Search results for "mito"

showing 10 items of 2513 documents

Fine Mapping of Gene Ordering by Elongated Chromosome Methods

2006

Publisher Summary Fluorescence in situ hybridization (FISH) can be used to localize specific DNA sequences on metaphase chromosomes, interphase nuclei, and experimentally extended DNA or chromatin fibers. Depending on the hybridization target, FISH techniques show widely different levels of DNA resolution. Mechanically stretched or elongated chromosomes fill the resolution gap between metaphase FISH and fiber FISH, allowing the rapid and straightforward ordering and localization of clones along the length of an entire chromosome with a 100- to 200-kb resolution. Although various genome projects have provided very high-resolution physical maps of human and important animal genomes, FISH is s…

medicine.diagnostic_testFiber FISHmedicineChromosomeGenome projectBiologyMolecular biologyGenomeMitosisMetaphaseFluorescence in situ hybridizationChromatinCell biology
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Cytotoxic effects of Jay Amin hydroxamic acid (JAHA), a ferrocene-based class I histone deacetylase inhibitor, on triple-negative MDA-MB231 breast ca…

2012

The histone deacetylase inhibitors (HDACis) are a class of chemically heterogeneous anticancer agents of which suberoylanilide hydroxamic acid (SAHA) is a prototypical member. SAHA derivatives may be obtained by three-dimensional manipulation of SAHA aryl cap, such as the incorporation of a ferrocene unit like that present in Jay Amin hydroxamic acid (JAHA) and homo-JAHA [ Spencer , et al. ( 2011 ) ACS Med. Chem. Lett. 2 , 358 - 362 ]. These metal-based SAHA analogues have been tested for their cytotoxic activity toward triple-negative MDA-MB231 breast cancer cells. The results obtained indicate that of the two compounds tested, only JAHA was prominently active on breast cancer cells with a…

medicine.drug_classCell SurvivalMetallocenesAntineoplastic AgentsApoptosisToxicologyHydroxamic AcidsStructure-Activity RelationshipIn vivoAnnexinmedicineTumor Cells CulturedCytotoxic T cellHumansFerrous CompoundsSettore BIO/06 - Anatomia Comparata E Citologiachemistry.chemical_classificationMembrane Potential MitochondrialReactive oxygen speciesDose-Response Relationship DrugMolecular StructureChemistryHistone deacetylase inhibitorCell CycleGeneral MedicineIn vitroHistone Deacetylase InhibitorsBiochemistryhistone deacetylase inhibitor breast cancer autophagy apoptosis mitochondria cell cycleApoptosisCancer researchHistone deacetylaseDrug Screening Assays AntitumorReactive Oxygen Species
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N-acetylcysteine protects against age-related increase in oxidized proteins in mouse synaptic mitochondria.

1997

Since it has been proposed that oxidized protein accumulation plays a critical role in brain aging, we have investigated the effect of a thiolic antioxidant on protein carbonyl content in synaptic mitochondria from female OF-1 mice. At 48 weeks of age, a control group was fed standard food pellets and another group received pellets containing 0.3% (w/w) of N-acetylcysteine. A 24-week treatment resulted in a significant decrease in protein carbonyl content in synaptic mitochondria of the N-acetylcysteine-treated animals as compared to age-matched controls.

medicine.medical_specialtyAgingAntioxidantmedicine.medical_treatmentProtein Carbonyl ContentMice Inbred StrainsMitochondrionBiologyAcetylcysteinechemistry.chemical_compoundMiceInternal medicineAge relatedmedicineAnimalsSulfhydryl CompoundsMolecular BiologyBrain agingchemistry.chemical_classificationNeuronsGeneral NeuroscienceGlutathioneFree Radical ScavengersGlutathioneAcetylcysteineMitochondriaEndocrinologychemistryBiochemistrySynapsesThiolFemaleNeurology (clinical)Oxidation-ReductionDevelopmental Biologymedicine.drugBrain research
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Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage.

2021

Background: Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty. Methods: Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigate…

medicine.medical_specialtyAging[SDV]Life Sciences [q-bio]Respiratory chainOxidative phosphorylationDiseases of the musculoskeletal systemGlucosephosphate DehydrogenaseMitocondrisLipid peroxidation03 medical and health scienceschemistry.chemical_compoundMice0302 clinical medicineEnvellimentPhysiology (medical)Internal medicineAdipocytemedicineNADPHAnimalsOrthopedics and Sports MedicineRespiratory exchange ratio030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesDisabilityFrailtybusiness.industryMusclesQM1-695Skeletal muscleGlucose 1-DehydrogenaseGlutathioneOriginal Articles3. Good healthMitochondriamedicine.anatomical_structureEndocrinologyGlucosechemistryRC925-935Human anatomyHealthspanOriginal ArticleAntioxidantbusinessReactive oxygen species030217 neurology & neurosurgeryJournal of cachexia, sarcopenia and muscle
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Exercise as a Model to Study Oxidative Stress

2011

Physical exercise generates free radicals. The major source of radicals in exercise appears to be extracellular. Our experiments show that xanthine oxidase is a key player in the generation of superoxide during exercise. Mitochondrial contribution appears to be less important: during high oxygen utilization by mitochondria in state 3, the proportion of oxygen that is converted to superoxide is on an order of magnitude lower than in resting, state 4 conditions. Exercise-induced radicals constitute a double-edged sword: high intensity ­exercise causes the generation of relatively high concentrations of radicals that cause oxidative stress and eventually damage. On the other hand, low intensit…

medicine.medical_specialtyAntioxidantChemistrySuperoxideRadicalmedicine.medical_treatmentPhysical exerciseMitochondrionmedicine.disease_causechemistry.chemical_compoundEndocrinologyInternal medicinemedicineExtracellularXanthine oxidaseOxidative stress
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Magnesium and Alzheimer’s Disease

2015

Environmental factors, including nutrition and metal elements, are implicated in the pathophysiology of Alzheimer’s disease (AD). Several in vitro and in vivo data indicate a role for magnesium (Mg) in many biological and clinical aspects of AD. Mg deficiency, aside from having a negative impact on the energy production pathways required by the mitochondria to generate adenosine triphosphate, also affects many biochemical mechanisms vital for neuronal properties and synaptic plasticity, including the response of N-methyl- d -aspartate receptors to excitatory amino acids, stability, and viscosity of the cell membrane. Mg also has an action as a mild calcium antagonist, and as an antioxidant …

medicine.medical_specialtyAntioxidantChemistrymedicine.medical_treatmentchemistry.chemical_elementInflammationMitochondrionCalciummedicine.disease_causePathogenesisEndocrinologyInternal medicineSynaptic plasticitymedicinemedicine.symptomCognitive declineOxidative stress
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Pentaerithrityl tetranitrate improves angiotensin II induced vascular dysfunction via induction of heme oxygenase-1

2010

The organic nitrate pentaerythritol tetranitrate is devoid of nitrate tolerance, which has been attributed to the induction of the antioxidant enzyme heme oxygenase (HO)-1. With the present study, we tested whether chronic treatment with pentaerythritol tetranitrate can improve angiotensin II–induced vascular oxidative stress and dysfunction. In contrast to isosorbide-5 mononitrate (75 mg/kg per day for 7 days), treatment with pentaerythritol tetranitrate (15 mg/kg per day for 7 days) improved the impaired endothelial and smooth muscle function and normalized vascular and cardiac reactive oxygen species production (mitochondria, NADPH oxidase activity, and uncoupled endothelial NO synthase)…

medicine.medical_specialtyAntioxidantNitric Oxide Synthase Type IIImedicine.medical_treatmentVasodilator AgentsBlotting WesternFluorescent Antibody TechniquePentaerythritol tetranitratemedicine.disease_causePentaerythritolArticlechemistry.chemical_compoundInternal medicineRats Inbred SHRInternal MedicinemedicineAnimalsPentaerythritol TetranitrateEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesAnalysis of VarianceAngiotensin IImedicine.diseaseAngiotensin IIMitochondriaRatsHeme oxygenaseOxidative StressEndocrinologychemistryHeminEndothelium VascularReactive Oxygen SpeciesOxidative stressHeme Oxygenase-1
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Antioxidant supplements in exercise: worse than useless?

2012

TO THE EDITOR: In a recent paper by Higashida et al. (5), the authors report that very large doses of antioxidant vitamins do not prevent the exercise-induced adaptive responses of muscle mitochondria, GLUT4, and insulin action to exercise. As clearly stated in the paper, their data disagree with those reported by three independent research groups from Germany (14), Australia (17), and Spain (4). Using a significantly different experimental protocol regarding exercise training intensity and duration, antioxidant supplementation (doses and types of antioxidants), and molecular parameters analyzed (mRNA vs. protein levels), Higashida et al. compared their data with ours and came to exactly th…

medicine.medical_specialtyAntioxidantVitamin CbiologyPhysiologybusiness.industryEndocrinology Diabetes and Metabolismmedicine.medical_treatmentInsulinSkeletal muscleClinical nutritionmedicine.anatomical_structureEndocrinologyMitochondrial biogenesisPhysiology (medical)Internal medicinemedicinebiology.proteinbusinessInhibitory effectGLUT4American Journal of Physiology-Endocrinology and Metabolism
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Redox modulation of mitochondriogenesis in exercise. Does antioxidant supplementation blunt the benefits of exercise training?

2015

Physical exercise increases the cellular production of reactive oxygen species (ROS) in muscle, liver, and other organs. This is unlikely due to increased mitochondrial production but rather to extramitochondrial sources such as NADPH oxidase or xanthine oxidase. We have reported a xanthine oxidase-mediated increase in ROS production in many experimental models from isolated cells to humans. Originally, ROS were considered as detrimental and thus as a likely cause of cell damage associated with exhaustion. In the past decade, evidence showing that ROS act as signals has been gathered and thus the idea that antioxidant supplementation in exercise is always recommendable has proved incorrect.…

medicine.medical_specialtyAntioxidantmedicine.medical_treatmentPhysical exerciseBiochemistryAntioxidantsSuperoxide dismutasechemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineAnimalsHumansMuscle SkeletalXanthine oxidaseExercisechemistry.chemical_classificationReactive oxygen speciesOrganelle BiogenesisNADPH oxidasebiologyMuscle adaptationGlutathione peroxidaseAdaptation PhysiologicalMitochondria MuscleOxidative StressEndocrinologychemistryDietary Supplementsbiology.proteinOxidation-ReductionFree Radical Biology and Medicine
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Moderate consumption of beer reduces liver triglycerides and aortic cholesterol deposit in LDLr-/- apoB100/100 mice.

2006

This study was designed to address the effects of a moderate consumption of beer on serum and liver lipid parameters and on the development of aortic lesions in a mouse model associated with a human atherogenic lipoprotein profile. LDLr(-/-) apoB(100/100) mice received each day during 12 weeks either water, mild beer (0.570g of ethanol/kg of body weight) or ethanol-free beer in a single pure dose. Serum and liver lipid parameters were analyzed and atherosclerotic lesions were estimated in heart and aorta through their total cholesterol content. mRNA levels of enzymes and receptors involved in lipoprotein uptake, in fatty acid esterification and oxidation, and in reverse cholesterol transpor…

medicine.medical_specialtyApolipoprotein BAlcohol DrinkingCholesterol VLDLAortic DiseasesPalmitatesDown-RegulationAorta ThoracicMitochondria LiverPolymerase Chain ReactionPhosphatidylcholine-Sterol O-Acyltransferasechemistry.chemical_compoundMiceInternal medicinemedicineAnimalsRNA MessengerScavenger receptorChromatography High Pressure LiquidTriglyceridesApolipoproteins BbiologyTriglycerideCholesterolReverse cholesterol transportCholesterol HDLfood and beveragesBeerLipoprotein(a)Cholesterol LDLScavenger Receptors Class BAtherosclerosisMice Inbred C57BLEndocrinologychemistryLiverReceptors LDLLDL receptorbehavior and behavior mechanismsbiology.proteinlipids (amino acids peptides and proteins)FemaleCardiology and Cardiovascular MedicineOxidation-ReductionLipoproteinSterol Regulatory Element Binding Protein 2Atherosclerosis
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