Search results for "CHON"

showing 10 items of 1866 documents

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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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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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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Characterization of cells with different mitochondrial membrane potential during apoptosis.

2005

Background Until now, the simultaneous analysis of several parameters during apoptosis, including DNA content and mitochondrial membrane potential (ΔΨ), has not been possible because of the spectral characteristics of the commonly used dyes. Using polychromatic flow cytometry based upon multiple laser and UV lamp excitation, we have characterized cells with different ΔΨ during apoptosis. Methods U937 cells were treated with the flavonoid quercetin (Qu) and stained with JC-1 to detect ΔΨ, propidium iodide (PI) for cell viability, Hoechst 33342 for DNA content, Annexin V conjugated with Alexa Fluor-647 for detection of phosphatidilserine (PS) exposure, marker of early apoptosis, or Mitotracke…

Programmed cell deathHistologyCell Membrane PermeabilityCell Survivalpolychromatic flow cytometry • mitochondrial membrane potential • apoptosis • JC-1 • propidium iodide • Hoechst • Annexin-VPopulationApoptosisHL-60 CellsDNA FragmentationPhosphatidylserinesBiologyPathology and Forensic MedicineFlow cytometryMembrane Potentialschemistry.chemical_compoundAnnexinCell Line TumormedicineHumansViability assayPropidium iodideeducationFluorescent Dyeseducation.field_of_studymedicine.diagnostic_testDaunorubicinCell BiologyDNAIntracellular MembranesU937 CellsCarbocyaninesFlow CytometryMolecular biologyMitochondriachemistryApoptosisCell cultureDoxorubicinLeukocytes MononuclearBenzimidazolesQuercetinCytometry. Part A : the journal of the International Society for Analytical Cytology
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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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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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Synthesis of a new class of pyrrolo[3,4-h]quinazolines with antimitotic activity

2014

Abstract A new series of pyrrolo[3,4- h ]quinazolines was conveniently prepared with a broad substitution pattern. A large number of derivatives was obtained and the cellular cytotoxicity was evaluated in vitro against 5 different human tumor cell lines with GI 50 values reaching the low micromolar level (1.3–19.8 μM). These compounds were able to induce cell death mainly by apoptosis through a mitochondrial dependent pathway. Selected compounds showed antimitotic activity and a reduction of tubulin polymerization in a concentration-dependent manner. Moreover, they showed anti-angiogenic properties since reduced in vitro endothelial cell migration and disrupted HUVEC capillary-like tube net…

Programmed cell deathMitosisAntiproliferative activityCell Line TumorDrug DiscoveryHuman Umbilical Vein Endothelial CellsPiHumansTubulin polymerizationPyrrolesPyrrolo[3Cell-mediated cytotoxicityPyrrolo[34-h]quinazolines Antiproliferative activity Antimitotic activity Tubulin polymerization Vascular disrupting activityTubulin polymerizationVascular disrupting activityPharmacologyMatrigelCell Death4-h]quinazolinesChemistryAntimitotic activityOrganic ChemistryGeneral MedicineSettore CHIM/08 - Chimica FarmaceuticaMitochondriaEndothelial stem cellBiochemistryCell cultureApoptosisPyrrolo[3; 4-h]quinazolines; Antiproliferative activity; Antimitotic activity; Tubulin polymerization; Vascular disrupting activityQuinazolinesLysosomes
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Differential Roles of JNK in ConA/GalN and ConA-Induced Liver Injury in Mice

2008

Tumor necrosis factor-alpha-mediated liver injury can be induced by several different means; however, the signaling events and mechanisms of cell death are likely different. We investigated the mechanism of both apoptotic and necrotic hepatocyte cell death as well as the role of c-Jun NH2-terminal kinase (JNK) in the ConA and ConA/D-galactosamine (GalN) models of murine liver injury. ConA alone induced primarily necrotic cell death with no caspase activation, whereas ConA/GalN induced apoptosis in addition to necrotic cell death. The bi-modal death pattern in the ConA/GalN model was confirmed by the use of transgenic mice expressing a dominant-negative form of Fas-associated death domain in…

Programmed cell deathNecrosisFas-Associated Death Domain ProteinApoptosisGalactosamineMitochondria Liverchemical and pharmacologic phenomenaCaspase 8Pathology and Forensic MedicineMiceNecrosisConcanavalin AmedicineAnimalsPhosphorylationDeath domainLiver injuryCaspase 8biologyLiver DiseasesJNK Mitogen-Activated Protein Kinasesmedicine.diseaseMolecular biologyEnzyme ActivationMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureConcanavalin AApoptosisHepatocytebiology.proteinMutant ProteinsChemical and Drug Induced Liver Injurymedicine.symptomGene DeletionRegular ArticlesBH3 Interacting Domain Death Agonist ProteinThe American Journal of Pathology
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Lipids Nutrients in Parkinson and Alzheimer’s Diseases: Cell Death and Cytoprotection

2020

Neurodegenerative diseases, particularly Parkinson’s and Alzheimer’s, have common features: protein accumulation, cell death with mitochondrial involvement and oxidative stress. Patients are treated to cure the symptoms, but the treatments do not target the causes; so, the disease is not stopped. It is interesting to look at the side of nutrition which could help prevent the first signs of the disease or slow its progression in addition to existing therapeutic strategies. Lipids, whether in the form of vegetable or animal oils or in the form of fatty acids, could be incorporated into diets with the aim of preventing neurodegenerative diseases. These different lipids can inhibit the cytotoxi…

Programmed cell deathParkinson's diseaseInflammationReviewDiseasePharmacologyMitochondrionmedicine.disease_causelipids nutrientsCatalysislcsh:ChemistryInorganic ChemistrysynucleinFish OilsAlzheimer DiseaseHumansPlant OilsMedicinePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopybusiness.industryFatty AcidsOrganic ChemistryapoptosisamyloidParkinson DiseaseNutrientsGeneral Medicinemedicine.diseaseLipidsCytoprotectionComputer Science ApplicationsmitochondriaOxidative Stresslcsh:Biology (General)lcsh:QD1-999CytoprotectionParkinson’s diseaseSynucleinTaumedicine.symptombusinessAlzheimer’s diseaseOxidative stressInternational Journal of Molecular Sciences
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Studies on the subcellular pathophysiology of acute lethal cell injury.

1974

Summary In this paper we have summarized the effects of acute lethal injury on the cell. Such injuries are defined as injuries that result in cell death within a relatively short period of time usually minutes or hours. Following death; the cell undergoes necrosis. Ultrastructural and biochemical methods are needed to study pathophysiology. The cell passes through a series of stages numbered 1 through 7. Stages 1 through 4 are reversible while 5 through 7 are irreversible. Injuries resulting in acute cell death and necrosis include direct damage to the cell membrane, for example by antibody and complement or non-penetrating mercurials or interference with mitochondrial energy supply as in i…

Programmed cell deathPathologymedicine.medical_specialtyNecrosisTime FactorsCell SurvivalCellsCellIschemiaMitochondrionBiologyPermeabilityPathology and Forensic MedicineCell Physiological PhenomenaCell membraneKidney Tubules Proximal03 medical and health sciencesNecrosis0302 clinical medicineIschemiamedicineAnimalsHypoxia030304 developmental biology0303 health sciencesCell MembraneGeneral MedicineHypoxia (medical)medicine.diseasePathophysiology3. Good healthMitochondriaRatsMicroscopy Electronmedicine.anatomical_structuremedicine.symptomMitochondrial Swelling030217 neurology & neurosurgeryBeitrage zur Pathologie
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