Search results for "relationship"

showing 10 items of 3616 documents

Cytotoxicity and induction of DNA double-strand breaks by components leached from dental composites in primary human gingival fibroblasts

2012

Abstract Introduction The public interest steadily increases in the biological adverse effects caused by components released from resin-based dental restorations. Objective In this study, the cytotoxicity and the genotoxicity were investigated of following released components from dental resin restorations in human gingival fibroblasts (HGF): tetraethyleneglycol dimethacrylate (TEEGDMA), neopentylglycol dimethacrylate (Neopen), diphenyliodoniumchloride (DPIC), triphenyl-stibane (TPSB) and triphenylphosphane (TPP). Methods XTT based cell viability assay was used for cytotoxicity screening of substances. γ-H2AX assay was used for genotoxicity screening. In the γ-H2AX assay, HGFs were exposed …

Programmed cell deathMaterials scienceNecrosisCell SurvivalCell Culture TechniquesGingivaTetrazolium SaltsApoptosismedicine.disease_causeComposite ResinsCell LinePolyethylene GlycolsHistonesDental MaterialsNecrosisOnium CompoundsOrganophosphorus CompoundsPolymethacrylic AcidsMaterials TestingStilbenesmedicineHumansDNA Breaks Double-StrandedGeneral Materials ScienceViability assayCytotoxicityGeneral DentistryDose-Response Relationship DrugBiphenyl CompoundsFibroblastsMolecular biologyBiphenyl compoundMicroscopy FluorescenceMechanics of MaterialsApoptosisToxicityMethacrylatesIndicators and Reagentsmedicine.symptomGenotoxicityMutagensDental Materials
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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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Lovastatin attenuates ionizing radiation-induced normal tissue damage in vivo.

2009

Abstract Background and purpose HMG-CoA-reductase inhibitors (statins) are widely used lipid-lowering drugs. Moreover, they have pleiotropic effects on cellular stress responses, proliferation and apoptosis in vitro . Here, we investigated whether lovastatin attenuates acute and subchronic ionizing radiation-induced normal tissue toxicity in vivo . Materials and methods Four hours to 24h after total body irradiation (6Gy) of Balb/c mice, acute pro-inflammatory and pro-fibrotic responses were analyzed. To comprise subchronic radiation toxicity, mice were irradiated twice with 2.5Gy and analyses were performed 3weeks after the first radiation treatment. Molecular markers of inflammation and f…

Programmed cell deathPathologymedicine.medical_specialtyStatinmedicine.drug_classCell SurvivalPharmacologyRadiation DosageMiceRandom AllocationIn vivoFibrosisReference ValuesRadiation IonizingmedicineAnimalsHumansRadiology Nuclear Medicine and imagingLovastatinRNA MessengerRadiation InjuriesLungProbabilityMice Inbred BALB CChemistryTumor Necrosis Factor-alphaNF-kappa BDose-Response Relationship RadiationHematologymedicine.diseaseCTGFIntestinesDisease Models AnimalRadiation Injuries ExperimentalOncologyLiverApoptosisToxicitylipids (amino acids peptides and proteins)FemaleLovastatinHydroxymethylglutaryl-CoA Reductase InhibitorsInflammation Mediatorsmedicine.drugDNA DamageRadiotherapy and oncology : journal of the European Society for Therapeutic Radiology and Oncology
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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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Combined inhibition of Bcl-2 and NFκB synergistically induces cell death in cutaneous T-cell lymphoma.

2019

Abstract Therapeutic options for cutaneous T-cell lymphoma (CTCL) are limited and curative treatment regimens are not available. Thus, new targeted and well-tolerated therapeutic approaches are urgently needed. In this respect, we have recently shown that dimethyl fumerate (DMF) inhibits NF-κB acting as a survival factor in CTCL. Similarly, inhibition of the antiapoptotic protein B-cell lymphoma 2 (Bcl-2) has been shown to induce cell death in CTCL especially when combined with histone deacetylase inhibitors. Therefore, we hypothesized that inhibition of Bcl-2 should potentiate NF-κB inhibition in a novel combination treatment of CTCL. We show that, in vitro, the Bcl-2 inhibitors ABT-199 an…

Programmed cell deathT cellImmunologyAntineoplastic AgentsApoptosisBiochemistryMicehemic and lymphatic diseasesCell Line TumormedicineAnimalsHumansRNA Small InterferingCell ProliferationNeoplasm StagingCell DeathDose-Response Relationship Drugbusiness.industryCutaneous T-cell lymphomaNF-kappa BDrug SynergismCell BiologyHematologymedicine.diseaseXenograft Model Antitumor AssaysLymphomaLymphoma T-Cell CutaneousHistone Deacetylase InhibitorsDisease Models Animalmedicine.anatomical_structureProto-Oncogene Proteins c-bcl-2ApoptosisCell cultureCancer researchRNA InterferenceHistone deacetylaseSignal transductionbusinessProtein BindingBlood
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Coffee Silverskin and Spent Coffee Suitable as Neuroprotectors against Cell Death by Beauvericin and α-Zearalenol: Evaluating Strategies of Treatment

2021

Coffee silverskin and spent coffee have been evaluated in a neuroblastoma cell line (SH-SY5Y cells) against beauvericin (BEA) and α-zearalenol (α-ZEL)-induced cytotoxicity with different strategies of treatment. First, the direct treatment of mycotoxins and coffee by-products extracts in SH-SY5Y cells was assayed. IC50 values for α-ZEL were 20.8 and 14.0 µM for 48 h and 72 h, respectively and, for BEA only at 72 h, it was 2.5 µM. Afterwards, the pre-treatment with spent coffee obtained by boiling water increased cell viability for α-ZEL at 24 h and 48 h from 10% to 16% and from 25% to 30%, respectively

Programmed cell deathTime Factors030309 nutrition & dieteticsHealth Toxicology and Mutagenesislcsh:MedicineToxicologyCoffeeArticleSH-SY5Y cells03 medical and health scienceschemistry.chemical_compoundInhibitory Concentration 500404 agricultural biotechnologyCell Line TumorDepsipeptidesIc50 valuesHumansViability assayFood scienceCytotoxicityMycotoxinNeuroblastoma cell linespent coffeeNeurons0303 health sciencesCell DeathDose-Response Relationship DrugPlant Extractslcsh:Rbeauvericin04 agricultural and veterinary sciences040401 food scienceCytoprotectionBeauvericinNeuroprotective AgentschemistryCytoprotectionSeedsZeranolα-zearalenolcoffee silverskinToxins
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Effect of ultraviolet light, methyl methanesulfonate and ionizing radiation on the genotoxic response and apoptosis of mouse fibroblasts lacking c-Fo…

2001

c-Fos and p53 are DNA damage-inducible proteins that are involved in gene regulation, cell cycle checkpoint control and cell proliferation following exposure to genotoxic agents. To investigate comparatively the role of c-Fos and p53 in the maintenance of genomic stability and the induction of apoptosis, we generated mouse fibroblast cell lines from knockout mice deficient for either c-fos (fos -/-) or p53 (p53-/-) or for both gene products (fosp53-/-). The sensitivity of these established cell lines was compared with the corresponding wild-type cells as to the cytotoxic, clastogenic and apoptosis-inducing effects of ultraviolet (UV-C) light and methyl methanesulfonate (MMS). Additionally, …

Programmed cell deathTime FactorsCell cycle checkpointCell SurvivalUltraviolet RaysHealth Toxicology and MutagenesisBlotting WesternApoptosisBiologyToxicologyPolymerase Chain ReactionCell LineMiceNecrosischemistry.chemical_compoundRadiation IonizingGeneticsUltraviolet lightAnimalsCytotoxic T cellCells CulturedGenetics (clinical)Chromosome AberrationsMice KnockoutCell growthDose-Response Relationship RadiationFibroblastsBlotting NorthernMethyl MethanesulfonateMolecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutagensMutagenesis
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Cisplatin-induced apoptosis in 43-3B and 27-1 cells defective in nucleotide excision repair

2001

Cisplatin is a highly potent cytotoxic and genotoxic agent used in the chemotherapy of various types of tumors. Its cytotoxic effect is supposed to be due to the induction of intra- and interstrand DNA cross-links which are repaired via the nucleotide excision repair (NER) pathway. Here, we elucidated the mechanism of cisplatin-induced cytotoxicity in mutants derived from CHO-9 cells defective in NER. We compared 43-3B and 27-1 cells deficient for ERCC1 and ERCC3, respectively, with the corresponding wild-type and ERCC1 complemented 43-3B cells. It is shown that cells defective in ERCC1 are more sensitive than cells defective in ERCC3 with regard to cisplatin-induced reproductive cell death…

Programmed cell deathTime FactorsDNA RepairCell SurvivalPoly ADP ribose polymeraseBlotting WesternDown-RegulationApoptosisCHO CellsToxicologyCell LineNecrosisCricetinaeGeneticsmedicineAnimalsDrosophila ProteinsCytotoxic T cellMolecular BiologyCaspaseCisplatinCaspase 8Dose-Response Relationship DrugbiologyCaspase 3ProteinsEndonucleasesMolecular biologyCaspase 9DNA-Binding ProteinsEnzyme ActivationApoptosisCaspasesMutationbiology.proteinCancer researchCisplatinPoly(ADP-ribose) PolymerasesERCC1Nucleotide excision repairmedicine.drugMutation Research/DNA Repair
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Effect of flupirtine on cell death of human umbilical vein endothelial cells induced by reactive oxygen species.

1999

Abstract Flupirtine (KATADOLON®), known as a nonopiate centrally acting analgesic drug, was tested as to its potential to prevent apoptosis of human endothelial cells induced by reactive oxygen species (ROS). It was found that Flupirtine displayed no effect on viability and cell proliferation of human umbilical vein endothelial cells (HUVEC) up to a concentration of 10 μg/mL. Apoptosis, induced by ROS and generated by hypoxanthine/xanthine oxidase (EC 1.1.3.22) (HX/XOD) or t-butyl hydroperoxide, was reduced after preincubation with Flupirtine for 3 hr by 35% and 41%, respectively. The maximal cytoprotective effect against apoptosis was observed at a drug concentration of 1 to 3 μg/mL. Flow …

Programmed cell deathUmbilical VeinsXanthine OxidaseAminopyridinesDNA FragmentationPharmacologyBiochemistryXanthineUmbilical veinchemistry.chemical_compoundNecrosismedicineHumansXanthine oxidaseHypoxanthineCells CulturedPharmacologychemistry.chemical_classificationReactive oxygen speciesCell DeathDose-Response Relationship DrugCell growthchemistryBiochemistryApoptosisCalciumEndothelium VascularFlupirtineReactive Oxygen Speciesmedicine.drugBiochemical pharmacology
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