Search results for "Active oxygen"

showing 10 items of 884 documents

Trans-10, cis-12 conjugated linoleic acid induced cell death in human colon cancer cells through reactive oxygen species-mediated ER stress

2013

Dietary conjugated linoleic acids (CLA) are fatty acid isomers with anticancer activities produced naturally in ruminants or from vegetable oil processing. The anticancer effects of CLA differ upon the cancer origin and the CLA isomers. In this study, we carried out to precise the effects of CLA isomers, c9,t11 and t10,c12 CLA, on mechanisms of cell death induction in colon cancer cells. We first showed that only t10,c12 CLA treatment (25 and 50μM) for 72h triggered apoptosis in colon cancer cells without affecting viability of normal-derived colon epithelial cells. Exposure of colon cancer cells to t10,c12 CLA activated ER stress characterized by induction of eIF2α phoshorylation, splicing…

Programmed cell deathConjugated linoleic acidCHOPBiologychemistry.chemical_compoundCell Line TumormedicineHumansCytotoxic T cellLinoleic Acids ConjugatedMolecular BiologyCell ProliferationCell Deathintegumentary systemReverse Transcriptase Polymerase Chain Reactionfood and beveragesCancerCell BiologyEndoplasmic Reticulum Stressmedicine.diseaseImmunohistochemistrychemistryBiochemistryCell cultureApoptosisCancer cellCancer researchlipids (amino acids peptides and proteins)Reactive Oxygen SpeciesBiochimica et Biophysica Acta (BBA) - Molecular and Cell Biology of Lipids
researchProduct

Comparative analysis of stress responses of H9c2 rat cardiomyoblasts following treatment with doxorubicin and tBOOH

2011

Abstract Cardiotoxicity is the major dose-limiting adverse effect of anthracyclines and is hypothesized to result from damage induced by reactive oxygen species (ROS) or inhibition of topoisomerase II. Here, we comparatively analyzed the effect of doxorubicin and the organic peroxide tertiary-butylhydroperoxide (tBOOH) on stress responses of rat cardiomyblast cells (H9c2). Moreover, we investigated the impact of serum factors and the novel prototypical protein kinase CK2 inhibitor resorufin on the sensentivity of H9c2 cells exposed to doxorubicin or tBOOH. Measuring cell viability by use of the WST assay as well as cell cycle progression and apoptotic death by FACS-based methods, we found t…

Programmed cell deathDNA damageCell SurvivalAntineoplastic AgentsApoptosisBiologyPharmacologyAntioxidantsCell Linetert-ButylhydroperoxidemedicineAnimalsDoxorubicinViability assayCytotoxicitychemistry.chemical_classificationReactive oxygen speciesCardiotoxicityDose-Response Relationship DrugKinaseCell BiologyMolecular biologyAcetylcysteineRatsOxidative StresschemistryDoxorubicinReactive Oxygen SpeciesMyoblasts Cardiacmedicine.drug
researchProduct

Deglycosylated bleomycin induces apoptosis in lymphoma cell via c-jun NH2-terminal kinase but not reactive oxygen species

2007

Bleomycin (BLM) has demonstrated potent activity in treating malignant lymphomas but its therapeutic efficacy is hampered by induction of lung fibrosis. This side effect is related to the ability of the drug to generate reactive oxygen species in lung cells. In the present study, we evaluated the consequences of deglycosylation of BLM in term of cytotoxic activity and generation of reactive oxygen species. When tested on U937 human lymphoma cells, both compounds generated a typical apoptotic phenotype. Cell death induction was associated with Bax oligomerization, dissipation of the mitochondrial membrane potential, release of cytochrome c, caspase activation, chromatin condensation and inte…

Programmed cell deathFas Ligand ProteinLymphomaCellApoptosisDNA FragmentationBiologymedicine.disease_causeBiochemistryTNF-Related Apoptosis-Inducing LigandBleomycinmedicineHumansDeath domainPharmacologychemistry.chemical_classificationReactive oxygen speciesAntibiotics AntineoplasticU937 cellCytochrome cJNK Mitogen-Activated Protein KinasesU937 CellsMolecular biologymedicine.anatomical_structurechemistryBiochemistryApoptosisCaspasesbiology.proteinReactive Oxygen SpeciesOxidative stressBiochemical Pharmacology
researchProduct

A novel pro-apoptotic role of zinc octacarboxyphthalocyanine in melanoma me45 cancer cell's photodynamic therapy (PDT)

2018

Abstract Zn-based phthalocyanine acts as drug or photosensitizer in photodynamic therapy (PDT) for the treatment of cancer cells. The activated zinc octacarboxyphthalocyanine (ZnPcOC) reacts with oxygen, to generate reactive oxygen species for the damage of melanoma cancer cells, Me45. This in vitro study aimed at investigating the cytotoxic effects of different concentrations of ZnPcOC activated with a diode laser (λ = 685 nm) on Me45, and normal human fibroblast cells, NHDF. To perform this study 104 cells/ml were seeded in 96-well plates and allowed to attach overnight, after which cells were treated with different concentrations of ZnPcOC (10, 20 and 30 μM). After 4 h, cells were irradi…

Programmed cell deathIndolesCell Survivalmedicine.medical_treatmentPhotodynamic therapy (PDT)030303 biophysicsBiophysicsApoptosisPhotodynamic therapy02 engineering and technologyIsoindolesZinc octacarboxyphthalocyanine (ZnPcOC)PhotosensitizersCell Line03 medical and health sciencesCell Line TumorOrganometallic CompoundsmedicineHumansCytotoxic T cellRadiology Nuclear Medicine and imagingPhotosensitizerViability assayMelanoma0303 health sciencesPhotosensitizing AgentsRadiationRadiological and Ultrasound TechnologyChemistryMelanomaReactive oxygen species (ROS)UV–Vis spectraFibroblasts021001 nanoscience & nanotechnologymedicine.diseasePhotochemotherapyZinc CompoundsApoptosisCancer cellCancer researchMelanoma Me45 cancer cellsLasers SemiconductorPro-apoptotic activityReactive Oxygen Species0210 nano-technologyJournal of Photochemistry and Photobiology B-Biology
researchProduct

Iron Metabolism in the Tumor Microenvironment-Implications for Anti-Cancer Immune Response

2021

New insights into the field of iron metabolism within the tumor microenvironment have been uncovered in recent years. Iron promotes the production of reactive oxygen species, which may either trigger ferroptosis cell death or contribute to malignant transformation. Once transformed, cancer cells divert tumor-infiltrating immune cells to satisfy their iron demand, thus affecting the tumor immunosurveillance. In this review, we highlight how the bioavailability of this metal shapes complex metabolic pathways within the tumor microenvironment and how this affects both tumor-associated macrophages and tumor-infiltrating lymphocytes functions. Furthermore, we discuss the potentials as well as th…

Programmed cell deathIronReviewMalignant transformationImmune systemNeoplasmsTumor MicroenvironmentmedicineHumanscanceriron metabolismlcsh:QH301-705.5chemistry.chemical_classificationReactive oxygen speciesTumor microenvironmentInnate immune systemImmunityCancerGeneral Medicinemedicine.diseaseferroptosisferroptosiadaptive immune response tumor microenvironmentlcsh:Biology (General)chemistryCancer cellCancer researchinnate immune response
researchProduct

Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
researchProduct

Targeting the mitochondrial pathway to induce apoptosis/necrosis through ROS by a newly developed Schiff’s base to overcome MDR in cancer

2011

Abstract Multidrug resistance (MDR) in cancer, a major obstacle to successful application of cancer chemotherapy, is often characterized by over-expression of multidrug resistance-related proteins such as MRP1, P-gp or elevated glutathione (GSH) level. Efflux of drugs by functional P-gp, MRP1 and elevated GSH level can confer resistance to apoptosis induced by a range of different stimuli. Therefore, it is necessary to develop new cell death inducers with relatively lower toxicity toward non-malignant cells that can overcome MDR by induction of apoptotic or non-apoptotic cell death pathways. Herein we report the synthesis and spectroscopic characterization of a GSH depleting, redox active S…

Programmed cell deathMagnetic Resonance SpectroscopyNecrosisApoptosisMitochondrionBiologymedicine.disease_causeBiochemistryEhrlich ascites carcinomaMiceNecrosisCell Line TumorNeoplasmsSpectroscopy Fourier Transform InfraredmedicineAnimalsCytotoxic T cellCytotoxicitySchiff BasesCalpainCaspase 3General MedicineFlow CytometryGlutathioneMitochondriaBiochemistryDrug Resistance NeoplasmApoptosisCancer researchCalciumSpectrophotometry Ultravioletmedicine.symptomReactive Oxygen SpeciesOxidative stressBiochimie
researchProduct

Lysosomal degradation of the carboxydextran shell of coated superparamagnetic iron oxide nanoparticles and the fate of professional phagocytes

2010

Contrast agents based on dextran-coated superparamagnetic iron oxide nanoparticles (SPIO) are internalized by professional phagocytes such as hepatic Kupffer cells, yet their role in phagocyte biology remains largely unknown. Here we investigated the effects of the SPIO ferucarbotran on murine Kupffer cells and human macrophages. Intravenous injection of ferucarbotran into mice led to rapid accumulation of the particles in phagocytes and to long-lasting increased iron deposition in liver and kidneys. Macrophages incorporate ferucarbotran in lysosomal vesicles containing α-glucosidase, which is capable of degrading the carboxydextran shell of the ferucarbotran particles. Intravenous injectio…

Programmed cell deathMaterials sciencePhagocyteKupffer Cellsmedicine.medical_treatmentIntracellular SpaceBiophysicsApoptosisBioengineeringProinflammatory cytokineBiomaterialsMiceEdaravonemedicineAnimalsHumansMacrophageMagnetite Nanoparticleschemistry.chemical_classificationPhagocytesReactive oxygen speciesTumor Necrosis Factor-alphaDextransFree Radical ScavengersMagnetic Resonance ImagingCell biologyKineticsmedicine.anatomical_structureCytokineLiverchemistryBiochemistryMechanics of MaterialsApoptosisCeramics and CompositesNanoparticlesTumor necrosis factor alphaLysosomesReactive Oxygen SpeciesAntipyrineBiomaterials
researchProduct

Zinc accelerates respiratory burst termination in human PMN

2021

The respiratory burst of phagocytes is essential for human survival. Innate immune defence against pathogens relies strongly on reactive oxygen species (ROS) production by the NADPH oxidase (NOX2). ROS kill pathogens while the translocation of electrons across the plasma membrane via NOX2 depolarizes the cell. Simultaneously, protons are released into the cytosol. Here, we compare freshly isolated human polymorphonuclear leukocytes (PMN) to the granulocytes-like cell line PLB 985. We are recording ROS production while inhibiting the charge compensating and pH regulating voltage-gated proton channel (HV1). The data suggests that human PMN and the PLB 985 generate ROS via a general mechanism,…

Programmed cell deathMedicine (General)PhagocyteQH301-705.5NeutrophilsClinical BiochemistryBiochemistryIon ChannelsFlow cytometryR5-920medicineHumansPhagocyte ; Zinc ; Zinkstoffwechsel ; pH ; H<sub>v</sub>1 ; ROSBiology (General)HV1Respiratory Burstchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseInnate immune systembiologymedicine.diagnostic_testChemistrypHOrganic ChemistryNADPH OxidasesROSCell biologyRespiratory burstCytosolZincmedicine.anatomical_structurePhagocytebiology.proteinReactive Oxygen SpeciesResearch Paper
researchProduct

Induction of oxiapoptophagy, a mixed mode of cell death associated with oxidative stress, apoptosis and autophagy, on 7-ketocholesterol-treated 158N …

2013

7-Ketocholesterol (7KC) has been suggested to induce a complex mode of cell death on monocytic cells: oxiapoptophagy (OXIdation, APOPTOsis, and autoPHAGY) (Monier et al. (2003) [12]). The aim of the present study, realized on 158N murine oligodendrocytes, was to bring new evidence on this mixed form of cell death. On 158N cells, 7KC induces an overproduction of reactive oxygen species (ROS) revealed by dihydroethidium staining, a loss of transmembrane mitochondrial potential measured with DiOC6(3), caspase-3 activation, and condensation and/or fragmentation of the nuclei which are typical criteria of oxidative stress and apoptosis. Moreover, 7KC enhances cytoplamic membrane permeability to …

Programmed cell deathMembrane permeabilityalpha-TocopherolBiophysicsApoptosisBiologymedicine.disease_causeBiochemistrychemistry.chemical_compoundMicemedicineAutophagyAnimalsMicroscopy Phase-ContrastPropidium iodideFragmentation (cell biology)Molecular BiologyKetocholesterolsCells Culturedchemistry.chemical_classificationReactive oxygen speciesCell DeathDose-Response Relationship DrugAutophagyCell BiologyCell biologyOligodendrogliaOxidative StresschemistryApoptosisMicrotubule-Associated ProteinsOxidative stressBiochemical and biophysical research communications
researchProduct