Search results for "oxidative phosphorylation"

showing 10 items of 284 documents

Effect of exercise training on in vitro LDL oxidation and free radical-induced hemolysis: the HERITAGE Family Study.

2006

Oxidant stress and overproduction of reactive oxygen species (ROS) contribute to the development of cardiovascular disease. Oxidative modifications of low-density lipoproteins (LDL) are thought to play an early and critical role in atherogenesis. LDL oxidation can be reproduced in vitro, but results usually show a large interindividual variation not entirely explained by the environment. Free radical-induced hemolysis is also proposed to reveal the overall antioxidant capacity. The roles of genetic factors and exercise on the variability of both measures were investigated. The study was conducted in 146 healthy individuals from 28 families participating in a 20-week exercise-training progra…

AdultMalemedicine.medical_specialtyErythrocytesAdolescentFree RadicalsPhysiologyClinical BiochemistryOxidative phosphorylationBiochemistryHemolysisInternal medicineMedicineHumansMolecular BiologyExerciseGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesbusiness.industryFamily aggregationCell BiologyMiddle Agedmedicine.diseaseLipidsIn vitroHemolysisLipoproteins LDLAntioxidant capacityEpidemiologic StudiesEndocrinologyBiochemistrychemistryHealthy individualsGeneral Earth and Planetary SciencesFemalebusinessOxidation-ReductionAntioxidantsredox signaling
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Lipid metabolism during exercise I: Physiological and biochemical characterization of normal healthy male subjects in relation to their physical fitn…

1978

On the basis of maximal oxygen uptake (\(\dot V\)O2 max) 18 normal, healthy men were divided into two groups of equal size: moderately trained subjects (MTR) each having \(\dot V\)O2 max below 65.0 ml·min−1·kg−1 body weight (54.0±8.3) and well trained subjects (WTR), whose \(\dot V\)O2 max exceeded 65.0 ml·min−1·kg−1 body weight (69.2±4.1). The WTR group had slightly (non significant, n.s.) higher percentage of slow twitch, oxidative (SO) fibers in M. vastus lateralis and higher (n.s.) activities of cytochrome c oxidase (CytOx), succinate dehydrogenase (SDH), 3-hydroxyacyl-CoA-dehydrogenase (HADH), and citrate synthase (CS), while lactate dehydrogenase (LDH) activity was lower (n.s.). In th…

AdultMalemedicine.medical_specialtyPhysiologyPhysical fitnessCitrate (si)-SynthaseOxidative phosphorylationBiologyModels BiologicalElectron Transport Complex IVchemistry.chemical_compoundOxygen ConsumptionPhysiology (medical)Internal medicineLactate dehydrogenasemedicineHumansCytochrome c oxidaseCitrate synthaseOrthopedics and Sports MedicineL-Lactate Dehydrogenasebusiness.industryMusclesSuccinate dehydrogenasePublic Health Environmental and Occupational Health3-Hydroxyacyl CoA DehydrogenasesOxo-Acid-LyasesVO2 maxGeneral MedicineSuccinate DehydrogenaseEndocrinologyBiochemistrychemistryPhysical Fitnessbiology.proteinLean body massOxidoreductasesbusinessEuropean Journal of Applied Physiology and Occupational Physiology
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Limb Ischemic Conditioning Induces Oxidative Stress Followed by a Correlated Increase of HIF-1α in Healthy Volunteers.

2019

Background Local and remote ischemic preconditioning has been used as a protective intervention against ischemia/reperfusion (I/R) damage in several preclinical and clinical studies. However, its physiological mechanisms are not completely known. I/R increases the production of reactive oxygen species, which also serve as messengers for a variety of functions. Hypoxia-inducible factor 1 alpha (HIF-1α) is probably the most important transcription factor mediator of hypoxic signaling. Objective We hypothesized that limb ischemic conditioning (LIC) induces a local oxidative/nitrosative stress and a correlated increase of HIF-1α plasma levels. Methods An observational, prospective, and single-c…

AdultMalemedicine.medical_specialtyTime FactorsIschemiaOxidative phosphorylation030204 cardiovascular system & hematologymedicine.disease_causeDinoprost030218 nuclear medicine & medical imagingUpper Extremity03 medical and health scienceschemistry.chemical_compoundYoung Adult0302 clinical medicineInternal medicineBlood plasmamedicineHumansProspective StudiesNitriteIschemic PreconditioningNitriteschemistry.chemical_classificationReactive oxygen speciesbusiness.industryGeneral MedicineVenous bloodmedicine.diseaseHypoxia-Inducible Factor 1 alpha SubunitHealthy VolunteersUp-RegulationOxidative StressEndocrinologychemistryNitrosative StressRegional Blood FlowSpainIschemic preconditioningSurgeryFemaleTherapeutic OcclusionCardiology and Cardiovascular MedicinebusinessOxidative stressBiomarkersAnnals of vascular surgery
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Low-intensity exercise stimulates bioenergetics and increases fat oxidation in mitochondria of blood mononuclear cells from sedentary adults.

2020

Aim Exercise training induces adaptations in muscle and other tissue mitochondrial metabolism, dynamics, and oxidative phosphorylation capacity. Mitochondrial fatty acid oxidation was shown to be pivotal for the anti‐inflammatory status of immune cells. We hypothesize that exercise training can exert effects influence mitochondrial fatty acid metabolism in peripheral blood mononuclear cells (PBMCs). The aim was to investigate the effect of exercise on the fatty acid oxidation‐dependent respiration in PBMCs. Design Twelve fasted or fed volunteers first performed incremental‐load exercise tests to exhaustion on a cycle ergometer to determine the optimal workload ensuring maximal health benefi…

AdultMalemedicine.medical_specialtyobesityBioenergeticsPhysiologyImmunologyOxidative phosphorylation030204 cardiovascular system & hematologylcsh:Physiologyexercise fat metabolism lipolysis obesity sedentary adultsSignalling Pathways03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicineRespirationHeart ratemedicineMetabolism and RegulationLipolysisHumansBeta oxidationSedentary lifestyleOriginal Researchchemistry.chemical_classificationlcsh:QP1-981exercisebusiness.industryEndurance and PerformanceFatty Acidsfat metabolismFatty acidFastingsedentary adultsLipid MetabolismMitochondriaEndocrinologychemistryExercise TestLeukocytes MononuclearPhysical EndurancelipolysisFemaleSedentary BehaviorbusinessEnergy MetabolismOxidation-Reduction030217 neurology & neurosurgeryPhysiological reports
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Oxidant mechanisms in childhood obesity: the link between inflammation and oxidative stress.

2011

Evidence of obesity-induced oxidative stress in adults has emerged in the past several years, and similar evidence has been demonstrated in children more recently. The reactive species of oxygen or nitrogen can chemically alter all major classes of biomolecules by modifying their structure and function. Organisms have developed mechanisms to protect biomolecules from the deleterious effects of free radicals. These include the enzymes superoxide dismutase, catalase, and glutathione peroxidase, as well as water and lipid-soluble antioxidants, such as glutathione, ascorbate (vitamin C), α-tocopherol (vitamin E), and β-carotene. Obesity creates oxidant conditions that favor the development of c…

Adultmedicine.medical_specialtyOxidative phosphorylationSystemic inflammationmedicine.disease_causeSuperoxide dismutasechemistry.chemical_compoundRisk FactorsPhysiology (medical)Internal medicinemedicineHumansObesityChildchemistry.chemical_classificationInflammationReactive oxygen speciesbiologybusiness.industryGlutathione peroxidaseBiochemistry (medical)Public Health Environmental and Occupational HealthGeneral MedicineGlutathioneMalondialdehydeOxidantsOxidative StressEndocrinologychemistrybiology.proteinmedicine.symptomMorbiditybusinessOxidative stressTranslational research : the journal of laboratory and clinical medicine
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Mitochondrial oxidative stress plays a key role in aging and apoptosis

2000

Harman first suggested in 1972 that mitochondria might be the biological clock in aging, noting that the rate of oxygen consumption should determine the rate of accumulation of mitochondrial damage produced by free radical reactions. Later in 1980 Miquel and coworkers proposed the mitochondrial theory of cell aging. Mitochondria from postmitotic cells use O2 at a high rate, hence releasing oxygen radicals that exceed the cellular antioxidant defences. The key role of mitochondria in cell aging has been outlined by the degeneration induced in cells microinjected with mitochondria isolated from fibroblasts of old rats, especially by the inverse relationship reported between the rate of mitoch…

AgingFree RadicalsClinical BiochemistryApoptosisOxidative phosphorylationMitochondrionBiologymedicine.disease_causeDNA MitochondrialBiochemistryLipid peroxidationMicechemistry.chemical_compoundGeneticsmedicineCardiolipinAnimalsHumansMolecular BiologyFree-radical theory of agingchemistry.chemical_classificationReactive oxygen speciesBrainCell BiologyGlutathioneMitochondriaOxygenOxidative StressLiverchemistryBiochemistryCell agingOxidative stress
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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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Biomarkers of oxidative and nitrosative damage in Alzheimer's disease and mild cognitive impairment

2009

Alzheimer's disease (AD) is the most common type of dementia in the elderly. Products of oxidative and nitrosative stress (OS and NS, respectively) accumulate with aging, which is the main risk factor for AD. This provides the basis for the involvement of OS and NS in AD pathogenesis. OS and NS occur in biological systems due to the dysregulation of the redox balance, caused by a deficiency of antioxidants and/or the overproduction of free radicals. Free radical attack against lipids, proteins, sugars and nucleic acids leads to the formation of bioproducts whose detection in fluids and tissues represents the currently available method for assessing oxidative/nitrosative damage. Post-mortem …

AgingPathologymedicine.medical_specialtyFree RadicalsAlzheimer’s disease Mild cognitive impairment Free radicals Nitrosative stress Oxidative stressBioenergeticsDiseaseOxidative phosphorylationmedicine.disease_causeBiochemistryPathogenesisAlzheimer DiseaseHumansMedicineDementiaMolecular BiologyFree-radical theory of agingbusiness.industryMetabolismmedicine.diseaseOxidative StressNeurologyImmunologySettore MED/26 - NeurologiaCognition DisordersReactive Oxygen SpeciesbusinessBiomarkersOxidative stressBiotechnology
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PGC-1α, Inflammation, and Oxidative Stress: An Integrative View in Metabolism

2020

Peroxisome proliferator-activated receptor-γ coactivator (PGC)-1α is a transcriptional coactivator described as a master regulator of mitochondrial biogenesis and function, including oxidative phosphorylation and reactive oxygen species detoxification. PGC-1α is highly expressed in tissues with high energy demands, and it is clearly associated with the pathogenesis of metabolic syndrome and its principal complications including obesity, type 2 diabetes mellitus, cardiovascular disease, and hepatic steatosis. We herein review the molecular pathways regulated by PGC-1α, which connect oxidative stress and mitochondrial metabolism with inflammatory response and metabolic syndrome. PGC-1α regula…

AgingThioredoxin reductaseReview ArticleOxidative phosphorylationmedicine.disease_causeBiochemistryAntioxidantsCoactivatormedicineAnimalsHumansInflammationMetabolic Syndromechemistry.chemical_classificationReactive oxygen speciesOrganelle BiogenesisQH573-671ChemistryCell BiologyGeneral MedicinePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMitochondriaCell biologyOxidative StressMitochondrial biogenesisOrgan SpecificityThioredoxinCytologyPeroxiredoxinOxidative stressOxidative Medicine and Cellular Longevity
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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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