Search results for "Reactive"

showing 10 items of 1469 documents

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
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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
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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
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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
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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
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Targeting Mitochondria: A New Promising Approach for the Treatment of Liver Diseases

2010

Mitochondrial dysfunction acts as a common pathogenetic mechanism in several acute and chronic liver diseases, such as Alcoholic and Non-Alcoholic Fatty Liver Disease (NAFLD), drug-induced steatohepatitis, viral hepatitis, biliary cirrhosis, hepatocellular carcinoma, ischemia/reperfusion injury and transplant rejection. In particular mitochondrial uncoupling has been recently identified to play a determinant role in the pathogenesis of liver diseases by causing decrease of mitochondrial proton motive force and ATP depletion. Damaged mitochondria present defects in lipid homeostasis, bioenergetics impairment and overproduction of Reactive Oxygen Species (ROS), leading to lipid accumulation a…

Programmed cell deathMitochondrionBiologymedicine.disease_causeBiochemistryLiver diseaseDrug Delivery SystemsDrug DiscoverymedicineAnimalsHumansPharmacologychemistry.chemical_classificationReactive oxygen speciesCell DeathLiver DiseasesOrganic ChemistryFatty livermedicine.diseaseMitochondriaOxidative StressBiochemistrychemistryCancer researchMolecular MedicineSteatohepatitisReactive Oxygen SpeciesReperfusion injuryOxidative stressCurrent Medicinal Chemistry
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ROS-Dependent ER Stress and Autophagy Mediate the Anti-Tumor Effects of Tributyltin (IV) Ferulate in Colon Cancer Cells

2020

Organotin compounds represent potential cancer therapeutics due to their pro-apoptotic action. We recently synthesized the novel organotin ferulic acid derivative tributyltin (IV) ferulate (TBT-F) and demonstrated that it displays anti-tumor properties in colon cancer cells related with autophagic cell death. The purpose of the present study was to elucidate the mechanism of TBT-F action in colon cancer cells. We specifically show that TBT-F-dependent autophagy is determined by a rapid generation of reactive oxygen species (ROS) and correlated with endoplasmic reticulum (ER) stress. TBT-F evoked nuclear factor erythroid-2 related factor 2 (Nrf2)-mediated antioxidant response and Nrf2 silenc…

Programmed cell deathNF-E2-Related Factor 2Glucose-regulated proteinApoptosismedicine.disease_causeArticleCatalysisInorganic Chemistrylcsh:ChemistrySettore BIO/10 - BiochimicaAutophagyTumor Cells CulturedmedicineHumansGene silencingoxidative stressPhysical and Theoretical ChemistryEndoplasmic Reticulum Chaperone BiPMolecular Biologylcsh:QH301-705.5tributyltin (IV) derivativeSpectroscopyCell Proliferationoxidative strebiologyChemistryEndoplasmic reticulumOrganic ChemistryAutophagyCancerROSGeneral Medicineendoplasmic reticulum stremedicine.diseaseComputer Science ApplicationsGene Expression Regulation Neoplasticlcsh:Biology (General)lcsh:QD1-999autophagic cell deathColonic NeoplasmsUnfolded protein responseCancer researchbiology.proteinendoplasmic reticulum stressTrialkyltin CompoundsReactive Oxygen SpeciesOxidative stress
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Cytotoxicity of ungeremine towards multi-factorial drug resistant cancer cells and induction of apoptosis, ferroptosis, necroptosis and autophagy

2018

Abstract Background Successful cancer chemotherapy is hampered by resistance of cancer cells to established anticancer drugs. Numerous natural products reveal cytotoxicity towards tumor cells. Purpose The present study was aimed to determine the cytotoxicity of a betaine-type alkaloid, ungeremine, towards 9 cancer cell lines including various sensitive and drug-resistant phenotypes. The mode of action of this compound was further investigated. Methods The cytotoxicity, ferroptotic and necroptotic cell death were determined by the resazurin reduction assay. Caspase activation was evaluated using the caspase-Glo assay. Flow cytometry was applied for the analysis of cell cycle analysis (PI sta…

Programmed cell deathNecroptosisPharmaceutical ScienceApoptosis03 medical and health sciencesAlkaloids0302 clinical medicineAnnexinCell Line TumorDrug DiscoveryAutophagyHumansCytotoxic T cellCytotoxicity030304 developmental biologyPharmacology0303 health sciencesCell DeathPlant ExtractsChemistryUngeremineIndolizinesAntineoplastic Agents PhytogenicDrug Resistance MultipleComplementary and alternative medicineDrug Resistance NeoplasmApoptosis030220 oncology & carcinogenesisCancer cellAmaryllidaceae AlkaloidsCancer researchMolecular MedicineReactive Oxygen SpeciesPhytomedicine
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Cytotoxicity of apigenin toward multiple myeloma cell lines and suppression of iNOS and COX-2 expression in STAT1-transfected HEK293 cells.

2020

Apigenin is one of the most abundant dietary flavonoids that possesses multiple bio-functions.This study was designed to determine the influence of apigenin on gene expressions, cancer cells, as well as STAT1/COX-2/iNOS pathway mediated inflammation and tumorigenesis in HEK293-STAT1 cells. Furthermore, the cytotoxic activity toward multiple myeloma (MM) cell lines was investigated.Bioinformatic analyses were used to predict the sensitivity and resistance of tumor cells toward apigenin and to determine cellular pathways influenced by this compound. The cytotoxic and ferroptotic activity of apigenin was examined by the resazurin reduction assay. Additionally, we evaluated apoptosis, and cell …

Programmed cell deathPharmaceutical ScienceNitric Oxide Synthase Type IIApoptosis03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDrug DiscoveryAntineoplastic Combined Chemotherapy ProtocolsAutophagyCytotoxic T cellHumansDAPIApigenin030304 developmental biologyCell ProliferationPharmacology0303 health sciencesDose-Response Relationship DrugChemistryCell CycleComputational BiologyCell cycleAntineoplastic Agents PhytogenicHEK293 CellsSTAT1 Transcription FactorComplementary and alternative medicineApoptosisCell cultureCyclooxygenase 2Doxorubicin030220 oncology & carcinogenesisApigeninCancer cellCancer researchMolecular MedicineMultiple MyelomaReactive Oxygen SpeciesPhytomedicine : international journal of phytotherapy and phytopharmacology
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Pyrazolo[3,4-h]quinolines promising photosensitizing agents in the treatment of cancer.

2015

A new series of pyrazolo[3,4-h]quinolines, heteroanalogues of angelicin was conveniently prepared with a broad substitution pattern. A large number of derivatives was obtained and the cellular photocytotoxicity was evaluated in vitro against 5 different human tumor cell lines with GI50 values reaching the nanomolar level (14.52e0.04 mM). Selected compounds were able to photoinduce a massive cell death with the involvement of mitochondria. Their photodamage cellular targets were proteins and lipids and they did not cause any kind of DNA photodamage. This latter event is of considerable importance in the modulation of long term side effects, generally associated with the use of classical furo…

Programmed cell deathPhotodynamic therapy; Antiproliferative activity; Photosensitizing agents; Reactive oxygen species; PUVA therapyPUVA therapymedicine.medical_treatmentPhotodynamic therapyAntineoplastic AgentsAntiproliferative activityPhotodynamic therapy Antiproliferative activity Photosensitizing agents Reactive oxygen species PUVA therapyMitochondrionPhotodynamic therapychemistry.chemical_compoundStructure-Activity RelationshipAngelicinCell Line TumorDrug DiscoverymedicineStructure–activity relationshipHumansCell ProliferationPharmacologyPhotosensitizing AgentsDose-Response Relationship DrugMolecular StructureCell growthOrganic ChemistryGeneral MedicinePhotosensitizing AgentSettore CHIM/08 - Chimica FarmaceuticaFurocoumarinsBiochemistrychemistryQuinolinesPyrazolesDrug Screening Assays AntitumorReactive oxygen speciesEuropean journal of medicinal chemistry
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