Search results for "CHON"

showing 10 items of 1866 documents

Respiratory chain cysteine and methionine usage indicate a causal role for thiyl radicals in aging

2011

The identification of longevity-related structural adaptations in biological macromolecules may yield relevant insights into the molecular mechanisms of aging. In screening fully sequenced animal proteomes for signals associated with longevity, it was found that cysteine depletion in respiratory chain complexes was the by far strongest predictor on the amino acid usage level to co-vary with lifespan. This association was though restricted to aerobic animals, whereas anaerobic animals showed variable cysteine accumulation. By contrast, methionine accumulation, a prominent feature of mitochondrially encoded proteins affording competitive antioxidant protection, was not predictive of longevity…

AgingAntioxidantmedicine.medical_treatmentLongevityRespiratory chainMitochondrionBiochemistryElectron Transportchemistry.chemical_compoundMethionineEndocrinologyGeneticsmedicineAnimalsHumansCysteineSulfhydryl CompoundsMolecular BiologyCysteine metabolismchemistry.chemical_classificationMethionineCell BiologyAerobiosisMitochondriaAmino acidchemistryBiochemistryThiolOxidation-ReductionCysteineExperimental Gerontology
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Induction of Mitochondrial Changes Associated with Oxidative Stress on Very Long Chain Fatty Acids (C22:0, C24:0, or C26:0)-Treated Human Neuronal Ce…

2012

In Alzheimer's disease, lipid alterations point towards peroxisomal dysfunctions. Indeed, a cortical accumulation of saturated very long chain fatty acids (VLCFAs: C22:0, C24:0, C26:0), substrates for peroxisomalβ-oxidation, has been found in Alzheimer patients. This study was realized to investigate the effects of VLCFAs at the mitochondrial level since mitochondrial dysfunctions play crucial roles in neurodegeneration. On human neuronal SK-NB-E cells treated with C22:0, C24:0, or C26:0 (0.1–20 μM; 48 h), an inhibition of cell growth and mitochondrial dysfunctions were observed by cell counting with trypan blue, MTT assay, and measurement of mitochondrial transmembrane potential (Δψm) with…

AgingArticle SubjectMitochondrionBiologymedicine.disease_causeBiochemistryMitochondrial apoptosis-induced channelchemistry.chemical_compoundSuperoxidesCell Line TumormedicineHumanslcsh:QH573-671Cell ShapeCell ProliferationMembrane Potential MitochondrialNeuronslcsh:CytologySuperoxideFatty AcidsNeurodegenerationCell BiologyGeneral MedicinePeroxisomeFlow Cytometrymedicine.diseaseMolecular biologyMitochondriaCell biologyOxidative StressProtein SubunitsMicroscopy FluorescencechemistryMultiprotein ComplexesDNAJA3ATP–ADP translocaseOxidative stressResearch ArticleOxidative Medicine and Cellular Longevity
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Oxidative Stress and Mitochondrial Damage in Neurodegenerative Diseases: From Molecular Mechanisms to Targeted Therapies

2020

The progression of Alzheimer's dementia is associated with neurovasculature impairment, which includes inflammation, microthromboses, and reduced cerebral blood flow. Here, we investigate the effects of β amyloid peptides on the function of platelets, the cells driving haemostasis. Amyloid peptide β1-42 (Aβ1-42), Aβ1-40, and Aβ25-35 were tested in static adhesion experiments, and it was found that platelets preferentially adhere to Aβ1-42 compared to other Aβ peptides. In addition, significant platelet spreading was observed over Aβ1-42, while Aβ1-40, Aβ25-35, and the scAβ1-42 control did not seem to induce any platelet spreading, which suggested that only Aβ1-42 activates platelet signalli…

AgingArticle SubjectPlatelet Glycoprotein GPIIb-IIIa Complexmedicine.disease_causeBiochemistryOxidative Stress Mitochondria Neurodegenerative DiseasesText miningMedicineHumansPlatelet activationQH573-671business.industryNADPH OxidasesNeurodegenerative DiseasesThrombosisCell BiologyGeneral Medicinemedicine.diseasePlatelet ActivationThrombosisPlatelet Glycoprotein GPIIb-IIIa ComplexOxidative StressCancer researchCytologybusinessOxidative stressResearch ArticleOxidative Medicine and Cellular Longevity
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2021 revised algorithm for the management of knee osteoarthritis-the Chinese viewpoint.

2021

Abstract Aim The European Society for Clinical and Economic Aspects of Osteoporosis, Osteoarthritis and Musculoskeletal Diseases (ESCEO) algorithm for the management of knee osteoarthritis (OA) is available worldwide from 2014, but in 2019 an update was published. Based on this algorithm, a Working Group (WG), including ESCEO members and Chinese experts, wished to see how the new ESCEO algorithm was perceived by Chinese experts in knee OA and how it was integrated into their clinical practice. Methods A WG was held between members of the international ESCEO task force and a group of Chinese experts. Results Non-pharmacological approach should be combined with pharmacological interventions. …

AgingChinaSymptomatic slow-acting drugs for osteoarthritisOsteoarthritis03 medical and health sciences0302 clinical medicineMedicineHumans030212 general & internal medicineKnee osteoartrhitis · Patented crystalline glucosamine sulfate · Symptomatic slow-acting drugs for osteoarthritis · Algorithm · ChinaConsensus Document030203 arthritis & rheumatologyGlucosamineKnee osteoartrhitisbusiness.industryGeriatrics gerontologyTask forceAnti-Inflammatory Agents Non-SteroidalChondroitin SulfatesPatented crystalline glucosamine sulfateOsteoarthritis Kneemedicine.diseaseClinical PracticeAlgorithmPharmacological interventionsGeriatrics and GerontologybusinessAlgorithmAlgorithmsAging clinical and experimental research
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Repair of oxidatively generated DNA damage in Cockayne syndrome

2013

Defects in the repair of endogenously (especially oxidatively) generated DNA modifications and the resulting genetic instability can potentially explain the clinical symptoms of Cockayne syndrome (CS), a hereditary disease characterized by developmental defects and neurological degeneration. In this review, we describe the evidence for the involvement of CSA and CSB proteins, which are mutated in most of the CS patients, in the repair and processing of DNA damage induced by reactive oxygen species and the implications for the induction of cell death and mutations. Taken together, the data demonstrate that CSA and CSB, in addition to their established role in transcription-coupled nucleotide…

AgingDNA RepairTranscription GeneticDNA damageDNA repairBiologymedicine.disease_causeCockayne syndromemedicineAnimalsHumansCockayne SyndromePoly-ADP-Ribose Binding ProteinsMutationDNA HelicasesBase excision repairmedicine.diseaseMolecular biologyCell biologyDNA Repair EnzymesMitochondrial DNA repairMutationDNA mismatch repairOxidation-ReductionDNA DamageTranscription FactorsDevelopmental BiologyNucleotide excision repairMechanisms of Ageing and Development
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The adverse redox biochemistry of intramembrane thiols accounts for the lifespan-dependent cysteine depletion in the inner mitochondrial membrane of …

2013

AgingEndocrinologyBiochemistryChemistryGeneticsCell BiologyInner mitochondrial membraneMolecular BiologyBiochemistryRedoxCysteineCell biologyExperimental Gerontology
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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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Mitochondrial Markers in Aging and Primary Open-Angle Glaucoma

2020

This review focuses on recent progress in understanding the role of mitochondrial markers in the context of mitochondrial dysfunction in glaucoma and discussing new therapeutic approaches to modulate mitochondrial function and potentially lead to improved outcomes in glaucoma.

AgingMitochondrial Diseasesgenetic structuresOpen angle glaucomabusiness.industryGlaucomaContext (language use)medicine.diseaseBioinformaticseye diseasesOphthalmologyRetinal DiseasesmedicineHumanssense organsbusinessBiomarkersGlaucoma Open-AngleJournal of Glaucoma
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Humanin: A mitochondria-derived peptide with emerging properties.

2020

AgingPeptideApoptosisMitochondrionDNA MitochondrialMitochondrial Proteinschemistry.chemical_compoundMedicineHumansInsulinProtein IsoformsAmino AcidsReceptors LipoxinReceptorHumaninchemistry.chemical_classificationbusiness.industryLipoxin metabolismIntracellular Signaling Peptides and ProteinsReceptors Formyl PeptideAmino acidMitochondriachemistryBiochemistryApoptosisCardiology and Cardiovascular MedicinebusinessEnergy MetabolismDNABiomarkersCiliary Neurotrophic Factor Receptor alpha SubunitAnnales de cardiologie et d'angeiologie
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