Search results for "Dative"

showing 10 items of 2381 documents

Transcriptomic study of the toxic mechanism triggered by beauvericin in Jurkat cells

2018

Beauvericin (BEA), an ionophoric cyclic hexadepsipeptide mycotoxin, is able to increase oxidative stress by altering membrane ion permeability and uncoupling oxidative phosphorylation. A toxicogenomic study was performed to investigate gene expression changes triggered by BEA exposure (1.5, 3 and 5 mu M; 24 h) in Jurkat cells through RNA-sequencing and differential gene expression analysis. Perturbed gene expression was observed in a concentration dependent manner, with 43 differentially expressed genes (DEGs) overlapped in the three studied concentrations. Gene ontology (GO) analysis showed several biological processes related to electron transport chain, oxidative phosphorylation, and cel…

0301 basic medicineProgrammed cell deathCYTOCHROME-C RELEASEBCL-2 FAMILYCell Membrane PermeabilityRespiratory chainCell Culture TechniquesCASPASE-3 ACTIVATIONApoptosisOxidative phosphorylationCHO-K1 CELLSToxicologyJurkat cellsOxidative PhosphorylationElectron Transport03 medical and health sciencesJurkat CellsFUSARIUM MYCOTOXINSImmunotoxicologyDepsipeptidesHumansREAL-TIME PCROXIDATIVE STRESSTranscriptomicsCaspaseINDUCED APOPTOSISLEUKEMIA-CELLS030102 biochemistry & molecular biologybiologyDose-Response Relationship DrugChemistryJurkatGene Expression ProfilingBcl-2 familyDEATHGeneral MedicineBeauvericinToxicogenomicsCell biologyGene expression profiling030104 developmental biologyMitochondrial respiratory chainGene Ontologybiology.proteinRNA-seqTranscriptomeToxicology Letters
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Oxytosis/Ferroptosis—(Re-) Emerging Roles for Oxidative Stress-Dependent Non-apoptotic Cell Death in Diseases of the Central Nervous System

2018

Although nerve cell death is the hallmark of many neurological diseases, the processes underlying this death are still poorly defined. However, there is a general consensus that neuronal cell death predominantly proceeds by regulated processes. Almost 30 years ago, a cell death pathway eventually named oxytosis was described in neuronal cells that involved glutathione depletion, reactive oxygen species production, lipoxygenase activation, and calcium influx. More recently, a cell death pathway that involved many of the same steps was described in tumor cells and termed ferroptosis due to a dependence on iron. Since then there has been a great deal of discussion in the literature about wheth…

0301 basic medicineProgrammed cell deathCell typebrain diseasesCentral nervous systemReviewoxytosisBiologymedicine.disease_causelcsh:RC321-57103 medical and health sciencesironmedicineoxidative stresslcsh:Neurosciences. Biological psychiatry. Neuropsychiatryprogrammed cell deathchemistry.chemical_classificationReactive oxygen speciesGeneral NeuroscienceFerroptosisBrain Diseases ; Ferroptosis ; Iron ; Oxidative Stress ; Oxytosis ; Programmed Cell Deathferroptosis030104 developmental biologymedicine.anatomical_structurechemistryApoptotic cell deathNeuroscienceCalcium influxOxidative stressNeuroscienceFrontiers in Neuroscience
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The Phytochemical Indicaxanthin Synergistically Enhances Cisplatin-Induced Apoptosis in HeLa Cells via Oxidative Stress-Dependent p53/p21waf1 Axis

2020

Combining phytochemicals with chemotherapics is an emerging strategy to treat cancer to overcome drug toxicity and resistance with natural compounds. We assessed the effects of indicaxanthin (Ind), a pigment obtained from Opuntia ficus-indica (L. Mill) fruit, combined with cisplatin (CDDP) against cervical cancer cells (HeLa). Measured cell viability via Trypan blue assay

0301 basic medicineProgrammed cell deathCelllcsh:QR1-502indicaxanthincisplatinCell morphologyBiochemistrylcsh:MicrobiologyHeLa03 medical and health sciences0302 clinical medicinemedicineoxidative stresscancerViability assayMolecular BiologybiologyChemistryfood and beveragesCell cyclebiology.organism_classificationphytochemicalsMolecular biology030104 developmental biologymedicine.anatomical_structureApoptosis030220 oncology & carcinogenesis<i>Opuntia ficus indica</i> (L. Mill)Cancer cellOpuntia ficus indica (L. Mill)combo-therapyBiomolecules
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2021

While the importance of the iron-load of lipocalin-2 (Lcn-2) in promoting tumor progression is widely appreciated, underlying molecular mechanisms largely remain elusive. Considering its role as an iron-transporter, we aimed at clarifying iron-loaded, holo-Lcn-2 (hLcn-2)-dependent signaling pathways in affecting renal cancer cell viability. Applying RNA sequencing analysis in renal CAKI1 tumor cells to explore highly upregulated molecular signatures in response to hLcn-2, we identified a cluster of genes (SLC7A11, GCLM, GLS), which are implicated in regulating ferroptosis. Indeed, hLcn-2-stimulated cells are protected from erastin-induced ferroptosis. We also noticed a rapid increase in rea…

0301 basic medicineProgrammed cell deathChemistryGCLMEndocrinology Diabetes and Metabolismmedicine.disease_causeBiochemistry03 medical and health sciences030104 developmental biology0302 clinical medicineDownregulation and upregulationTumor progression030220 oncology & carcinogenesisCancer cellCancer researchmedicineIntegrated stress responseSignal transductionMolecular BiologyOxidative stressMetabolites
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Glutathione in metastases: From mechanisms to clinical applications.

2016

Metastatic spread, not primary tumors, is the leading cause of cancer death. Glutathione (γ-glutamyl-cysteinyl-glycine, GSH) is particularly relevant in cancer cells as it is involved in regulating carcinogenic mechanisms, growth and dissemination, and multidrug and radiation resistance. Upon interaction of metastatic cells with the vascular endothelium, a high percentage of metastatic cells with high GSH levels survive the combined nitrosative and oxidative stresses elicited by the vascular endothelium. GSH release from different organs, mainly the liver, and its interorgan transport through the blood circulation to metastatic foci, promote their growth. This review focuses on the relation…

0301 basic medicineProgrammed cell deathClinical BiochemistryCancer therapyOxidative phosphorylationBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineMetastatic cellNeoplasmsmedicineAnimalsHumansNeoplasm MetastasisCarcinogenBiochemistry (medical)CancerGlutathionemedicine.diseaseGlutathione030104 developmental biologychemistry030220 oncology & carcinogenesisCancer cellImmunologyCancer researchCritical reviews in clinical laboratory sciences
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Docosahexaenoic Acid Attenuates Mitochondrial Alterations and Oxidative Stress Leading to Cell Death Induced by Very Long-Chain Fatty Acids in a Mous…

2020

In the case of neurodegenerative pathologies, the therapeutic arsenal available is often directed towards the consequences of the disease. The purpose of this study is, therefore, to evaluate the ability of docosahexaenoic acid (DHA), a molecule present in certain foods and considered to have health benefits, to inhibit the cytotoxic effects of very long-chain fatty acids (C24:0, C26:0), which can contribute to the development of some neurodegenerative diseases. The effect of DHA (50 &micro

0301 basic medicineProgrammed cell deathDocosahexaenoic AcidsCell SurvivalVery long chain fatty acidoligodendrocytesvery long-chain fatty acidmedicine.disease_causeCatalysisArticleCell Linelcsh:ChemistryInorganic Chemistry03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicinemedicineAnimalsViability assayPropidium iodidePhysical and Theoretical Chemistrylcsh:QH301-705.5Molecular BiologySpectroscopyMembrane Potential MitochondrialOrganic ChemistryAutophagyFatty Acidsfood and beveragesGeneral Medicinelipotoxicitydocosahexaenoic acidComputer Science ApplicationsCell biologyMitochondriaOligodendrogliaOxidative Stress030104 developmental biologylcsh:Biology (General)lcsh:QD1-999chemistryLipotoxicityDocosahexaenoic acidModels Animallipids (amino acids peptides and proteins)Reactive Oxygen Species030217 neurology & neurosurgeryOxidative stressInternational Journal of Molecular Sciences
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Peroxisome proliferator-activated receptor-γ coactivator-1α mediates neuroprotection against excitotoxic brain injury in transgenic mice: role of mit…

2016

Peroxisome proliferator-activated receptor gamma coactivator-1α (PGC-1α) is a transcriptional coactivator involved in the regulation of mitochondrial biogenesis and cell defense. The functions of PGC-1α in physiology of brain mitochondria are, however, not fully understood. To address this we have studied wild-type and transgenic mice with a two-fold overexpression of PGC-1α in brain neurons. Data showed that the relative number and basal respiration of brain mitochondria were increased in PGC-1α transgenic mice compared with wild-type mitochondria. These changes occurred concomitantly with altered levels of proteins involved in oxidative phosphorylation (OXPHOS) as studied by proteomi…

0301 basic medicineProgrammed cell deathKainic acidTransgenebcl-X ProteinPeroxisome proliferator-activated receptorBiologyInhibitor of apoptosisSettore BIO/09 - FisiologiaNeuroprotectionOxidative PhosphorylationInhibitor of Apoptosis ProteinsMice03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineBrain InjurieInhibitor of Apoptosis ProteinAnimalsCA1 Region HippocampalCells CulturedNeuronschemistry.chemical_classificationNeuroscience (all)Kainic AcidCell DeathAnimalNeuron survivalGeneral NeuroscienceProteomicXIAP; Kainic acid; Mitochondria; Neuron survival; PGC-1α; Proteomics; Animals; Brain Injuries; CA1 Region Hippocampal; Cell Death; Cells Cultured; Inhibitor of Apoptosis Proteins; Kainic Acid; Mice; Mitochondria; Neurons; Oxidative Phosphorylation; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha; Proto-Oncogene Proteins c-bcl-2; bcl-X Protein; Neuroscience (all)NeuronPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyXIAP030104 developmental biologyProto-Oncogene Proteins c-bcl-2chemistryMitochondrial biogenesisBrain InjuriesImmunologyPGC-1α030217 neurology & neurosurgeryEuropean Journal of Neuroscience
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The anti-cancer drug doxorubicin induces substantial epigenetic changes in cultured cardiomyocytes.

2019

Abstract The anthracycline doxorubicin (DOX) is widely used in cancer therapy with the limitation of cardiotoxicity leading to the development of congestive heart failure. DOX-induced oxidative stress and changes of the phosphoproteome as well as epigenome were described but the exact mechanisms of the adverse long-term effects are still elusive. Here, we tested the impact of DOX treatment on cell death, oxidative stress parameters and expression profiles of proteins involved in epigenetic pathways in a cardiomyocyte cell culture model. Markers of oxidative stress, apoptosis and expression of proteins involved in epigenetic processes were assessed by immunoblotting in cultured rat myoblasts…

0301 basic medicineProgrammed cell deathMethyltransferaseApoptosisToxicologymedicine.disease_causeHistone DeacetylasesEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicinemedicineAnimalsMyocytes CardiacEpigeneticsCells CulturedHistone DemethylasesAntibiotics AntineoplasticbiologyDose-Response Relationship DrugHistone deacetylase 2ChemistryGeneral MedicineEpigenomeHydrogen PeroxideCardiotoxicityCell biologyRatsOxidative Stress030104 developmental biologyHistoneAcetylationDoxorubicin030220 oncology & carcinogenesisbiology.proteinOxidative stressBiomarkersChemico-biological interactions
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Taking up the cudgels for the traditional reactive oxygen and nitrogen species detection assays and their use in the cardiovascular system

2017

Reactive oxygen and nitrogen species (RONS such as H2O2, nitric oxide) confer redox regulation of essential cellular functions (e.g. differentiation, proliferation, migration, apoptosis), initiate and catalyze adaptive stress responses. In contrast, excessive formation of RONS caused by impaired break-down by cellular antioxidant systems and/or insufficient repair of the resulting oxidative damage of biomolecules may lead to appreciable impairment of cellular function and in the worst case to cell death, organ dysfunction and severe disease phenotypes of the entire organism. Therefore, the knowledge of the severity of oxidative stress and tissue specific localization is of great biological …

0301 basic medicineProgrammed cell deathRedox signalingClinical BiochemistrySevere diseaseReview ArticleBiologymedicine.disease_causeCardiovascular SystemBiochemistry03 medical and health sciencesPhysiology (medical)medicineDihydroethidium oxidative fluorescence microtopographyAnimalsHumanslcsh:QH301-705.5Organismchemistry.chemical_classificationlcsh:R5-920Reactive oxygen speciesFluorescence and chemiluminescence-based assaysOrganic ChemistrySpecies detectionNADPH OxidasesPhenotypeReactive Nitrogen SpeciesOxidative Stress030104 developmental biologylcsh:Biology (General)chemistryBiochemistryL-012-enhanced chemiluminescenceLuminescent MeasurementsLucigenin-enhanced chemiluminescencelcsh:Medicine (General)Reactive Oxygen SpeciesNeuroscienceOxidation-ReductionFunction (biology)Oxidative stressFree Radical Biology and Medicine
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Anticancer activity of biogenerated silver nanoparticles: an integrated proteomic investigation

2018

Silver nanoparticles (AgNPs), embedded into a specific polysaccharide (EPS), were biogenerated by Klebsiella oxytoca DSM 29614 under aerobic (AgNPs-EPSaer) and anaerobic conditions (AgNPs-EPSanaer). Both AgNPs-EPS matrices were tested by MTT assay for cytotoxic activity against human breast (SKBR3 and 8701-BC) and colon (HT-29, HCT 116 and Caco-2) cancer cell lines, revealing AgNPs-EPSaer as the most active, in terms of IC50, with a more pronounced efficacy against breast cancer cell lines. Therefore, colony forming capability, morphological changes, generation of reactive oxygen species (ROS), induction of apoptosis and autophagy, inhibition of migratory and invasive capabilities and prote…

0301 basic medicineProgrammed cell deathSettore BIO/11 - Biologia MolecolareMitochondrionmedicine.disease_causeSettore BIO/19 - Microbiologia Generale03 medical and health sciencesproteomicsbreast cancer cellmedicineMTT assaySettore BIO/06 - Anatomia Comparata E Citologiabacteriachemistry.chemical_classificationAnticancer activity; Bacteria; Breast cancer cells; Proteomics; Silver nanoparticles (AgNPs); OncologyReactive oxygen speciesBreast cancer cellsChemistryAutophagysilver nanoparticles (AgNPs)Cell biology030104 developmental biologyanticancer activitysilver nanoparticles (AgNPs); bacteria; breast cancer cells; anticancer activity; proteomicsOncologyApoptosisSKBR3Oxidative stressResearch Paper
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