Search results for "Mitochondrial Size"

showing 6 items of 6 documents

Mitochondria, oxidative stress and aging

2000

In the eighties, Miquel and Fleming suggested that mitochondria play a key role in cellular aging. Mitochondria, and specially mitochondrial DNA (mtDNA), are major targets of free radical attack. At present, it is well established that mitochondrial deficits accumulate upon aging due to oxidative damage. Thus, oxidative lesions to mtDNA accumulate with age in human and rodent tissues. Furthermore, levels of oxidative damage to mtDNA are several times higher than those of nuclear DNA. Mitochondrial size increases whereas mitochondrial membrane potential decreases with age in brain and liver. Recently, we have shown that treatment with certain antioxidants, such as sulphur-containing antioxid…

AgingMitochondrial DNAFree RadicalsDNA damageAge FactorsGeneral MedicineOxidative phosphorylationBiologyMitochondrionMitochondrial Sizemedicine.disease_causeBiochemistryAntioxidantsMitochondriaLipid peroxidationOxidative Stresschemistry.chemical_compoundBiochemistrychemistrymedicineReactive Oxygen SpeciesOxidative stressDNA DamageFree-radical theory of agingFree Radical Research
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Mitochondrial glutathione depletion by glutamine in growing tumor cells.

2000

The effect of L-glutamine (Gln) on mitochondrial glutathione (mtGSH) levels in tumor cells was studied in vivo in Ehrlich ascites tumor (EAT)-bearing mice. Tumor growth was similar in mice fed a Gln-enriched diet (GED; where 30% of the total dietary nitrogen was from Gln) or a nutritionally complete elemental diet (SD). As compared with non-tumor-bearing mice, tumor growth caused a decrease of blood Gln levels in mice fed an SD but not in those fed a GED. Tumor cells in mice fed a GED showed higher glutaminase and lower Gln synthetase activities than did cells isolated from mice fed an SD. Cytosolic glutamate concentration was 2-fold higher in tumor cells from mice fed a GED ( approximately…

AnionsMalemedicine.medical_specialtyFree RadicalsGlutamineOxidative phosphorylationBiologyMitochondrionMitochondrial Sizemedicine.disease_causeBiochemistryGlutaminase activitychemistry.chemical_compoundMiceAdenosine TriphosphatePhysiology (medical)Internal medicinemedicineAnimalsHumansAmino AcidsCarcinoma Ehrlich TumorGlutaminaseTumor Necrosis Factor-alphaGlutathioneHydrogen-Ion ConcentrationGlutathioneRecombinant ProteinsMitochondriaGlutamineOxidative StressEndocrinologyBiochemistrychemistryOxidative stressFree radical biologymedicine
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Altered Mitochondrial Function and Oxidative Stress in Leukocytes of Anorexia Nervosa Patients

2014

ContextAnorexia nervosa is a common illness among adolescents and is characterised by oxidative stress.ObjectiveThe effects of anorexia on mitochondrial function and redox state in leukocytes from anorexic subjects were evaluated.Design and settingA multi-centre, cross-sectional case-control study was performed.PatientsOur study population consisted of 20 anorexic patients and 20 age-matched controls, all of which were Caucasian women.Main outcome measuresAnthropometric and metabolic parameters were evaluated in the study population. To assess whether anorexia nervosa affects mitochondrial function and redox state in leukocytes of anorexic patients, we measured mitochondrial oxygen consumpt…

Anorexia NervosaEating DisordersMitochondrionmedicine.disease_causeBiochemistryElectron Transport Complex IIIchemistry.chemical_compoundLeukocytesMedicine and Health SciencesEnergy-Producing OrganellesMembrane Potential Mitochondrialchemistry.chemical_classificationeducation.field_of_studyMultidisciplinaryQRGlutathioneMitochondriaAnorexia nervosa (differential diagnoses)MedicineFemaleCellular Structures and Organellesmedicine.symptomResearch ArticleAdultmedicine.medical_specialtyAdolescentSciencePopulationContext (language use)AnorexiaBioenergeticsYoung AdultOxygen ConsumptionInternal medicineMental Health and PsychiatrymedicineHumanseducationReactive oxygen speciesElectron Transport Complex Ibusiness.industryBiology and Life SciencesCell BiologyGlutathioneOxidative StressEndocrinologychemistryMitochondrial SizeReactive Oxygen SpeciesbusinessOxidative stressPLoS ONE
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Mitochondria as sources and targets of damage in cellular aging.

2011

Mitochondria are considered as the most important cellular sources and targets of free radicals. They are also a source of signalling molecules that regulate cell cycle, proliferation, and apoptosis. Denham Harman postulated the free radical theory of aging in 1956. Previously Rebecca Gershman showed that radiation toxicity could be attributed to free radical damage. Subsequently, Jaime Miquel formulated the mitochondrial free radical theory of aging. We have shown that mitochondrial size, membrane potential, inner membrane mass and peroxide production is altered inside cells in old animals. These result in an increase in the oxidative damage to mitochondrial DNA with aging that can be prev…

Mitochondrial DNAFree RadicalsDNA damageBiochemistry (medical)Clinical BiochemistryGeneral MedicineMitochondrionBiologyMitochondrial Sizemedicine.disease_causeAntioxidantsCell biologyMitochondriaOxidative StressMitochondrial biogenesisApoptosismedicineAnimalsHumansOxidative stressCellular SenescenceFree-radical theory of agingDNA DamageClinical chemistry and laboratory medicine
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Mitochondrial defects and neuromuscular degeneration caused by altered expression of Drosophila Gdap1: implications for the Charcot–Marie–Tooth neuro…

2014

One of the genes involved in Charcot-Marie-Tooth (CMT) disease, an inherited peripheral neuropathy, is GDAP1. In this work, we show that there is a true ortholog of this gene in Drosophila, which we have named Gdap1. By up- and down-regulation of Gdap1 in a tissue-specific manner, we show that altering its levels of expression produces changes in mitochondrial size, morphology and distribution, and neuronal and muscular degeneration. Interestingly, muscular degeneration is tissue-autonomous and not dependent on innervation. Metabolic analyses of our experimental genotypes suggest that alterations in oxidative stress are not a primary cause of the neuromuscular degeneration but a long-term c…

Nerve Tissue ProteinsDiseaseDegeneration (medical)BiologyMitochondrionMitochondrial Sizemedicine.disease_causeRetinaCharcot-Marie-Tooth DiseaseGeneticsmedicineAnimalsDrosophila ProteinsHumansMolecular BiologyGenePhylogenyGenetics (clinical)F-Box ProteinsNeurodegenerationNeuromuscular DiseasesGeneral MedicineAnatomymedicine.diseaseMitochondriaCell biologyTissue DegenerationDisease Models AnimalDrosophila melanogasterGene Expression RegulationMitochondrial SizeOxidative stressHuman Molecular Genetics
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Aging of the liver: Age-associated mitochondrial damage in intact hepatocytes

1996

Mitochondrial damage may be a major cause of cellular aging. So far, this hypothesis had only been tested using isolated mitochondria. The aim of this study was to investigate the involvement of mitochondria in aging using whole liver cells and not isolated mitochondria only. Using flow cytometry, we found that age is associated with a decrease in mitochondrial membrane potential (30%), an increase in mitochondrial size, and an increase in mitochondrial peroxide generation (23%). Intracellular peroxide levels were also increased. The number of mitochondria per cell and inner mitochondrial membrane mass did not change. Gluconeogenesis from glycerol or fructose (mitochondrial-independent) did…

medicine.medical_specialtyHepatologyMitochondrionBiologyMitochondrial SizePyruvate carboxylaseEndocrinologyMitochondrial permeability transition poreGluconeogenesisInternal medicinemedicinesense organsATP–ADP translocaseInner mitochondrial membranePhosphoenolpyruvate carboxykinaseHepatology
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