Search results for "MITOCHONDRION"

showing 10 items of 491 documents

Cajanol, a novel anticancer agent from Pigeonpea [Cajanus cajan (L.) Millsp.] roots, induces apoptosis in human breast cancer cells through a ROS-med…

2010

Cajanol (5-hydroxy-3-(4-hydroxy-2-methoxyphenyl)-7-methoxychroman-4-one) is an isoflavanone from Pigeonpea [Cajanus cajan (L.) Millsp.] roots. As the most effective phytoalexin in pigeonpea, the cytotoxic activity of cajanol towards cancer cells has not been report as yet. In the present study, the anticancer activity of cajanol towards MCF-7 human breast cancer cells was investigated. In order to explore the underlying mechanism of cell growth inhibition of cajanol, cell cycle distribution, DNA fragmentation assay and morphological assessment of nuclear change, ROS generation, mitochondrial membrane potential (DeltaPsim) disruption, and expression of caspase-3 and caspase-9, Bax, Bcl-2, PA…

Cell growthCytochrome cApoptosisBreast NeoplasmsGeneral MedicineMitochondrionCell cycleBiologyToxicologyFlow CytometryMolecular biologyAntineoplastic Agents PhytogenicIsoflavonesPlant RootsMitochondriaCajanusCell cultureApoptosisCell Line TumorCancer cellbiology.proteinCytotoxic T cellHumansFemaleReactive Oxygen SpeciesChemico-biological interactions
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Mitochondrial biogenesis in exercise and in ageing☆

2009

Mitochondrial biogenesis is critical for the normal function of cells. It is well known that mitochondria are produced and eventually after normal functioning they are degraded. Thus, the actual level of mitochondria in cells is dependent both on the synthesis and the degradation. Ever since the proposal of the mitochondrial theory of ageing by Jaime Miquel in the 70's, it was appreciated that mitochondria, which are both a target and a source of radicals in cells, are most important organelles to understand ageing. Thus, a common feature between cell physiology of ageing and exercise is that in both situations mitochondria are critical for normal cell functioning. Mitochondrial synthesis i…

Cell physiologySenescenceAgingmedicine.medical_specialtyMitochondrial DNAPharmaceutical ScienceTFAMMitochondrionBiologyAntioxidantsMitochondria MuscleCell biologyEndocrinologyMitochondrial biogenesisAgeingInternal medicinemedicineHumansNRF1Muscle SkeletalReactive Oxygen SpeciesExerciseAdvanced Drug Delivery Reviews
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Resveratrol reduces oxidative stress and cell death and increases mitochondrial antioxidants and XIAP in PC6.3-cells.

2010

Resveratrol, a polyphenol derived e.g. from red grapes, has been shown to mediate several positive biological actions such as protection of cells against oxidative stress. It can also influence cell signaling, but the mechanisms behind its antioxidant properties are largely unknown. Here we show that RSV reduces oxidative stress and enhances cell survival in PC6.3 cells depending on the concentration. In these cells, RSV increased the levels of antioxidants, SOD2 and TRX2, and of X chromosome-linked inhibitor of apoptosis protein. RSV also activated NFκB signaling as shown using luciferase reporter constructs. These findings show that RSV regulates oxidative stress and mitochondrial antioxi…

Cell signalingProgrammed cell deathBlotting WesternSOD2Settore BIO/11 - Biologia MolecolareApoptosisX-Linked Inhibitor of Apoptosis ProteinMitochondrionBiologyResveratrolmedicine.disease_causeInhibitor of apoptosisSettore BIO/09 - FisiologiaPolymerase Chain ReactionAntioxidantsCell LineMitochondrial Proteins03 medical and health scienceschemistry.chemical_compoundXIAP0302 clinical medicineThioredoxinsStilbenesmedicineTRX2Humans030304 developmental biologyNeurons0303 health sciencesSuperoxide DismutaseGeneral Neurosciencefood and beveragesROSSOD23. Good healthXIAPCell biologyMitochondriaOxidative StressBiochemistrychemistryResveratrolSettore BIO/14 - FarmacologiaOxidative stre030217 neurology & neurosurgeryOxidative stressNFκBNeuroscience letters
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PON3 is upregulated in cancer tissues and protects against mitochondrial superoxide-mediated cell death

2012

To achieve malignancy, cancer cells convert numerous signaling pathways, with evasion from cell death being a characteristic hallmark. The cell death machinery represents an anti-cancer target demanding constant identification of tumor-specific signaling molecules. Control of mitochondrial radical formation, particularly superoxide interconnects cell death signals with appropriate mechanistic execution. Superoxide is potentially damaging, but also triggers mitochondrial cytochrome c release. While paraoxonase (PON) enzymes are known to protect against cardiovascular diseases, recent data revealed that PON2 attenuated mitochondrial radical formation and execution of cell death. Another famil…

Cell signalingProgrammed cell deathMAP Kinase Signaling SystemApoptosisMitochondrionBiologyEndoplasmic ReticulumGene Expression Regulation EnzymologicMicechemistry.chemical_compoundSuperoxidesNeoplasmsAnimalsHumansMolecular BiologyOriginal PaperAryldialkylphosphataseSuperoxideCytochromes cCell BiologyMitochondriaNeoplasm ProteinsUp-RegulationCell biologyGene Expression Regulation NeoplasticHEK293 CellschemistryApoptosisCancer cellDNAJA3Signal transductionCell Death & Differentiation
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Transcriptional study after Beauvericin and Enniatin B combined exposure in Jurkat T cells

2019

Simultaneous mycotoxins toxicity is complex and non-predictable based on their individual toxicities. Beauvericin and Enniatins are emerging mycotoxins highly co-occurrent in food and feed, and their cytotoxicity has been reported in several human cell lines. RNA-seq studies of individual exposure in Jurkat cells demonstrated human genome perturbation mainly affecting mitochondrial pathways, however, both mycotoxins showed differences between their toxic responses. This study investigates the transcriptional effects of combined exposure to Beauvericin and Enniatin B (1:1) (0.1, 0.5, 1.5 μM; 24 h) in Jurkat cells by qPCR on 30 selected target genes (10 mitochondrial, 20 nuclear). Gene expres…

Cell signalingTranscription GeneticBiologyMitochondrionToxicologyJurkat cellsJurkat Cells03 medical and health scienceschemistry.chemical_compound0404 agricultural biotechnologyDepsipeptidesGene expressionTranscriptional regulationHumansCytotoxicityGene030304 developmental biology0303 health sciences04 agricultural and veterinary sciencesGeneral Medicine040401 food scienceBeauvericinCell biologyGene Expression RegulationchemistryDrug Therapy CombinationTranscriptomeFood ScienceFood and Chemical Toxicology
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New neuroprotective effect of lemon integropectin on neuronal cellular model

2021

Lemon IntegroPectin obtained via hydrodynamic cavitation of organic lemon processing waste in water shows significant neuroprotective activity in vitro, as first reported in this study investigating the effects of both lemon IntegroPectin and commercial citrus pectin on cell viability, cell morphology, reactive oxygen species (ROS) production, and mitochondria perturbation induced by treatment of neuronal SH-SY5Y human cells with H2O2. Mediated by ROS, including H2O2 and its derivatives, oxidative stress alters numerous cellular processes, such as mitochondrial regulation and cell signaling, propagating cellular injury that leads to incurable neurodegenerative diseases. These results, and t…

Cell signalingantioxidantPhysiologyhesperidin;Antioxidant Flavonoids Hesperidin Mitochondria Neu-roprotective Neurological disease Oxidative stress PectinClinical BiochemistryRM1-950antioxidant;MitochondrionCell morphologymedicine.disease_causeBiochemistryNeuroprotectionArticleflavonoids;03 medical and health sciences0302 clinical medicinehesperidinmedicineoxidative stressViability assayneurological diseaseMolecular Biology030304 developmental biologychemistry.chemical_classificationpectinoxidative stress;neuroprotective;0303 health sciencesReactive oxygen speciespectin;neuroprotectiveCell BiologyCell biologymitochondriachemistryneurological disease;flavonoidsTherapeutics. PharmacologyCellular model030217 neurology & neurosurgeryOxidative stress
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Electron microscopic demonstration of intracelluar promethazine accumulation sites by a precipitation technique: application to the cerebellar cortex…

1996

A method is described that allows electron microscopic identification of the phenothiazine neuroleptic promethazine after supravital intracardiac injection of high drug concentrations (greater than or equal to 3 %). The cerebellar cortex of the mouse was used for the investigation. This procedure is based on simultaneous fixation of drug and tissue by immersion in a paraformaldehyde-glutaraldehyde solution with the addition of phosphomolybdic acid. The electron microscopic investigation revealed that the drug could easily be identified as an electron-dense precipitate. Subpopulations of neurons exhibited a higher affinity for the drug than others, but no preference for any nerve cell type …

Cell typeTissue FixationHistologyChromatographyChemistryEndoplasmic reticulumMitochondrionPromethazinePromethazineCerebellar CortexMiceMicroscopy Electronchemistry.chemical_compoundCytoplasmCerebellar cortexPhenothiazineUltrastructureBiophysicsmedicineAnimalsAnatomymedicine.drugJournal of Histochemistry & Cytochemistry
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Role of humanin, a mitochondrial-derived peptide, in cardiovascular disorders

2020

The mitochondria produce specific peptides-mitochondrial-derived peptides-that mediate the transcriptional stress response by their translocation into the nucleus and interaction with deoxyribonucleic acid. Mitochondrial-derived peptides are regulators of metabolism. This class of peptides comprises humanin, mitochondrial open reading frame of the 12S ribosomal ribonucleic acid type c (MOTS-c) and small humanin-like peptides (SHLPs). Humanin inhibits mitochondrial complex 1 activity and limits the level of oxidative stress in the cell. Data show that mitochondrial-derived peptides have a role in improving metabolic diseases, such as type 2 diabetes. Perhaps humanin can be used as a marker f…

CellPeptide030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causeCardiovascular System03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemAnimalsHumansMedicine030212 general & internal medicineEndothelial dysfunctionComputingMilieux_MISCELLANEOUSHumaninchemistry.chemical_classificationbusiness.industryIntracellular Signaling Peptides and ProteinsGeneral Medicinemedicine.diseaseMitochondriaUp-RegulationCell biologyOxidative StressOpen reading framemedicine.anatomical_structurechemistryCardiovascular DiseasesInflammation MediatorsCardiology and Cardiovascular MedicinebusinessFunction (biology)Oxidative stressSignal TransductionArchives of Cardiovascular Diseases
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Cadmium and mitochondria

2009

The heavy metal cadmium (Cd) a pollutant associated with several modern industrial processes, is absorbed in significant quantities from cigarette smoke, water, food and air contaminations. It is known to have numerous undesirable effects on health in both experimental animals and humans, targeting kidney, liver and vascular system. The molecular mechanism accounting for most of the biological effects of Cd are not well-understood and the toxicity targets are largely unidentified. The present review focuses on important recent advances about the effects of cadmium on mitochondria of mammalian cells. Mitochondria are the proverbial powerhouses of the cell, running the fundamental biochemical…

Cellchemistry.chemical_elementMitochondrionBiologyModels BiologicalmedicineAnimalsHumansSettore BIO/06 - Anatomia Comparata E CitologiaCytotoxicityMolecular BiologyMembrane potentialMammalsPollutantCadmiumMitochondrial gene expressionApoptosiROSCell BiologyMitochondriamedicine.anatomical_structurechemistryBiochemistryApoptosisToxicityMolecular MedicineEnergy MetabolismIntracellularInner membrane ion permeabilityCadmiumMitochondrion
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High levels of exogenous C2-ceramide promote morphological and biochemical evidences of necrotic features in thyroid follicular cells

2002

CD95 and ceramide are known to be involved in the apoptotic mechanism. The triggering of CD95 induces a cascade of metabolic events that progressively and dramatically modifies the cell shape by intense membrane blebbing, leading to apoptotic bodies production. Although the CD95 pathway has been abundantly described in normal thyrocytes, the effects of cell permeable synthetic ceramide at morphological and biochemical levels are not fully known. In the present study, we show that thyroid follicular cells (TFC) exposed to 20 microM of C(2)-ceramide for 4 h are characterized by morphological features of necrosis, such as electron-lucent cytoplasm, mitochondrial swelling, and loss of plasma me…

CeramideCell BiologyMitochondrionBiologyBiochemistryCell biologychemistry.chemical_compoundBcl-2-associated X proteinchemistryApoptosisNecrotic Processbiology.proteinDNA fragmentationInner mitochondrial membraneMolecular BiologyBcl-2 Homologous Antagonist-Killer ProteinJournal of Cellular Biochemistry
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