal pigment epitheliumEthanolAutophagyRetinalEpithelial CellsCell BiologyCell biologyMitochondriaOxidative Stressmedicine.anatomical_structurechemistryBiochemistryMitochondrial fissionOriginal ArticleReactive Oxygen SpeciesOxidative stressCell Death & Disease
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