Search results for "mitochondrion"

showing 10 items of 491 documents

3'-Untranslated regions of oxidative phosphorylation mRNAs function in vivo, as enhancers of translation

2000

Recent findings have indicated that the 3´-untranslated region (3´-UTR) of the mRNA encoding the β-catalytic subunit of the mitochondrial H+-ATP synthase has an in vitro translation-enhancing activity (TEA) [Izquierdo and Cuezva, Mol. Cell. Biol. (1997) 17, 5255–5268; Izquierdo and Cuezva, Biochem. J. (2000) 346, 849–855]. In the present work, we have expressed chimaeric plasmids that encode mRNA variants of green fluorescent protein in normal rat kidney and liver clone 9 cells to determine whether the 3´-UTRs of nuclear-encoded mRNAs involved in the biogenesis of mitochondria have an intrinsic TEA. TEA is found in the 3´-UTR of the mRNAs encoding the α- and β-subunits of the rat H+-ATP syn…

Untranslated regionTranscription GeneticProtein subunitBlotting WesternGreen Fluorescent ProteinsMitochondrionKidneyTransfectionBiochemistryOxidative PhosphorylationCell LineElectron Transport Complex IVMitochondrial ProteinsMitochondrial transcription factor AGenes ReporterAnimalsCytochrome c oxidaseGreen fluorescent proteinRNA MessengerEnhancer3' Untranslated RegionsMolecular BiologyCell NucleusAU-rich elementMessenger RNAbiologyThree prime untranslated regionNuclear ProteinsCell BiologyH+-ATP synthaseMolecular biologyRatsMitochondriaDNA-Binding ProteinsLuminescent ProteinsProton-Translocating ATPasesLiverMicroscopy FluorescenceProtein Biosynthesisbiology.proteinElectrophoresis Polyacrylamide GelResearch ArticlePlasmidsTranscription FactorsCytochrome c oxidase
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A Deficiency in Respiratory Complex I in Heart Mitochondria from Vitamin A-Deficient Rats Is Counteracted by an Increase in Coenzyme Q

1997

Defects of NADH:coenzyme Q oxidoreductase (complex I) of mitochondria have been described in many congenital and acquired diseases. Administration of coenzyme Q (CoQ, ubiquinone) has been shown to benefit patients with some of these diseases. However, the mechanisms by which CoQ exerts the therapeutic effects are not clearly understood. A reason could be the lack of saturation of CoQ, in kinetic terms, for complex I activity. However, this hypothesis has not been proved in vivo because of the difficulty to incorporate CoQ into the mitochondrial membranes. We have found a deficiency in respiratory complex I in heart mitochondria from vitamin A-deficient rats which was accompanied by high CoQ…

Vitaminmedicine.medical_specialtyAcquired diseasesUbiquinoneBiophysicsMitochondrionBiologyBiochemistryMitochondria Heartchemistry.chemical_compoundRespiratory Complex IOxidoreductaseInternal medicinemedicineAnimalsNADH NADPH OxidoreductasesMolecular Biologychemistry.chemical_classificationElectron Transport Complex IVitamin A Deficiencyfood and beveragesCell BiologyRatsElectron transfer rateKineticsEndocrinologychemistryCoenzyme Q – cytochrome c reductaseBiochemical and Biophysical Research Communications
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Vitamin A deficiency causes oxidative damage to liver mitochondria in rats.

2000

Mitochondrial damage in rat liver induced by chronic vitamin A-deficiency was studied using three different groups of rats: (i) control rats, (ii) rats fed a vitamin A-free diet until 50 d after birth and (iii) vitamin A-deficient rats re-fed a control diet for 30 d. No statistical difference in body weight and food intake was found between control and vitamin A-deficient rats. Liver GSH concentration was similar in both groups. However, in vitamin A-deficient rats, the mitochondrial GSH/GSSG ratio was significantly lower and the levels of malondialdehyde (MDA) and 8-oxo-7, 8-dihydro-2'-deoxyguanosine (oxo8dG) were higher when compared to control rats. These values were partially restored i…

Vitaminmedicine.medical_specialtyAgingPopulationMitochondria LiverBiologyMitochondrionmedicine.disease_causeWeight GainBiochemistryMembrane Potentialschemistry.chemical_compoundMembrane LipidsPhysiology (medical)Internal medicineMalondialdehydemedicineDeoxyguanosineAnimalseducationVitamin Aeducation.field_of_studyGlutathione DisulfideVitamin A DeficiencyDeoxyguanosineGlutathioneIntracellular Membranesmedicine.diseaseMalondialdehydeFlow CytometryGlutathioneRatsVitamin A deficiencyEndocrinologychemistry8-Hydroxy-2'-DeoxyguanosineFemaleEnergy IntakeOxidative stressFree radical biologymedicine
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Induction of mitochondrial xanthine oxidase activity during apoptosis in the rat mammary gland

2006

Oxidative stress is an important signal for apoptosis to start. So far the mitochondrial respiratory chain has been considered as the major, if not the only, cause of such stress. Here we report that this is not the case. Xanthine oxidase, a O2(-) and H2O2 generating enzyme which is important in causing significant oxidative stress in the cytosol, is also present in the mitochondrial fraction of rat mammary gland. After weaning, during the involution of the mammary gland, massive apoptosis occurs. Mitochondrial xanthine oxidase activity increases and high mitochondrial H2O2 production takes place. Inhibition of xanthine oxidase activity by allopurinol, a specific inhibitor of xanthine oxida…

Xanthine OxidaseAllopurinolRespiratory chainAllopurinolApoptosisWeaningMitochondrionmedicine.disease_causeMitochondrial Proteinschemistry.chemical_compoundMammary Glands AnimalmedicineAnimalsInvolution (medicine)Enzyme InhibitorsXanthine oxidaseChemistryHydrogen PeroxideMitochondriaRatsCell biologyOxidative StressMitochondrial respiratory chainBiochemistryApoptosisOxidative stressmedicine.drugFrontiers in Bioscience
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Stilbenes and resveratrol metabolites improve mitochondrial fatty acid oxidation defects in human fibroblasts

2014

International audience; Background: Inborn enzyme defects of mitochondrial fatty acid beta-oxidation (FAO) form a large group of genetic disorders associated to variable clinical presentations ranging from life-threatening pediatric manifestations up to milder late onset phenotypes, including myopathy. Very few candidate drugs have been identified in this group of disorders. Resveratrol (RSV) is a natural polyphenol with anti-oxidant and anti-inflammatory effects, recently shown to have beneficial metabolic properties in mice models. Our study explores its possible effects on FAO and mitochondrial energy metabolism in human cells, which are still very little documented.Methods: Using cells …

[SDV]Life Sciences [q-bio]Blotting WesternStimulationMitochondrionResveratrolBiologyPharmacology03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoStilbenesmedicineHumansGenetics(clinical)Pharmacology (medical)CarnitinePatient fibroblastsGenetics (clinical)030304 developmental biologyPiceidEC50Medicine(all)chemistry.chemical_classification0303 health sciencesResearchFatty Acidsfood and beveragesMitochondrial FAO defectsPharmacological therapyGeneral MedicineFibroblastsMitochondria3. Good health[SDV] Life Sciences [q-bio]EnzymechemistryResveratrolOxidation-Reduction030217 neurology & neurosurgerymedicine.drug
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New molecular aspects of regulation of mitochondrial activity by fenofibrate and fasting

2000

Abstract Fenofibrate and fasting are known to regulate several genes involved in lipid metabolism in a similar way. In this study measuring several mitochondrial enzyme activities, we demonstrate that, in contrast to citrate synthase and complex II, cytochrome c oxidase (COX) is a specific target of these two treatments. In mouse liver organelles, Western blot experiments indicated that mitochondrial levels of p43, a mitochondrial T3 receptor, and mitochondrial peroxisome proliferator activated receptor (mt-PPAR), previously described as a dimeric partner of p43 in the organelle, are increased by both fenofibrate and fasting. In addition, in PPARα-deficient mice, this influence was abolishe…

[SDV]Life Sciences [q-bio]Receptors Cytoplasmic and NuclearPeroxisome proliferator-activated receptorMitochondria LiverMitochondrionBiochemistryMice0302 clinical medicineFenofibrateStructural BiologyBIOLOGIE CELLULAIRECitrate synthaseFibrateReceptorComputingMilieux_MISCELLANEOUSMice Knockoutchemistry.chemical_classification0303 health sciencesFenofibratebiologyElectron Transport Complex IIFastingPeroxisomeDNA-Binding ProteinsSuccinate Dehydrogenase[SDV] Life Sciences [q-bio]OxidoreductasesDimerizationmedicine.drugPeroxisome proliferator activated receptormedicine.medical_specialtyBiophysicsCitrate (si)-Synthase[INFO] Computer Science [cs]Mitochondrial T3 receptorElectron Transport Complex IV03 medical and health sciencesMultienzyme ComplexesInternal medicineGeneticsmedicineAnimalsCytochrome c oxidase[INFO]Computer Science [cs]MitochondrionMolecular BiologyCrosses Genetic030304 developmental biologyOrganellesLipid metabolismCell BiologyMice Inbred C57BLEndocrinologychemistrybiology.protein030217 neurology & neurosurgeryTranscription Factors
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Sea Urchin Mitochondrial Matrix Contains a 56-kDa Chaperonine-like Protein

1997

Abstract Paracentrotus lividus mitochondrial matrix contains a constitutive hsp of 56-KDa which cross reacts with a serum anti-hsp-60 chaperonine from yeast mitochondria. The localization of hsps preexisting or newly synthesized in different subcellular fractions of gastrula embryos is also analyzed by two-dimensional electrophoresis.

animal structuresChaperoninsBlotting WesternBiophysicsMitochondrionBiochemistryParacentrotus lividusbiology.animalAnimalsElectrophoresis Gel Two-DimensionalImmunoelectrophoresisMolecular BiologySea urchinbiologyEmbryoCell Biologybiology.organism_classificationMolecular biologyYeastMitochondriaGastrulationBiochemistryMitochondrial matrixSea Urchinsbiological sciencesembryonic structuresBiochemical and Biophysical Research Communications
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ISOLATION OF CYTOCHROME OXIDASE COMPLEX FROM SEA URCHIN MITOCHONDRIAL INNER MEMBRANES

1996

Cytochrome oxidase complex has been isolated and purified from sea urchin mitochondrial inner membranes. The complex exhibited a discrete number of bands in PAGE and a 17 kDa band was recognized by an anti-human subunit IV antibody. No bands were recognized by an anti-yeast hsp60 antibody and an anti-sea urchin β ATPase subunit.

animal structuresProtein subunitATPaseCell BiologyGeneral MedicineMitochondrionBiologyMolecular biologyMembraneBiochemistrybiology.animalembryonic structuresbiology.proteinCytochrome c oxidaseHSP60AntibodySea urchinCell Biology International
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Hsp60 in Modifications of Nervous System Homeostasis and Neurodegeneration

2019

Hsp60 is a critical chaperonin for its role in preserving cell survival and protecting mitochondria against stress conditions. Indeed, mutations or malfunctions of Hsp60 are involved in several human diseases, either genetic or acquired, some of them affecting also the brain. In this chapter, we present several experimental observations supporting the role of Hsp60 in some neurodegenerative diseases. Further, Hsp60, as multifunctional protein, contributes to the protein folding system, to protect mitochondria and is involved in several other cellular pathways that are known to be affected in these diseases. Furthermore, due to its role outside of the mitochondria and in the extracellular fl…

animal structuresfungiNeurodegenerationchemical and pharmacologic phenomenamacromolecular substancesBiologyMitochondrionmedicine.diseasecomplex mixturesMicrovesiclesCell biologyChaperoninmedicineHSP60Protein foldingNeuroinflammationHomeostasis
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Glutathione in Cancer Cell Death

2011

Glutathione (L-γ-glutamyl-L-cysteinyl-glycine; GSH) in cancer cells is particularly relevant in the regulation of carcinogenic mechanisms; sensitivity against cytotoxic drugs, ionizing radiations, and some cytokines; DNA synthesis; and cell proliferation and death. The intracellular thiol redox state (controlled by GSH) is one of the endogenous effectors involved in regulating the mitochondrial permeability transition pore complex and, in consequence, thiol oxidation can be a causal factor in the mitochondrion-based mechanism that leads to cell death. Nevertheless GSH depletion is a common feature not only of apoptosis but also of other types of cell death. Indeed rates of GSH synthesis and…

autophagyCancer ResearchProgrammed cell deathCell growthapoptosisReviewGlutathioneMitochondrionBiologylcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogenslcsh:RC254-282necrosisCell biologychemistry.chemical_compoundcell deathOncologyMitochondrial permeability transition porechemistryApoptosisCancer cellcancerglutathioneIntracellularCancers
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