Search results for "mito"

showing 10 items of 2513 documents

Alteration of the Mitochondrial Effects of Ceria Nanoparticles by Gold: An Approach for the Mitochondrial Modulation of Cells Based on Nanomedicine

2020

Ceria nanoparticles are cell compatible antioxidants whose activity can be enhanced by gold deposition and by surface functionalization with positive triphenylphosphonium units to selectively target the mitochondria. The antioxidant properties of these nanoparticles can serve as the basis of a new strategy for the treatment of several disorders exhibiting oxidative stress, such as cancer, diabetes or Alzheimer&rsquo

AntioxidantantioxidantGeneral Chemical Engineeringmedicine.medical_treatmentNanoparticleceria nanoparticles02 engineering and technologyMitochondrionmedicine.disease_causeArticlelcsh:Chemistry03 medical and health scienceschemistry.chemical_compoundQUIMICA ORGANICAmitochondrial functionmedicineGeneral Materials ScienceNRF1Gold-supported ceria nanoparticles030304 developmental biology0303 health sciencesChemistryfungigold-supported ceria nanoparticlesfood and beveragestriphenylphosphonium gold-supported ceria nanoparticles021001 nanoscience & nanotechnologylcsh:QD1-999Colloidal goldBiophysicsNanomedicineMitochondrial functionAntioxidant0210 nano-technologyAdenosine triphosphateCeria nanoparticlesOxidative stressTriphenylphosphonium gold-supported ceria nanoparticles
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Direct and indirect antioxidant properties of α-lipoic acid and therapeutic potential.

2012

International audience; Diabetes has emerged as a major threat to worldwide health. The exact mechanisms underlying the disease are unknown; however, there is growing evidence that the excess generation of reactive oxygen species (ROS) associated with hyperglycemia, causes oxidative stress in a variety of tissues. In this context, various natural compounds with pleiotropic actions like lipoic acid (LA) are of interest, especially in metabolic diseases such as diabetes. LA, either as a dietary supplement or a therapeutic agent, modulates redox potential because of its ability to match the redox status between different subcellular compartments as well as extracellularly. Both the oxidized (d…

Antioxidantmedicine.medical_treatmentContext (language use)InflammationBiologymedicine.disease_causeAntioxidants03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemDiabetes mellitusmedicineDiabetes MellitusAnimalsHumans030304 developmental biologyChelating Agentschemistry.chemical_classificationInflammation0303 health sciencesReactive oxygen speciesThioctic AcidEndothelial CellsMetabolismmedicine.disease3. Good health[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemMitochondriaLipoic acidOxidative StresschemistryBiochemistryCardiovascular Diseases030220 oncology & carcinogenesisHyperglycemiaDietary Supplementsmedicine.symptomReactive Oxygen SpeciesOxidation-ReductionOxidative stressFood ScienceBiotechnologyMolecular nutritionfood research
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Novel imine antioxidants at low nanomolar concentrations protect dopaminergic cells from oxidative neurotoxicity.

2009

Strong evidence indicates that oxidative stress may be causally involved in the pathogenesis of Parkinson's disease. We have employed human dopaminergic neuroblastoma cells and rat primary mesencephalic neurons to assess the protective potential of three novel bisarylimine antioxidants on dopaminergic cell death induced by complex I inhibition or glutathione depletion. We have found that exceptionally low concentrations (EC(50) values approximately 20 nM) of these compounds (iminostilbene, phenothiazine, and phenoxazine) exhibited strong protective effects against the toxicities of MPP(+), rotenone, and l-buthionine sulfoximine. Investigating intracellular glutathione levels, it was found t…

Antioxidantmedicine.medical_treatmentDopamineGlutathione reductaseNeurotoxinsBiologymedicine.disease_causeProtein oxidationBiochemistryAntioxidantsLipid peroxidationRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundCell Line TumormedicineAnimalsHumansCells CulturedMembrane Potential MitochondrialCell DeathDose-Response Relationship DrugNeurotoxicityParkinson DiseaseRotenoneGlutathionemedicine.diseaseGlutathioneMitochondriaRatsSubstantia NigraOxidative StressNeuroprotective AgentschemistryBiochemistryElectron Transport Chain Complex ProteinsCytoprotectionNerve DegenerationIminesOxidation-ReductionOxidative stressJournal of neurochemistry
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Impact of Hydrogen Peroxide on Protein Synthesis in Yeast.

2021

This article belongs to the Special Issue Thiol-Based Redox Regulation of Cellular and Organismal Function.

Antioxidantprotein synthesisPhysiologymedicine.medical_treatmentClinical Biochemistryhydrogen peroxideReviewRM1-950Mitochondrionmedicine.disease_causeBiochemistryCysteine thiolscysteine thiolschemistry.chemical_compoundmedicineProtein biosynthesisHydrogen peroxideMolecular Biologychemistry.chemical_classificationReactive oxygen speciesTranslation (biology)Cell BiologyHydrogen peroxideSignalingCell biologychemistryTherapeutics. PharmacologyProtein synthesissignalingOxidative stressIntracellularAntioxidants (Basel, Switzerland)
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Le forme del tempo. Miti, fiabe, immagini di Italo Calvino

2004

Monografia su Italo Calvino attaverso una disamina antropologica della sua intera produzione, con particolare attenzione alla presenza del mito, della fiaba e ai problemi della visione.

Antropologia mito fiaba visione
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To the research of treatments for the typical calcific disease of old aortic valve in the omics era: Is the miR-195 a therapeutic signature via targe…

2020

Calcific aortic valve disease (CAVD) is the most frequent form of val-vular pathology [1,2], with high percentages of mortality and morbidityin Western populations, so much to be a very public health problem [2].Diverse millions of subjects are affected by CAVD and the major numberare old individuals (65- older), even if some have a younger age and aregenerally affected by congenital bicuspid aortic valve (BAV) disease[2,3]. CAVD in BAV individuals arises decades earlier respect to subjectswith the physiological tricuspid aortic valve [3]. Furthermore, it can leadto death if untreated with surgical aortic valve replacement or trans-catheter aortic valve implantation, its unique treatments […

Aortic valvemedicine.medical_specialtybicuspid aortic valvebusiness.industryp38 mitogen-activated protein kinasesDiseasemedicine.diseaseOmicsBicuspid aortic valvemedicine.anatomical_structuremiR-195Internal medicinemedicineCardiologyCardiology and Cardiovascular Medicinebusiness
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DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK).

2009

Abstract The impact of DNA damage-induced replication blockage for early activation of stress kinases [stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)] is largely unknown. Here, we show that induction of dual phosphorylation of SAPK/JNK by the DNA polymerase inhibitor aphidicolin was not ameliorated by additional exposure to ultraviolet (UV) light, indicating that overlapping mechanisms participate in signaling to SAPK/JNK triggered by both agents. UV-induced DNA replication blockage, cyclobutane pyrimidine dimer formation and DNA strand break induction coincided with SAPK/JNK phosphorylation at early (≤ 30 min) but not late (≥ 2 h) time points after exposure. Genotoxin…

AphidicolinDNA ReplicationDNA damageUltraviolet RaysPoly ADP ribose polymeraseCell Linechemistry.chemical_compoundMiceAphidicolinStructural BiologyCricetinaeAnimalsHumansLymphocytesPhosphorylationProtein kinase AMolecular BiologyNucleic Acid Synthesis InhibitorsBRCA2 ProteinMice KnockoutbiologyKinaseCell CycleDNA replicationJNK Mitogen-Activated Protein KinasesFibroblastsMolecular biologyProliferating cell nuclear antigenDNA-Binding ProteinsEnzyme ActivationchemistryPyrimidine Dimersbiology.proteinPhosphorylationApoptosis Regulatory ProteinsDNA DamageJournal of molecular biology
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Deficiency of glutathione peroxidase-1 accelerates the progression of atherosclerosis in apolipoprotein E-deficient mice.

2007

Background— We have recently demonstrated that activity of red blood cell glutathione peroxidase-1 is inversely associated with the risk of cardiovascular events in patients with coronary artery disease. The present study analyzed the effect of glutathione peroxidase-1 deficiency on atherogenesis in the apolipoprotein E-deficient mouse. Methods and Results— Female apolipoprotein E-deficient mice with and without glutathione peroxidase-1 deficiency were placed on a Western-type diet for another 6, 12, or 24 weeks. After 24 weeks on Western-type diet, double-knockout mice (GPx-1 −/− ApoE −/− ) developed significantly more atherosclerosis than control apolipoprotein E-deficient mice. Moreover…

Apolipoprotein Emedicine.medical_specialtyGPX1AntioxidantApolipoprotein Bmedicine.medical_treatmentLipoproteinsApoptosisBlood Pressuremedicine.disease_causeNitric OxideMitochondria HeartMonocyteschemistry.chemical_compoundMiceApolipoproteins EGlutathione Peroxidase GPX1SuperoxidesInternal medicinePeroxynitrous AcidmedicineAnimalsAortaCell Proliferationchemistry.chemical_classificationMice KnockoutReactive oxygen speciesGlutathione PeroxidaseMembranesbiologyGlutathione peroxidaseGlutathioneAtherosclerosisEndocrinologyPhenotypechemistryImmunologybiology.proteinDisease ProgressionFemaleCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidation-ReductionOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Neuronal cell cycle: the neuron itself and its circumstances.

2015

Neurons are usually regarded as postmitotic cells that undergo apoptosis in response to cell cycle reactivation. Nevertheless, recent evidence indicates the existence of a defined developmental program that induces DNA replication in specific populations of neurons, which remain in a tetraploid state for the rest of their adult life. Similarly, de novo neuronal tetraploidization has also been described in the adult brain as an early hallmark of neurodegeneration. The aim of this review is to integrate these recent developments in the context of cell cycle regulation and apoptotic cell death in neurons. We conclude that a variety of mechanisms exists in neuronal cells for G1/S and G2/M check…

ApoptosisBrdU 5-bromo-2′-deoxyuridineReviewp75NTR neurotrophin receptor p75Nervous SystemG0 quiescent stateCKI Cdk-inhibitorNeuronsCell DeathNeurodegenerationCell CycleapoptosisNeurodegenerative DiseasesCell cycleCell biologymedicine.anatomical_structureInk inhibitor of kinaseBDNF brain-derived neurotrophic factorp38MAPK p38 mitogen-activated protein kinaseG2 growth phase 2Programmed cell deathS-phasePD Parkinson diseaseRb RetinoblastomaMcm2 minichromosome maintenance 2PCNA proliferating cell nuclear antigenMitosisContext (language use)BiologyCdk cyclin-dependent kinaseCNS central nervous systemS-phase synthesis phase.Cip/Kip cyclin inhibitor protein/kinase inhibitor proteinmedicineAnimalsHumansMolecular BiologyMitosisTetraploidAD Alzheimer diseasecell cycle re-entryDNA replicationCell BiologyNeuronmedicine.diseaseG1 growth phase 1neuronRGCs retinal ganglion cellsCell cycle re-entrytetraploidnervous systemApoptosisNeuronDevelopmental BiologyCell cycle (Georgetown, Tex.)
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Superoxide Flux in Endothelial Cells via the Chloride Channel-3 Mediates Intracellular Signaling

2007

Reactive oxygen species (ROS) have been implicated in both cell signaling and pathology. A major source of ROS in endothelial cells is NADPH oxidase, which generates superoxide (O2.−) on the extracellular side of the plasma membrane but can result in intracellular signaling. To study possible transmembrane flux of O2.−, pulmonary microvascular endothelial cells were preloaded with the O2.−-sensitive fluorophore hydroethidine (HE). Application of an extracellular bolus of O2.−resulted in rapid and concentration-dependent transient HE oxidation that was followed by a progressive and nonreversible increase in nuclear HE fluorescence. These fluorescence changes were inhibited by superoxide dism…

ApoptosisMembrane PotentialsSuperoxide dismutasechemistry.chemical_compoundChloride ChannelsSuperoxidesExtracellularAnimalsHumansEnzyme InhibitorsRNA Small InterferingMolecular BiologyLungCells CulturedFluorescent Dyeschemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideAngiotensin IIThrombinAcetophenonesEndothelial CellsNADPH OxidasesCell BiologyArticlesCell biologyMitochondriaPhenanthridinesOxygenchemistryDIDSbiology.proteinCalciumSignal transductionOxidation-ReductionIntracellularSignal Transduction
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