Search results for "mitochondria"

showing 10 items of 1306 documents

Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
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Biological and biophysics aspects of metformin-induced effects: cortex mitochondrial dysfunction and promotion of toxic amyloid pre-fibrillar aggrega…

2016

The onset of Alzheimer disease (AD) is influenced by several risk factors comprising diabetes. Within this context, antidiabetic drugs, including metformin, are investigated for their effect on AD. We report that in the C57B6/J mice, metformin is delivered to the brain where activates AMP-activated kinase (AMPK), its molecular target. This drug affects the levels of β- secretase (BACE1) and β-amyloid precursor protein (APP), promoting processing and aggregation of β-amyloid (Aβ), mainly in the cortex region. Moreover, metformin induces mitochondrial dysfunction and cell death by affecting the level and conformation of Translocase of the Outer Membrane 40 (TOM40), voltage-dependent anion-sel…

0301 basic medicineAgingmedicine.medical_specialtyMitochondrial poreAmyloidTranslocase of the outer membraneContext (language use)AMP-Activated Protein KinasesBiologyAmyloid beta-Protein PrecursorMice03 medical and health sciences0302 clinical medicineβ-amyloid aggregationAlzheimer DiseaseHexokinaseInternal medicine?-amyloid aggregationmitochondrial dysfunctionmedicineAnimalsHypoglycemic Agentsmitochondrial poresMitochondrial transportAmyloid beta-PeptidesVoltage-Dependent Anion Channel 1BrainAMPKcell degenerationCell BiologyAlzheimer's diseasemedicine.diseaseMitochondriaMetformin030104 developmental biologyEndocrinologyAmyloid Precursor Protein SecretasesAlzheimer's diseasemetforminVDAC1030217 neurology & neurosurgeryResearch Papermedicine.drug
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Estrogenic regulation of skeletal muscle proteome : a study of premenopausal women and postmenopausal MZ cotwins discordant for hormonal therapy

2017

Female middle age is characterized by a decline in skeletal muscle mass and performance, predisposing women to sarcopenia, functional limitations, and metabolic dysfunction as they age. Menopausal loss of ovarian function leading to low circulating level of 17b-estradiol has been suggested as a contributing factor to aging-related muscle deterioration. However, the underlying molecular mechanisms remain largely unknown and thus far androgens have been considered as a major anabolic hormone for skeletal muscle. We utilized muscle samples from 24 pre- and postmenopausal women to establish proteome-wide profiles, associated with the difference in age (30–34 years old vs. 54– 62 years old), men…

0301 basic medicineAgingnaisetlabel‐free protein quantitationProteomeAnabolismvaihdevuodetmedicine.medical_treatmentTwinsmenopausenano‐LC‐HD‐MSElihakset0302 clinical medicineSTRENGTHBRAIN315 Sport and fitness sciencesta315luustoINHIBITORHormone replacement therapy (menopause)ta3142MITOCHONDRIAL BIOGENESISMiddle AgedPostmenopauseMenopauseREPLACEMENThormone replacement therapyEditorialmedicine.anatomical_structurehormonihoitoHormonal therapyOriginal ArticleFemalemuscleswomenAdultestrogeenitnano-LC-HD-MSEEXPRESSIONmedicine.medical_specialtyBiologyestrogenic regulation03 medical and health sciencesmitochondrial functionInternal medicinemedicineHumansMuscle Skeletallabel-free protein quantitationmuscle proteomeAgedSkeletal muscleEstrogenslabel-free proteinquantitationOriginal ArticlesCell Biologyfunctional annotationmedicine.diseaseMiddle ageMONOZYGOTIC TWIN PAIRS030104 developmental biologyEndocrinologyPremenopauselihasmassaSarcopeniaCELLS3111 BiomedicineEnergy Metabolismfemale muscle030217 neurology & neurosurgeryskeletal musclesHormone
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Longevity-related molecular pathways are subject to midlife “switch” in humans

2019

Emerging evidence indicates that molecular aging may follow nonlinear or discontinuous trajectories. Whether this occurs in human neuromuscular tissue, particularly for the noncoding transcriptome, and independent of metabolic and aerobic capacities, is unknown. Applying our novel RNA method to quantify tissue coding and long noncoding RNA (lncRNA), we identified ~800 transcripts tracking with age up to ~60 years in human muscle and brain. In silico analysis demonstrated that this temporary linear “signature” was regulated by drugs, which reduce mortality or extend life span in model organisms, including 24 inhibitors of the IGF‐1/PI3K/mTOR pathway that mimicked, and 5 activators that oppos…

0301 basic medicineAgingved/biology.organism_classification_rank.speciesMuscle Fibers SkeletallihaksetTranscriptome0302 clinical medicineGene expressionGene Regulatory NetworksRNA-Seqmedia_commonCerebral CortexNeuronsreactive oxygen speciesihoTOR Serine-Threonine Kinasesmitochondrial complex 1LongevityBrainNon-coding RNAAlzheimer'sECSITCell biologytranskriptio (biologia)mTORRNA Long NoncodingOriginal ArticleaivotSignal TransductionAdultTranscriptional ActivationskinIn silicomedia_common.quotation_subjectLongevityBiology03 medical and health sciencesHumanslong noncoding RNAskeletal muscleModel organismGeneSirolimusved/biologyagingRNACell BiologyTwins MonozygoticOriginal Articles030104 developmental biologyikääntyminenRNATranscriptome030217 neurology & neurosurgery
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Tenofovir-induced toxicity in renal proximal tubular epithelial cells

2017

OBJECTIVE In-vivo studies suggest that mitochondria is involved in tenofovir (TFV)-induced renal toxicity, but the underlying mechanisms are still unclear. The aim of the present study was to assess the effects of TFV and its prodrug, TFV disoproxil fumarate, on mitochondrial function and cell survival/viability in a renal proximal tubular cell line. DESIGN AND METHODS We evaluated parameters of cellular proliferation/survival (cell count, cell cycle, viability) and mitochondrial function (oxygen consumption, mitochondrial membrane potential, reactive oxygen species production) in NRK-52E cells. Intracellular TFV was measured by HPLC and expression of antioxidant genes was analysed by real-…

0301 basic medicineAnti-HIV AgentsCell Survival030106 microbiologyImmunologyCellOxidative phosphorylationMitochondrionPharmacologyCell Line03 medical and health sciencesmedicineHumansImmunology and AllergyTenofovirCell Proliferationchemistry.chemical_classificationKidneyReactive oxygen speciesCell growthEpithelial Cellsmedicine.diseaseMitochondriaMitochondrial toxicity030104 developmental biologyInfectious Diseasesmedicine.anatomical_structurechemistryIntracellularAIDS
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Zinc oxide nanoparticles mediated cytotoxicity, mitochondrial membrane potential and level of antioxidants in presence of melatonin.

2017

Zinc oxide nanoparticles (ZnO NPs) are widely used in a variety of products and are currently being investigated for biomedical applications. However, they have the potential to interact with macromolecules like proteins, lipids and DNA within the cells which makes the safe biomedical application difficult. The toxicity of the ZnO NP is mainly attributed reactive oxygen species (ROS) generation. Different strategies like iron doping, polymer coating and external supply of antioxidants have been evaluated to minimize the toxic potential of ZnO NPs. Melatonin is a hormone secreted by the pineal gland with great antioxidant properties. The melatonin is known to protect cells from ROS inducing …

0301 basic medicineAntioxidantFree RadicalsCell Survivalmedicine.medical_treatment02 engineering and technologyNitric OxideBiochemistryAntioxidantsNitric oxideCell LineMelatonin03 medical and health sciencesPineal glandchemistry.chemical_compoundMiceStructural BiologymedicineAnimalsDrug InteractionsCytotoxicityMolecular BiologyMelatoninchemistry.chemical_classificationMembrane potentialMembrane Potential MitochondrialReactive oxygen speciesBrainGeneral Medicine021001 nanoscience & nanotechnology030104 developmental biologymedicine.anatomical_structurechemistryBiochemistryToxicityNanoparticlesZinc Oxide0210 nano-technologyReactive Oxygen Specieshormones hormone substitutes and hormone antagonistsmedicine.drugInternational journal of biological macromolecules
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Physiological Levels of Nitric Oxide Diminish Mitochondrial Superoxide. Potential Role of Mitochondrial Dinitrosyl Iron Complexes and Nitrosothiols.

2017

Mitochondria are the major source of superoxide radicals and superoxide overproduction contributes to cardiovascular diseases and metabolic disorders. Endothelial dysfunction and diminished nitric oxide levels are early steps in the development of these pathological conditions. It is known that physiological production of nitric oxide reduces oxidative stress and inflammation, however, the precise mechanism of “antioxidant” effect of nitric oxide is not clear. In this work we tested the hypothesis that physiological levels of nitric oxide diminish mitochondrial superoxide production without inhibition of mitochondrial respiration. In order to test this hypothesis we analyzed effect of low p…

0301 basic medicineAntioxidantPhysiologymedicine.medical_treatmentdinitrosyl iron complexesMitochondrionmedicine.disease_causelcsh:PhysiologyNitric oxide03 medical and health scienceschemistry.chemical_compoundnitric oxidePhysiology (medical)medicineHydrogen peroxideOriginal Researchchemistry.chemical_classificationReactive oxygen specieslcsh:QP1-981SuperoxideNitrosylationelectron spin resonancenitrosothiolsmitochondria030104 developmental biologychemistryBiophysicssuperoxideOxidative stressFrontiers in physiology
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Redox Imbalance and Mitochondrial Release of Apoptogenic Factors at the Forefront of the Antitumor Action of Mango Peel Extract

2021

Today, an improved understanding of cancer cell response to cellular stress has become more necessary. Indeed, targeting the intracellular pro-oxidant/antioxidant balance triggering the tumor commitment to cell demise could represent an advantageous strategy to develop cancer-tailored therapies. In this scenario, the present study shows how the peel extract of mango—a tropical fruit rich in phytochemicals with nutraceutical properties—can affect the cell viability of three colon cancer cell lines (HT29, Caco-2 and HCT116), inducing an imbalance of cellular redox responses. By using hydro-alcoholic mango peel extract (MPE), we observed a consistent decline in thiol group content, which was a…

0301 basic medicineAntioxidantmedicine.medical_treatmentCellPharmaceutical ScienceOrganic chemistryApoptosisphytochemicalArticleAnalytical Chemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineQD241-441Downregulation and upregulationCell Line TumorNeoplasmsDrug DiscoverymedicineHumansViability assayPhysical and Theoretical ChemistryMethyl gallateMembrane Potential MitochondrialMangiferaPlant Extractsmitochondrial apoptogenic proteinsphytochemicalsAntineoplastic Agents PhytogenicBcl-2 family proteinCell biologyMitochondriaBcl-2 family proteins030104 developmental biologymedicine.anatomical_structurechemistryChemistry (miscellaneous)030220 oncology & carcinogenesisCancer cellMolecular MedicineVDAC1Oxidation-ReductionIntracellularmitochondria injuryMolecules
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Oxygen Use in Neonatal Care: A Two-edged Sword

2017

In the neonatal period, the clinical use of oxygen should be taken into consideration for its beneficial and toxicity effects. Oxygen toxicity is due to the development of reactive oxygen species (ROS) such as OH• that is one of the strongest oxidants in nature. Of note, generation of ROS is a normal occurrence in human and it is involved in a myriad of physiological reactions. Anyway an imbalance between production of oxidant species and antioxidant defenses, called oxidative stress, could affect various aspect of organisms' physiology and it could determine pathological consequences to living beings. Neonatal oxidative stress is essentially due to decreased antioxidants, increased ROS, or…

0301 basic medicineAntioxidantmedicine.medical_treatmentIschemiaPhysiologyReviewmedicine.disease_causePediatrics03 medical and health sciences0302 clinical medicine030225 pediatricsnewborn infantsmedicineoxidative stressOxygen toxicitychemistry.chemical_classificationHyperoxiareactive oxygen speciesReactive oxygen speciesbusiness.industryHypoxia (medical)medicine.diseasemitochondria030104 developmental biologyMitochondrial respiratory chainchemistryfree ironPediatrics Perinatology and Child HealthImmunologymedicine.symptombusinessoxygenOxidative stressFrontiers in Pediatrics
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Regulation of vascular function and inflammation via cross talk of reactive oxygen and nitrogen species from mitochondria or nadph oxidase—implicatio…

2020

Oxidative stress plays a key role for the development of cardiovascular, metabolic, and neurodegenerative disease. This concept has been proven by using the approach of genetic deletion of reactive oxygen and nitrogen species (RONS) producing, pro-oxidant enzymes as well as by the overexpression of RONS detoxifying, antioxidant enzymes leading to an amelioration of the severity of diseases. Vice versa, the development and progression of cardiovascular diseases is aggravated by overexpression of RONS producing enzymes as well as deletion of RONS detoxifying enzymes. We have previously identified cross talk mechanisms between different sources of RONS, which can amplify the oxidative stress-m…

0301 basic medicineAntioxidantmedicine.medical_treatmentReview030204 cardiovascular system & hematologyMitochondrionmedicine.disease_causelcsh:Chemistry0302 clinical medicineEndothelial dysfunctionEndothelial dysfunctionlcsh:QH301-705.5SpectroscopyNADPH oxidasebiologyChemistryGeneral MedicineReactive Nitrogen SpeciesComputer Science ApplicationsCell biologyMitochondriaCardiovascular DiseasesDisease Progressionmedicine.symptomInflammationENOS uncouplingOxidative phosphorylationEndothelial dysfunction; ENOS uncoupling; Kindling radicals; Low-grade inflammation; Mitochondria; NADPH oxidase; Oxidative stress; Redox cross talkLow-grade inflammationCatalysisRedox cross talkInorganic Chemistry03 medical and health sciencesmedicineDiabetes MellitusAnimalsHumansPhysical and Theoretical ChemistryMolecular BiologyInflammationNADPH oxidaseOrganic ChemistryNADPH Oxidasesmedicine.diseaseAngiotensin II030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Oxidative stressbiology.proteinKindling radicalsReactive Oxygen SpeciesOxidative stress
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