Search results for "mito"

showing 10 items of 2513 documents

Mitogenomics of the Olive Seed Weevil, Anchonocranus oleae Marshall and Implications for Its Phylogenetic Position in Curculionidae

2022

Anchonocranus oleae Marshall (Coleoptera: Curculionidae) is a seed-feeding weevil native to southern Africa; its larvae are known to develop in the fruits of the African Wild Olive and, more rarely, cultivated olives. The species has been mainly found in the Western Cape province of South Africa, but it has remained in relative obscurity because it does not seem to represent a current threat to commercial olive production. As part of an ongoing effort to produce baseline genetic data for olive-associated entomofauna in South Africa, we generated reference DNA barcodes for A. oleae collected from wild and cultivated olives and sequenced its mitogenome for assessment of the phylogenetic posit…

African Wild Olive; <i>Olea europaea</i> subsp. <i>europaea</i>; <i>O. europaea</i> subsp. <i>cuspidata</i>; mitochondrial phylogenyAfrican Wild OliveSettore AGR/11 - Entomologia Generale E ApplicataInsect Sciencemitochondrial phylogenyOlea europaea subsp. europaeaO. europaea subsp. cuspidataInsects; Volume 13; Issue 7; Pages: 607
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Oxidative Stress in Neurodegenerative Diseases: From a Mitochondrial Point of View

2019

Age is the main risk factor for a number of human diseases, including neurodegenerative disorders such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, which increasing numbers of elderly individuals suffer. These pathological conditions are characterized by progressive loss of neuron cells, compromised motor or cognitive functions, and accumulation of abnormally aggregated proteins. Mitochondrial dysfunction is one of the main features of the aging process, particularly in organs requiring a high-energy source such as the heart, muscles, brain, or liver. Neurons rely almost exclusively on the mitochondria, which produce the energy required for most of the cel…

AgingAntioxidantMitochondrial Diseasesmedicine.medical_treatmentneurodegeneration oxidative stress mitochondiaDiseaseReview ArticleMitochondrionBiologymedicine.disease_causeBiochemistryAntioxidantsAlzheimer DiseasemedicineHumansAmyotrophic lateral sclerosislcsh:QH573-671lcsh:CytologyNeurodegenerationParkinson DiseaseCell BiologyGeneral Medicinemedicine.diseaseMitochondriaOxidative Stressmedicine.anatomical_structureSynaptic plasticityNeuronNeuroscienceOxidative stress
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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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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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Activation by mitogens and superantigens of axolotl lymphocytes: functional characterization and ontogenic study.

1996

Urodele amphibians have weak and slow immune responses compared to mammals and anuran amphibians. Using new culture conditions, we tested the ability of lymphocytes of a well-studied salamander, the Mexican axolotl (Ambystoma mexicanum) to proliferate in vitro with diverse mitogenic agents. We demonstrated that the axolotl has a population of B lymphocytes that proliferate specifically and with a high stimulation index to the lipopolysaccharide (LPS) known as a B-cell mitogen in mammals. This proliferative capacity is observed without significant changes throughout ontogenesis. In the presence of LPS, axolotl B lymphocytes are able to synthesize and secrete both isotopes of immunoglobulin d…

AgingLymphocyteT-LymphocytesImmunologyPopulationCell Culture TechniquesMajor histocompatibility complexLymphocyte ActivationAxolotlmedicineSuperantigenImmunology and AllergyAnimalsFunctional abilityeducationPhytohaemagglutinineducation.field_of_studyB-LymphocytesSuperantigensbiologyCell Differentiationbiology.organism_classificationCell biologyAmbystoma mexicanummedicine.anatomical_structureConcanavalin AImmunologybiology.proteinMitogensCell DivisionSpleenResearch Article
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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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