Search results for "MITO"

showing 10 items of 2513 documents

Biological activities of the LXRα and β agonist, 4β-hydroxycholesterol, and of its isomer, 4α-hydroxycholesterol, on oligodendrocytes: effects on cel…

2013

The biochemical and biological properties of 4β-hydroxycholesterol and of its isomer, 4α-hydroxycholesterol, are not well known. So, we determined the ability of 4α- and 4β-hydroxycholesterol to react with LXRα and LXRβ, and we characterized the activities of these oxysterols on oligodendrocytes which are myelin synthesizing cells. The effects of 4α- and 4β-hydroxycholesterol were studied on 158N murine oligodendrocytes to assess their activities on cell growth and viability, oxidative and inflammatory status. To this end different parameters were used: cell counting with trypan blue; identification of dead cells and cell cycle analysis with propidium iodide; evaluation of mitochondrial dep…

Programmed cell deathCell SurvivalBiologyBiochemistrychemistry.chemical_compoundMiceIsomerismpolycyclic compoundsmedicineAnimalsPropidium iodideProtein Structure QuaternaryCell ProliferationLiver X ReceptorsInflammationSuperoxideCell growthAcridine orangeDepolarizationGeneral MedicineOrphan Nuclear ReceptorsOligodendrocyteActinsHydroxycholesterolsCell biologyMitochondriaOligodendrogliamedicine.anatomical_structurechemistryCytokineslipids (amino acids peptides and proteins)Trypan blueProtein MultimerizationLysosomesReactive Oxygen SpeciesOxidation-ReductionBiochimie
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Regulation of tumour cell sensitivity to TNF-induced oxidative stress and cytotoxicity: Role of glutathione

1998

Glutathione (GSH) and the rate of cellular proliferation determine tumour cell sensitivity to tumour necrosis factor (TNF). Buthionine sulphoximine (BSO), a selective inhibitor of GSH synthesis, inhibits tumour growth and increases recombinant human TNF (rhTNF)-alpha cytoxicity in vitro. Administration of sublethal doses of rhTNF-alpha to Ehrlich ascites-tumour (EAT)-bearing mice induces oxidative stress (as measured by increases in intracellular peroxide levels, O2.- generation and mitochondrial GSSG). ATP-induced selective GSH depletion, when combined with rhTNF-alpha administration, affords a 61% inhibition of tumour growth and results in a significant extent of host survival. Administra…

Programmed cell deathCell SurvivalClinical BiochemistryMitochondrionPharmacologyBiologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesmedicineAnimalsHumansCarcinoma Ehrlich TumorGlutathione DisulfideTumor Necrosis Factor-alphaGeneral MedicineGlutathioneGlutathioneRecombinant ProteinsOxidative StresschemistryBiochemistryCancer cellMolecular MedicineGlutathione disulfideTumor necrosis factor alphaOxidative stressIntracellularBioFactors
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Molecular mechanisms of rosmarinic acid from Salvia miltiorrhiza in acute lymphoblastic leukemia cells

2015

Abstract Ethnopharmacological relevance Rosmarinic acid (RA), a major hydrosoluble bioactive compound found in the Chinese medicinal herb, Salvia miltiorrhiza Bunge, which has been used in traditional Chinese medicine to treat various diseases, including cancer. However, the mechanisms have not been fully elucidated. Aim of the study Guided by microarray hybridization and Ingenuity Pathway Analysis, we identified modes of action of rosmarinic acid (RA) isolated from S. miltiorrhiza on acute lymphoblastic leukemia cells. Materials and methods Microarray data were verified by independent methods: Real-time RT-PCR (mRNA expression), resazurin assay (cytotoxicity of RA towards parental CCRF-CEM…

Programmed cell deathCell SurvivalDNA damageNecroptosisCellAntineoplastic AgentsApoptosisSalvia miltiorrhizaPharmacologyCell morphologyDepsidesSalvia miltiorrhizaCell Line TumorDrug DiscoveryCell AdhesionmedicineHumansLymphocytesCells CulturedMembrane Potential MitochondrialPharmacologybusiness.industryGene Expression ProfilingCell CycleNF-kappa BPrecursor Cell Lymphoblastic Leukemia-LymphomaCell cycleMolecular biologyDrug Resistance MultipleMolecular Docking Simulationmedicine.anatomical_structureCinnamatesDrug Resistance NeoplasmApoptosisComet AssayReactive Oxygen SpeciesbusinessDNA DamageJournal of Ethnopharmacology
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Cytotoxicity of 40 Egyptian plant extracts targeting mechanisms of drug-resistant cancer cells

2019

Abstract Background The multidrug resistance (MDR) phenotype encounters a major challenge to the success of established chemotherapy in cancer patients. We hypothesized that cytotoxic medicinal plants with novel phytochemicals can overcome MDR and kill MDR-cells with similar efficacy as drug sensitive cells. Purpose We evaluated plant extracts from an unexplored ecosystem in Egypt with unusual climate and nutrient conditions for their activity against sensitive and multidrug-resistant cancer cell lines. Material and methods/study design Methylene chloride: methanol (1:1) and methanol: H2O (7:3) extracts of 40 plants were prepared resulting in a sum of 76 fraction containing compounds with v…

Programmed cell deathCell SurvivalPhytochemicalsPharmaceutical ScienceApoptosisCentaureaWithaniaPulicariaMagnoliopsida03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsDrug DiscoveryHumansCytotoxic T cellViability assayCytotoxicity030304 developmental biologyMembrane Potential MitochondrialPharmacology0303 health sciencesPlants MedicinalbiologyPlant ExtractsChemistryWithaniabiology.organism_classificationAntineoplastic Agents PhytogenicMolecular biologyDrug Resistance MultipleMultiple drug resistanceComplementary and alternative medicineDrug Resistance NeoplasmCell culture030220 oncology & carcinogenesisCancer cellMolecular MedicineEgyptReactive Oxygen SpeciesPhytotherapyPhytomedicine
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Poriferan survivin exhibits a conserved regulatory role in the interconnected pathways of cell cycle and apoptosis

2010

Survivin orchestrates intracellular pathways during cell division and apoptosis. Its central function as mitotic regulator and inhibitor of cell death has major implications for tumor cell proliferation. Analyses in early-branching Metazoa so far propose an exclusive role of survivin as a chromosomal passenger protein, whereas only later during evolution a complementary antiapoptotic function might have arisen, concurrent with increased organismal complexity. To lift the veil on the ancestral function(s) of this key regulator, a survivin-like protein (SURVL) of one of the earliest-branching metazoan taxa was identified and functionally characterized. SURVL of the sponge Suberites domuncula …

Programmed cell deathCell divisionRecombinant Fusion ProteinsMolecular Sequence DataApoptosisTransfectionCell LineInhibitor of Apoptosis ProteinsLipopeptidesSurvivinAnimalsHumansAmino Acid SequenceMolecular BiologyMitosisGeneticsOriginal PaperBase SequencebiologyCell CycleCell BiologyCell cyclebiology.organism_classificationCell biologySuberites domunculaCell cultureCaspasesSuberitesSequence AlignmentCell DivisionIntracellularCadmiumCell Death & Differentiation
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Heat shock proteins: essential proteins for apoptosis regulation

2008

Abstract Many different external and intrinsic apoptotic stimuli induce the accumulation in the cells of a set of proteins known as stress or heat shock proteins (HSPs). HSPs are conserved proteins present in both prokaryotes and eukaryotes. These proteins play an essential role as molecular chaperones by assisting the correct folding of nascent and stress-accumulated misfolded proteins, and by preventing their aggregation. HSPs have a protective function, that is they allow the cells to survive to otherwise lethal conditions. Various mechanisms have been proposed to account for the cytoprotective functions of HSPs. Several of these proteins have demonstrated to directly interact with compo…

Programmed cell deathCell signalingReviewsMitochondrionBiologyModels BiologicallysosomesLysosomeHeat shock proteindeath receptorsmedicineAnimalsHumansemerging chemotherapeutic treatmentsHeat-Shock ProteinsCell Deathhaematopoietic malignanciesapoptosiscell signallingCell BiologyMitochondriaNeoplasm ProteinsCell biologymedicine.anatomical_structurecaspasesHematologic Neoplasmsheat shock proteinsMolecular MedicineProtein foldingHSP60Signal transductionMolecular ChaperonesSignal TransductionJournal of Cellular and Molecular Medicine
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Variability of ecdysteroid-induced cell cycle alterations in Drosophila Kc sublines.

1987

. The cell cycle of two lines isolated from Drosophila Kc cells was followed by flow cytofluorometry and cell counting. The first line is the 8-9K clone which grew in a medium supplemented with 5% serum; the second, named subline Kc0, grew in a serum-free medium. The stationary phase is characterized by a G2 cell accumulation: 73% in the 8-9K clone and 50% in the Kc0 subline. When the medium was supplemented with the steroid moulting hormone 20-hydroxyecdysone, more than 90% of 8-9K cells and 65% of Kc0 cells were progressively arrested in G2. In the continuous presence of 20-hydroxyecdysone, most of the 8-9K cells remain G2-arrested; no massive G2 release into M was observed and only a few…

Programmed cell deathCellClone (cell biology)MitosisCell CountBiologyCell Linechemistry.chemical_compoundmedicineAnimalsInterphaseEcdysteroidCell CycleCell BiologyGeneral MedicineAnatomyDNACell cycleCell countingFlow CytometryMolecular biologyCulture Mediamedicine.anatomical_structureEcdysteronechemistryCell cultureDrosophilaMoultingCell and tissue kinetics
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GD3 ganglioside directly targets mitochondria in a bcl-2-controlled fashion.

2000

Lipid and glycolipid diffusible mediators are involved in the intracellular progression and amplification of apoptotic signals. GD3 ganglioside is rapidly synthesized from accumulated ceramide after the clustering of death-inducing receptors and triggers apoptosis. Here we show that GD3 induces dissipation of DeltaPsim and swelling of isolated mitochondria, which results in the mitochondrial release of cytochrome c, apoptosis inducing factor, and caspase 9. Soluble factors released from GD3-treated mitochondria are sufficient to trigger DNA fragmentation in isolated nuclei. All these effects can be blocked by cyclosporin A, suggesting that GD3 is acting at the level of the permeability tran…

Programmed cell deathCeramideApoptosisMitochondria LiverMitochondrionliverBiochemistryMembrane Potentialschemistry.chemical_compoundGangliosidesGeneticsAnimalsMolecular BiologySettore MED/04 - Patologia GeneralebiologyCytochrome cCaspase 9SialyltransferasesCell biologyRatsmitochondriaEnzyme ActivationchemistryMitochondrial permeability transition poreProto-Oncogene Proteins c-bcl-2ApoptosisCaspasesbiology.proteinCyclosporinecaspases; cyclosporine; proto-oncogene proteins c-bcl-2; sialyltransferases; caspase 9; rats; animals; enzyme activation; apoptosis; membrane potentials; gangliosides; mitochondria liver; subcellular fractionsApoptosis-inducing factorlipids (amino acids peptides and proteins)ApoptosomeBiotechnologySubcellular FractionsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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DNA damage-induced cell death by apoptosis

2006

Following the induction of DNA damage, a prominent route of cell inactivation is apoptosis. During the last ten years, specific DNA lesions that trigger apoptosis have been identified. These include O6-methylguanine, base N-alkylations, bulky DNA adducts, DNA cross-links and DNA double-strand breaks (DSBs). Repair of these lesions are important in preventing apoptosis. An exception is O6-methylguanine-thymine lesions, which require mismatch repair for triggering apoptosis. Apoptosis induced by many chemical genotoxins is the consequence of blockage of DNA replication, which leads to collapse of replication forks and DSB formation. These DSBs are thought to be crucial downstream apoptosis-tr…

Programmed cell deathDNA RepairDNA repairDNA damageApoptosisp38 Mitogen-Activated Protein KinasesAnimalsHumansE2F1Molecular BiologybiologyCaspase 2DNA replicationDNAProliferating cell nuclear antigenCaspasesbiology.proteinCancer researchMolecular MedicineDNA mismatch repairTumor Suppressor Protein p53biological phenomena cell phenomena and immunityProto-Oncogene Proteins c-aktAtaxia telangiectasia and Rad3 relatedDNA DamageMutagensSignal TransductionTrends in Molecular Medicine
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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
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