Search results for "Apoptosis"

showing 10 items of 1809 documents

Dibutyltin(IV) and Tributyltin(IV) Derivatives of meso-Tetra(4 sulfonatophenyl)porphine Inhibit the Growth and the Migration of Human Melanoma Cells.

2019

Melanoma is the most aggressive and deadly form of skin cancer, which is largely due to its propensity to metastasize. Therefore, with the aim to inhibit the growth and the metastatic dissemination of melanoma cells and to provide a novel treatment option, we studied the effects of the melanoma treatment with two organotin(IV) complexes of the meso-tetra(4-sulfonato-phenyl)porphine, namely (Bu2Sn)2TPPS and (Bu3Sn)4TPPS. In particular, we showed that nanomolar concentrations of (Bu2Sn)2TPPS and (Bu3Sn)4TPPS are sufficient to inhibit melanoma cell growth, to increase the expression of the full-length poly (ADP-ribose) polymerase (PARP-1), to induce the cell cycle arrest respectively at G2/M a…

0301 basic medicinePorphyrinsCellAntineoplastic AgentsApoptosisorganotin(IV)migrationArticleBRAF03 medical and health sciences0302 clinical medicineCyclin D1Cell MovementCell Line Tumormelanoma; organotin(IV); cellular growth; BRAF; cell cycle; migrationmedicinemelanomaHumansSTAT3Cell ProliferationDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryMelanomaCell migrationCell Cycle CheckpointsGeneral Medicinecellular growthCell cyclemedicine.disease030104 developmental biologymedicine.anatomical_structureFocal Adhesion Kinase 1030220 oncology & carcinogenesisbiology.proteinCancer researchcell cycleSkin cancerSignal Transduction
researchProduct

Autophagy as a defense strategy against stress: focus on Paracentrotus lividus sea urchin embryos exposed to cadmium

2015

Autophagy is used by organisms as a defense strategy to face environmental stress. This mechanism has been described as one of the most important intracellular pathways responsible for the degradation and recycling of proteins and organelles. It can act as a cell survival mechanism if the cellular damage is not too extensive or as a cell death mechanism if the damage/stress is irreversible; in the latter case, it can operate as an independent pathway or together with the apoptotic one. In this review, we discuss the autophagic process activated in several aquatic organisms exposed to different types of environmental stressors, focusing on the sea urchin embryo, a suitable system recently in…

0301 basic medicineProgrammed cell deathAquatic Organismsfood.ingredientEmbryo NonmammalianStreMini ReviewApoptosis; Autophagy; Cadmium; Defense strategies; Sea urchin embryos; Stress; Biochemistry; Cell BiologyApoptosisBiochemistryParacentrotus lividusToxicology03 medical and health scienceschemistry.chemical_compoundfoodStress PhysiologicalDefense strategieParacentrotusAutophagyAnimalsSettore BIO/06 - Anatomia Comparata E CitologiaSea urchin embryobiologyMechanism (biology)AutophagyApoptosiCell BiologyEnvironmental exposureEnvironmental Exposurebiology.organism_classificationAdaptation PhysiologicalCell biology030104 developmental biologychemistryParacentrotusIntracellularToxicantCadmium
researchProduct

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
researchProduct

Mechanisms of beauvericin toxicity and antioxidant cellular defense

2015

Beauvericin (BEA) is a secondary metabolite produced by many species of fungus Fusarium. This study determines the injury (cell viability, cell proliferation, mitochondrial membrane potential, cell death and DNA damage) and the intracellular defense mechanisms (catalase and superoxide dismutase) in Chinese Hamster ovary (CHO-K1) cells after BEA exposure. The results obtained in this study demonstrated that BEA induces cytotoxicity in a dose- and time-dependent manner in CHO-K1 cells. Moreover, disruption in mitochondrial enzymatic activity and cell proliferation has been observed after BEA exposure, which can lead or be consequence of cell death. BEA inhibits cell proliferation by arresting…

0301 basic medicineProgrammed cell deathCell SurvivalDNA damageApoptosisCHO CellsToxicologyAntioxidantsSuperoxide dismutase03 medical and health sciencesCricetulus0404 agricultural biotechnologyDepsipeptidesAnimalsViability assayCell ProliferationMembrane Potential MitochondrialbiologySuperoxide DismutaseCell growthChinese hamster ovary cell04 agricultural and veterinary sciencesGeneral MedicineCatalase040401 food scienceCell biology030104 developmental biologyBiochemistryApoptosisbiology.proteinIntracellularDNA DamageToxicology Letters
researchProduct

Neurotoxicity of zearalenone’s metabolites and beauvericin mycotoxins via apoptosis and cell cycle disruption

2021

Cell cycle progression and programmed cell death are imposed by pathological stimuli of extrinsic or intrinsic including the exposure to neurotoxins, oxidative stress and DNA damage. All can cause abrupt or delayed cell death, inactivate normal cell survival or cell death networks. Nevertheless, the mechanisms of the neuronal cell death are unresolved. One of the cell deaths triggers which have been wildly studied, correspond to mycotoxins produced by Fusarium species, which have been demonstrated cytotoxicity and neurotoxicity through impairing cell proliferation, gene expression and induction of oxidative stress. The aim of present study was to analyze the cell cycle progression and cell …

0301 basic medicineProgrammed cell deathCellPopulationApoptosisToxicology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell Line TumorDepsipeptidesmedicineHumansEstrogens Non-SteroidaleducationCell Proliferationeducation.field_of_studyCell growthCell CycleNeurotoxicityMycotoxinsCell cyclemedicine.diseaseMolecular biologyBeauvericin030104 developmental biologymedicine.anatomical_structurechemistryApoptosisZearalenone030217 neurology & neurosurgeryToxicology
researchProduct

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
researchProduct

Apoptosis of Hepatocytes: Relevance for HIV-Infected Patients under Treatment.

2021

Due to medical advances over the past few decades, human immunodeficiency virus (HIV) infection, once a devastatingly mortal pandemic, has become a manageable chronic condition. However, available antiretroviral treatments (cART) cannot fully restore immune health and, consequently, a number of inflammation-associated and/or immunodeficiency complications have manifested themselves in treated HIV-infected patients. Among these chronic, non-AIDS (acquired immune deficiency syndrome)-related conditions, liver disease is one of the deadliest, proving to be fatal for 15–17% of these individuals. Aside from the presence of liver-related comorbidities, including metabolic disturbances and co-infe…

0301 basic medicineProgrammed cell deathChronic conditionantiretroviral drugs; apoptosis; hepatic cell death; HIV; liver; toxicityInflammationApoptosisHIV InfectionsReviewliverModels Biological03 medical and health sciencesLiver disease0302 clinical medicineImmune systemAntiretroviral Therapy Highly ActivemedicineHumans030212 general & internal medicinelcsh:QH301-705.5antiretroviral drugsImmunodeficiencybusiness.industryapoptosisHIVtoxicityGeneral Medicinemedicine.diseasehepatic cell death030104 developmental biologylcsh:Biology (General)LiverApoptosisImmunologyUnfolded protein responseHepatocytesmedicine.symptombusinessCells
researchProduct

BAX inhibitor-1 is a Ca(2+) channel critically important for immune cell function and survival.

2015

The endoplasmic reticulum (ER) serves as the major intracellular Ca(2+) store and has a role in the synthesis and folding of proteins. BAX (BCL2-associated X protein) inhibitor-1 (BI-1) is a Ca(2+) leak channel also implicated in the response against protein misfolding, thereby connecting the Ca(2+) store and protein-folding functions of the ER. We found that BI-1-deficient mice suffer from leukopenia and erythrocytosis, have an increased number of splenic marginal zone B cells and higher abundance and nuclear translocation of NF-κB (nuclear factor-κ light-chain enhancer of activated B cells) proteins, correlating with increased cytosolic and ER Ca(2+) levels. When put into culture, purifie…

0301 basic medicineProgrammed cell deathCytoplasmEncephalomyelitis Autoimmune ExperimentalCell SurvivalT-LymphocytesActive Transport Cell NucleusApoptosisBiologyEndoplasmic Reticulum03 medical and health sciencesAnimalsCalcium SignalingObesityMolecular BiologyCalcium signalingMice KnockoutOriginal PaperB-LymphocytesBAX inhibitor 1Endoplasmic reticulumNF-kappa BMembrane ProteinsCell BiologyLeukopeniaNFKB1Acquired immune systemCell biologyEnzyme ActivationMice Inbred C57BLCytosol030104 developmental biologyApoptosisCaspasesCalciumFemaleSpleen
researchProduct

A naturally occuring triterpene saponin ardisiacrispin B displayed cytotoxic effects in multi-factorial drug resistant cancer cells via ferroptotic a…

2018

WOS: 000432722700010

0301 basic medicineProgrammed cell deathCytotoxicitySaponinPharmaceutical ScienceApoptosisFlow cytometryCell Cycle Distribution03 medical and health sciencesArdisiacrispin BCell Line TumorDrug DiscoverymedicineFerroptosisHumansCytotoxic T cellOleanolic AcidCytotoxicityCaspaseMembrane Potential MitochondrialPharmacologybiologymedicine.diagnostic_testMitochondrial Membrane PotentialChemistryHep G2 CellsSaponinsHCT116 Cellsmedicine.diseaseAntineoplastic Agents PhytogenicDrug Resistance MultipleLeukemia030104 developmental biologyComplementary and alternative medicineDoxorubicinDrug Resistance NeoplasmApoptosisCaspasesCancer cellbiology.proteinCancer researchMolecular MedicineReactive Oxygen SpeciesPhytomedicine
researchProduct

Triclosan-Evoked Neurotoxicity Involves NMDAR Subunits with the Specific Role of GluN2A in Caspase-3-Dependent Apoptosis

2018

Triclosan (TCS) is an antimicrobial agent that is used extensively in personal care and in sanitising products. A number of studies have shown the presence of TCS in different human tissues such as blood, adipose tissue, the liver, brain as well as in breast milk and urine. N-Methyl-D-aspartate receptors (NMDARs) are glutamate-gated ion channels that are widely expressed in the central nervous system and which play key roles in excitatory synaptic transmission. There is, however, no data on the involvement of NMDAR subunits in the apoptotic and neurotoxic effects of TCS. Our experiments are the first to show that TCS used at environmentally relevant concentrations evoked NMDA-dependent effe…

0301 basic medicineProgrammed cell deathGluN1Protein subunitNeurotoxinsNeuroscience (miscellaneous)Glutamic AcidCaspase 3ApoptosisReceptors N-Methyl-D-AspartateArticle03 medical and health sciencesCellular and Molecular NeuroscienceMice0302 clinical medicinemedicineAnimalsGene SilencingRNA MessengerReceptorNeuronsL-Lactate DehydrogenaseChemistryCaspase 3fungiNeurotoxicityROSTransfectionmedicine.diseaseTriclosanCell biologyGluN2BGluN2AProtein Subunits030104 developmental biologyNeurologyNMDAApoptosisNMDA receptorFemale030217 neurology & neurosurgeryMolecular Neurobiology
researchProduct