Search results for "MITOCHONDRION"

showing 10 items of 491 documents

The role of mitochondrial reactive oxygen species, NO and H2S in ischaemia/reperfusion injury and cardioprotection

2020

Redox signalling in mitochondria plays an important role in myocardial ischaemia/reperfusion (I/R) injury and in cardioprotection. Reactive oxygen and nitrogen species (ROS/RNS) modify cellular structures and functions by means of covalent changes in proteins including among others S‐nitros(yl)ation by nitric oxide (NO) and its derivatives, and S‐sulphydration by hydrogen sulphide (H2S). Many enzymes are involved in the mitochondrial formation and handling of ROS, NO and H2S under physiological and pathological conditions. In particular, the balance between formation and removal of reactive species is impaired during I/R favouring their accumulation. Therefore, various interventions aimed a…

0301 basic medicineMitochondrial ROSIschemiaEndogenyheartMitochondrionRedoxNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinenitric oxidemedicinechemistry.chemical_classificationCardioprotectionreactive oxygen speciesReactive oxygen speciesVDP::Medisinske Fag: 700::Basale medisinske odontologiske og veterinærmedisinske fag: 710Cell Biologymedicine.diseaseVDP::Medical disciplines: 700::Basic medical dental and veterinary science disciplines: 710Cell biologyreperfusionmitochondria030104 developmental biologychemistry030220 oncology & carcinogenesiscardioprotectionMolecular Medicineischaemiahydrogen sulphidecardioprotection; heart; hydrogen sulphide; ischaemia; mitochondria; nitric oxide; reactive oxygen species; reperfusion
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The mitochondrial antioxidant SS-31 increases SIRT1 levels and ameliorates inflammation, oxidative stress and leukocyte-endothelium interactions in t…

2018

AbstractThere is growing focus on mitochondrial impairment and cardiovascular diseases (CVD) in type 2 diabetes (T2D), and the development of novel therapeutic strategies in this context. It is unknown whether mitochondrial-targeting antioxidants such as SS-31 protect sufficiently against oxidative damage in diabetes. We aimed to evaluate if SS-31 modulates SIRT1 levels and ameliorates leukocyte-endothelium interactions, oxidative stress and inflammation in T2D patients. Anthropometric and metabolic parameters were studied in 51 T2D patients and 57 controls. Production of mitochondrial reactive oxygen species (ROS), mitochondrial membrane potential, glutathione content, leukocyte-endotheliu…

0301 basic medicineMitochondrial ROSMaleAntioxidantendocrine system diseasesmedicine.medical_treatmentMitochondrionPharmacologymedicine.disease_causeAntioxidantsLeukocyte-endothelial Interactionschemistry.chemical_compoundSirtuin 1Leukocyteschemistry.chemical_classificationMembrane Potential MitochondrialMultidisciplinaryQRMiddle AgedMitochondriaUp-RegulationMedicineFemalemedicine.symptomOligopeptidesRolling FluxScienceInflammationContext (language use)SIRT1 LevelsArticle03 medical and health sciencesmedicineCell AdhesionHuman Umbilical Vein Endothelial CellsHumansAgedInflammationReactive oxygen speciesTranscription Factor RelAGlutathioneSirtuins (SIRT1)Oxidative Stress030104 developmental biologychemistryDiabetes Mellitus Type 2Case-Control StudiesReactive Oxygen SpeciesLeukocyte Rolling VelocityOxidative stressScientific Reports
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Revisiting the Warburg effect: historical dogma versus current understanding

2020

Contrary to Warburg's original thesis, accelerated aerobic glycolysis is not a primary, permanent and universal consequence of dysfunctional or impaired mitochondria compensating for poor ATP yield per mole of glucose. Instead, in most tumours the Warburg effect is an essential part of a 'selfish' metabolic reprogramming, which results from the interplay between (normoxic/hypoxic) hypoxia-inducible factor-1 (HIF-1) overexpression, oncogene activation (cMyc, Ras), loss of function of tumour suppressors (mutant p53, mutant phosphatase and tensin homologue (PTEN), microRNAs and sirtuins with suppressor functions), activated (PI3K-Akt-mTORC1, Ras-Raf-MEK-ERK-cMyc, Jak-Stat3) or deactivated (LKB…

0301 basic medicineMitochondrial ROSPhysiologyCellular respirationChemistryMitochondrionWarburg effectCell biologyddc:Citric acid cycle03 medical and health sciencesPhosphatidylinositol 3-Kinases030104 developmental biology0302 clinical medicineGlucoseMitochondrial biogenesisAnaerobic glycolysisNeoplasmsTumor MicroenvironmentHumansGlycolysisGlycolysis030217 neurology & neurosurgery
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Ribosome-Targeting Antibiotics Impair T Cell Effector Function and Ameliorate Autoimmunity by Blocking Mitochondrial Protein Synthesis

2019

Summary While antibiotics are intended to specifically target bacteria, most are known to affect host cell physiology. In addition, some antibiotic classes are reported as immunosuppressive for reasons that remain unclear. Here, we show that Linezolid, a ribosomal-targeting antibiotic (RAbo), effectively blocked the course of a T cell-mediated autoimmune disease. Linezolid and other RAbos were strong inhibitors of T helper-17 cell effector function in vitro, showing that this effect was independent of their antibiotic activity. Perturbing mitochondrial translation in differentiating T cells, either with RAbos or through the inhibition of mitochondrial elongation factor G1 (mEF-G1) progressi…

0301 basic medicineMitochondrial translationmedicine.medical_treatmentT-LymphocytesCellMitochondrionmedicine.disease_causeRibosomemitochondrial translationOxidative PhosphorylationantibioticsAutoimmunityACTIVATIONMice0302 clinical medicineribosome-targetingMedicine and Health SciencesImmunology and AllergyTRANSCRIPTION FACTORMolecular Targeted TherapyMice Knockout0303 health sciencesEffectorExperimental autoimmune encephalomyelitisautoimmunityCell DifferentiationPeptide Elongation Factor GAnti-Bacterial Agents3. Good healthCell biologymitochondriaInfectious DiseasesCytokinemedicine.anatomical_structureRESPIRATION030220 oncology & carcinogenesisEncephalomyelitis Autoimmune ExperimentalMultiple SclerosisT cellImmunologyINHIBITIONT cellsBiologyOXAZOLIDINONEPeptides CyclicArticleMitochondrial Proteins03 medical and health sciencesNAD+medicineAnimalsHumanselongation factor G1030304 developmental biologyAutoimmune diseaseBacteriaLinezolidBiology and Life SciencesPATHWAYSDNANADmedicine.diseaseIn vitroMice Inbred C57BL030104 developmental biologyTh17 CellsArgyrinCHLORAMPHENICOLMEMBRANERibosomesImmunity
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Inhibited fatty acid β-oxidation impairs stress resistance ability in Nile tilapia (Oreochromis niloticus)

2017

Energy metabolism plays important roles in stress resistance and immunity in mammals, however, such functions have not been established in fish. In the present study, Nile tilapia (Oreochromis niloticus) was fed with mildronate, an inhibitor of mitochondrial fatty acid (FA) β-oxidation, for six weeks subsequently challenged with Aeromonas hydrophila and ammonia nitrogen exposure. Mildronate treatment reduced significantly l-carnitine concentration and mitochondrial FA β-oxidation efficiency, while it increased lipid accumulation in liver. The fish with inhibited hepatic FA catabolism had lower survival rate when exposed to Aeromonas hydrophila and ammonia nitrogen. Moreover, fish fed mildro…

0301 basic medicineNitrogenAquatic ScienceMitochondrionFish DiseasesRandom Allocation03 medical and health sciencesNile tilapiaImmune systemAmmoniaStress PhysiologicalCarnitinemedicineAnimalsEnvironmental ChemistryCarnitinechemistry.chemical_classificationbiologyCatabolismFatty AcidsFatty acidCichlids04 agricultural and veterinary sciencesGeneral Medicinebiology.organism_classificationAnimal FeedAeromonas hydrophilaDietMitochondriaOreochromisAeromonas hydrophila030104 developmental biologychemistryBiochemistryDietary Supplements040102 fisheries0401 agriculture forestry and fisheriesGram-Negative Bacterial InfectionsOxidation-ReductionMethylhydrazinesmedicine.drugFish & Shellfish Immunology
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Bcl-xL knockout attenuates mitochondrial respiration and causes oxidative stress that is compensated by pentose phosphate pathway activity

2017

Bcl-xL is an anti-apoptotic protein that localizes to the outer mitochondrial membrane and influences mitochondrial bioenergetics by controlling Ca2+ influx into mitochondria. Here, we analyzed the effect of mitochondrial Bcl-xL on mitochondrial shape and function in knockout (KO), wild type and rescued mouse embryonic fibroblast cell lines. Mitochondria of KO cells were more fragmented, exhibited a reduced ATP concentration, and reduced oxidative phosphorylation (OXPHOS) suggesting an increased importance of ATP generation by other means. Under steady-state conditions, acidification of the growth medium as a readout for glycolysis was similar, but upon inhibition of ATP synthase with oligo…

0301 basic medicineOligomycinBioenergeticsOxidative phosphorylationBH4 DOMAINMitochondrionPentose phosphate pathwaymedicine.disease_causeBiochemistryCYTOCHROME-C03 medical and health scienceschemistry.chemical_compoundCHANNEL VDAC0302 clinical medicinePhysiology (medical)BCL-XLmedicineJournal ArticleGlycolysisRELEASEATP synthasebiologyGLUCOSE-METABOLISMFISSIONAPOPTOSIS030104 developmental biologyBiochemistrychemistryCELLSbiology.proteinMEMBRANE030217 neurology & neurosurgeryOxidative stressFree Radical Biology and Medicine
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Prenatal Ambient Air Pollution, Placental Mitochondrial DNA Content, and Birth Weight in the INMA (Spain) and ENVIRONAGE (Belgium) Birth Cohorts

2016

The research leading to these results was funded by the Spanish Ministry of Health (FIS-PI11/00610, FIS-PI041436, FIS-PI081151, FIS-PI042018, and FIS-PI09/02311), the European Union (EU) (FP7-ENV-2011 cod 282957 and HEALTH.2010.2.4.5-1), the Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314, 09/02647, 11/01007, 11/02591, CP11/00178, FIS-PI06/0867, and FIS-PS09/00090), the Conselleria de Sanitat Generalitat Valenciana, the Generalitat de Catalunya-CIRIT (1999SGR 00241), the Obre Social Cajastur, the Universidad de Oviedo, the Department of Health of the Basque Government (2005111093 and 2009111069),…

0301 basic medicinePediatrics:Phenomena and Processes::Physiological Phenomena::Body Constitution::Body Weights and Measures::Body Size::Body Weight::Birth Weight [Medical Subject Headings]:Phenomena and Processes::Physiological Phenomena::Physiological Processes::Growth and Development::Morphogenesis::Embryonic and Fetal Development::Fetal Development [Medical Subject Headings]Health Toxicology and MutagenesisPlacentaEspañaPhysiology:Diseases::Pathological Conditions Signs and Symptoms::Pathologic Processes::Growth Disorders::Fetal Growth Retardation [Medical Subject Headings]ADN mitocondrial010501 environmental sciencesMitochondrion01 natural sciencesFetal DevelopmentBélgicaPregnancyBirth Weightskin and connective tissue diseasesPeso al nacerNews | Science SelectionsMitocondrias:Phenomena and Processes::Reproductive and Urinary Physiological Phenomena::Reproductive Physiological Phenomena::Reproductive Physiological Processes::Reproduction::Pregnancy [Medical Subject Headings]:Anatomy::Cells::Cellular Structures::Intracellular Space::Cytoplasm::Cytoplasmic Structures::Organelles::Mitochondria [Medical Subject Headings]2. Zero hunger:Geographicals::Geographic Locations::Europe::Spain [Medical Subject Headings]Air PollutantsAmbient air pollutionAire -- ContaminacióFemenino3. Good healthmedicine.anatomical_structureMaternal ExposureFemaleBirth cohort:Health Care::Environment and Public Health::Public Health::Environmental Pollution::Air Pollution [Medical Subject Headings]Mitochondrial DNAmedicine.medical_specialtyModelos LinealesEmbarazoBirth weightInfants -- DesenvolupamentBiology:Chemicals and Drugs::Inorganic Chemicals::Gases::Nitrogen Oxides::Nitrogen Dioxide [Medical Subject Headings]DNA Mitochondrial:Phenomena and Processes::Genetic Phenomena::Genetic Structures::Genome::Genome Components::Genes::Genes Mitochondrial [Medical Subject Headings]03 medical and health sciencesAir pollutantsPlacentaAir PollutionmedicineHumans:Geographicals::Geographic Locations::Europe::Belgium [Medical Subject Headings]:Analytical Diagnostic and Therapeutic Techniques and Equipment::Investigative Techniques::Epidemiologic Methods::Statistics as Topic::Models Statistical::Linear Models [Medical Subject Headings]Contaminación del aire0105 earth and related environmental sciencesRetardo del crecimiento fetal:Chemicals and Drugs::Nucleic Acids Nucleotides and Nucleosides::Nucleic Acids::DNA::DNA Circular::DNA Mitochondrial [Medical Subject Headings]Genes mitocondrialesPregnancyPublic Health Environmental and Occupational HealthDesarrollo fetalmedicine.disease:Anatomy::Embryonic Structures::Placenta [Medical Subject Headings]030104 developmental biology:Check Tags::Female [Medical Subject Headings]13. Climate actionSpainsense organsDióxido de nitrógeno
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Lon protease: a novel mitochondrial matrix protein in the interconnection between drug-induced mitochondrial dysfunction and endoplasmic reticulum st…

2017

Background and Purpose Mitochondria-associated membranes (MAMs) are specific endoplasmic reticulum (ER) domains that enable it to interact directly with mitochondria and mediate metabolic flow and Ca2+ transfer. A growing list of proteins have been identified as MAMs components, but how they are recruited and function during complex cell stress situations is still not understood, while the participation of mitochondrial matrix proteins is largely unrecognized. Experimental Approach This work compares mitochondrial/ER contact during combined ER stress/mitochondrial dysfunction using a model of human hepatoma cells (Hep3B cell line) treated for 24 h with classic pharmacological inducers of ER…

0301 basic medicinePharmacologyMitochondrial DNAChemistryEndoplasmic reticulumMitochondrionmedicine.diseaseCarbonyl cyanide m-chlorophenyl hydrazoneCell biology03 medical and health sciencesMitofusin-2chemistry.chemical_compound030104 developmental biology0302 clinical medicineMitochondrial matrixUnfolded protein responsemedicineOptic Atrophy 1030217 neurology & neurosurgeryBritish Journal of Pharmacology
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Role of p62/SQSTM1 beyond autophagy: a lesson learned from drug-induced toxicity in vitro

2018

Background and Purpose SQSTM1/p62 is a multifunctional, stress-induced, scaffold protein involved in multiple cellular processes including autophagic clearance, regulation of inflammatory responses and redox homeostasis. Its altered function has been associated with different human pathologies, such as neurodegenerative, metabolic and bone diseases (down-regulation), and cancerogenesis (up-regulation). However, its role in the off-target effects of clinically used drugs is still not understood. Experimental Approach We evaluated the expression of p62 in cultured Hep3B cells and their derived ρ° cells (lacking mitochondria), along with markers of autophagy and mitochondrial dysfunction. The …

0301 basic medicinePharmacologyMitochondrial ROSScaffold proteinAutophagyATG5InflammasomePharmacologyMitochondrionBiologyCell biology03 medical and health sciences030104 developmental biologymedicineGene silencingViability assaymedicine.drugBritish Journal of Pharmacology
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Antioxidant effects of resveratrol in the cardiovascular system

2016

The antioxidant effects of resveratrol (3,5,4'-trihydroxy-trans-stilbene) contribute substantially to the health benefits of this compound. Resveratrol has been shown to be a scavenger of a number of free radicals. However, the direct scavenging activities of resveratrol are relatively poor. The antioxidant properties of resveratrol in vivo are more likely to be attributable to its effect as a gene regulator. Resveratrol inhibits NADPH oxidase-mediated production of ROS by down-regulating the expression and activity of the oxidase. This polyphenolic compound reduces mitochondrial superoxide generation by stimulating mitochondria biogenesis. Resveratrol prevents superoxide production from un…

0301 basic medicinePharmacologyOxidase testAntioxidantendocrine system diseasesbiologySuperoxideSirtuin 1organic chemicalsmedicine.medical_treatmentfood and beveragesMitochondrionResveratrolmedicine.disease_cause03 medical and health scienceschemistry.chemical_compound030104 developmental biologychemistryBiochemistrymedicinebiology.proteinProtein deacetylaseOxidative stressBritish Journal of Pharmacology
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