Search results for "Mitochondria"

showing 10 items of 1306 documents

(+)-Pentazocine reduces oxidative stress and apoptosis in microglia following hypoxia/reoxygenation injury

2016

Abstract Background Sigma-1 receptors (σ 1 R) are highly expressed in neurons as well as microglia and have been shown to modulate the inflammatory response in the central nervous system and thus may serve as possible target for neuroprotective strategies. The aim of the present study was to test the effect of (+)-pentazocine, a putative σ 1 R agonist, in an in vitro model of microglia activation. Methods Microglia (BV2 cells) was exposed (3 h) to 1% oxygen and reoxygenation was allowed for 24 h. Cells were treated with different concentrations (1, 10, 25 and 50 μM) of (+)-pentazocine in the presence or absence of NE-100 (1 μM), a well established σ 1 R antagonist. Cell viability and apopto…

0301 basic medicinePentazocineSigma receptorCell SurvivalmicrogliaApoptosisPharmacologyBiologymedicine.disease_causeNeuroprotection(+)-PentazocineCell LineMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePentazocine; microglia; SIGMAmedicineAnimalsReceptors sigmaViability assayAnnexin A5PhosphorylationHypoxiaMembrane Potential MitochondrialMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3MicrogliaAnimalGeneral NeuroscienceApoptosiOxidative StreGlutathioneGlutathioneOxidative Stress030104 developmental biologymedicine.anatomical_structurePentazocineBiochemistrychemistryApoptosis030217 neurology & neurosurgeryIntracellularOxidative stressSIGMAmedicine.drug
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Cytotoxicity and mode of action of a naturally occurring naphthoquinone, 2-acetyl-7-methoxynaphtho[2,3-b]furan-4,9-quinone towards multi-factorial dr…

2017

Abstract Introduction Malignacies are still a major public concern worldwide and despite the intensive search of new chemotherapeutic agents, treatment still remains a challenging issue. The present study was designed to evaluate the cytotoxicity of 2-acetyl-7-methoxynaphtho[2,3-b]furan-4,9-quinone (AMNQ) isolated from the bark of Milletia versicolor towards a panel of drug-sensitive and multidrug-resistant (MDR) cancer cell lines. Methods The resazurin reduction assay was used to evaluate the cytotoxicity of AMNQ against 9 drug-sensitive and multidrug-resistant (MDR) cancer cell lines. Cell cycle, mitochondrial membrane potential (MMP) and levels of reactive oxygen species were all analyze…

0301 basic medicinePharmaceutical ScienceApoptosisPharmacologyFlow cytometry03 medical and health sciences0302 clinical medicineCell Line TumorDrug DiscoverymedicineHumansCytotoxic T cellCytotoxicityMembrane Potential MitochondrialPharmacologymedicine.diagnostic_testPlant ExtractsChemistryCell CycleCancerCell cyclemedicine.diseaseAntineoplastic Agents PhytogenicDrug Resistance MultipleMultiple drug resistance030104 developmental biologyComplementary and alternative medicineDoxorubicinDrug Resistance NeoplasmApoptosisCaspases030220 oncology & carcinogenesisCancer cellCancer researchMolecular MedicineReactive Oxygen SpeciesNaphthoquinonesPhytomedicine
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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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Development of an Analytical Assay for Electrochemical Detection and Quantification of Protein-Bound 3-Nitrotyrosine in Biological Samples and Compar…

2020

Reactive oxygen and nitrogen species (RONS) cause oxidative damage, which is associated with endothelial dysfunction and cardiovascular disease, but may also contribute to redox signaling. Therefore, their precise detection is important for the evaluation of disease mechanisms. Here, we compared three different methods for the detection of 3-nitrotyrosine (3-NT), a marker of nitro-oxidative stress, in biological samples. Nitrated proteins were generated by incubation with peroxynitrite or 3-morpholino sydnonimine (Sin-1) and subjected to total hydrolysis using pronase, a mixture of different proteases. The 3-NT was then separated by high performance liquid chromatography (HPLC) and quantifi…

0301 basic medicinePhysiologyClinical BiochemistryDot blotmitochondrial superoxidePronase030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryHigh-performance liquid chromatographyArticleperoxynitritePeroxynitrite03 medical and health sciences0302 clinical medicineProtein-bound 3-nitrotyrosinemedicineoxidative stressBovine serum albuminMolecular Biologychemistry.chemical_classificationDetection limitReactive oxygen speciesChromatographyHPLC with electrochemical detectionbiologylcsh:RM1-950Cell Biology3. Good health030104 developmental biologylcsh:Therapeutics. PharmacologychemistryOxidative stressbiology.proteinprotein-bound 3-nitrotyrosineOxidative stressEx vivoMitochondrial superoxide
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Metal homeostasis regulators suppress FRDA phenotypes in a drosophila model of the disease

2016

Friedreich's ataxia (FRDA), the most commonly inherited ataxia in populations of European origin, is a neurodegenerative disorder caused by a decrease in frataxin levels. One of the hallmarks of the disease is the accumulation of iron in several tissues including the brain, and frataxin has been proposed to play a key role in iron homeostasis. We found that the levels of zinc, copper, manganese and aluminum were also increased in a Drosophila model of FRDA, and that copper and zinc chelation improve their impaired motor performance. By means of a candidate genetic screen, we identified that genes implicated in iron, zinc and copper transport and metal detoxification can restore frataxin def…

0301 basic medicinePhysiologyGene Expressionlcsh:MedicineMitochondrionmedicine.disease_causeAntioxidantsIron-Binding ProteinsMedicine and Health SciencesHomeostasislcsh:ScienceGeneticsMultidisciplinarybiologyDrosophila MelanogasterIron-binding proteinsAnimal ModelsPhenotypeMitochondria3. Good healthInsectsDNA-Binding ProteinsChemistryZincPhenotypesPhysical SciencesDrosophilaAnatomymedicine.symptomDrosophila melanogasterResearch ArticleChemical ElementsAtaxiaArthropodaIronResearch and Analysis Methods03 medical and health sciencesModel OrganismsOcular SystemmedicineGeneticsAnimalsHumansGenetikManganeselcsh:ROrganismsBiology and Life SciencesCell Biologybiology.organism_classificationInvertebratesOxidative StressDisease Models Animal030104 developmental biologyFriedreich AtaxiaFrataxinbiology.proteinEyeslcsh:QPhysiological ProcessesCarrier ProteinsHeadCopperOxidative stressAluminumTranscription FactorsGenetic screen
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MYC and MCL1 Cooperatively Promote Chemotherapy-Resistant Breast Cancer Stem Cells via Regulation of Mitochondrial Oxidative Phosphorylation

2017

Summary Most patients with advanced triple-negative breast cancer (TNBC) develop drug resistance. MYC and MCL1 are frequently co-amplified in drug-resistant TNBC after neoadjuvant chemotherapy. Herein, we demonstrate that MYC and MCL1 cooperate in the maintenance of chemotherapy-resistant cancer stem cells (CSCs) in TNBC. MYC and MCL1 increased mitochondrial oxidative phosphorylation (mtOXPHOS) and the generation of reactive oxygen species (ROS), processes involved in maintenance of CSCs. A mutant of MCL1 that cannot localize in mitochondria reduced mtOXPHOS, ROS levels, and drug-resistant CSCs without affecting the anti-apoptotic function of MCL1. Increased levels of ROS, a by-product of a…

0301 basic medicinePhysiologyMice NudeTriple Negative Breast NeoplasmsOxidative phosphorylationTumor initiationMitochondrionBiologyOxidative PhosphorylationArticleProto-Oncogene Proteins c-myc03 medical and health sciencesCancer stem cellCell Line TumorAnimalsHumansMCL1Molecular BiologyTriple-negative breast cancerchemistry.chemical_classificationReactive oxygen speciesCell BiologyMitochondria030104 developmental biologychemistryDrug Resistance NeoplasmNeoplastic Stem CellsCancer researchMyeloid Cell Leukemia Sequence 1 ProteinFemaleStem cellReactive Oxygen SpeciesCell Metabolism
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Mitoprotective Clinical Strategies in Type 2 Diabetes and Fanconi Anemia Patients: Suggestions for Clinical Management of Mitochondrial Dysfunction

2020

Oxidative stress (OS) and mitochondrial dysfunction (MDF) occur in a number of disorders, and several clinical studies have attempted to counteract OS and MDF by providing adjuvant treatments against disease progression. The present review is aimed at focusing on two apparently distant diseases, namely type 2 diabetes (T2D) and a rare genetic disease, Fanconi anemia (FA). The pathogenetic links between T2D and FA include the high T2D prevalence among FA patients and the recognized evidence for OS and MDF in both disorders. This latter phenotypic/pathogenetic feature—namely MDF—may be regarded as a mechanistic ground both accounting for the clinical outcomes in both diseases, and…

0301 basic medicinePhysiologymedicine.medical_treatmentClinical Biochemistrymitochondrial nutrientsDiseaseType 2 diabetesReviewBioinformaticsmedicine.disease_causeBiochemistry03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoFanconi anemiamitochondrial dysfunctionmedicineoxidative stressMolecular Biologyfanconi anemiaCoenzyme Q10business.industrylcsh:RM1-950Mitochondrial nutrientCell Biologymedicine.diseasePhenotype030104 developmental biologylcsh:Therapeutics. Pharmacologychemistry030220 oncology & carcinogenesisOxidative stretype 2 diabetesbusinessAdjuvantOxidative stressAntioxidants
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Effects of air pollution particles (ultrafine and fine particulate matter) on mitochondrial function and oxidative stress – Implications for cardiova…

2020

Environmental pollution is a major cause of global mortality and burden of disease. All chemical pollution forms together may be responsible for up to 12 million annual excess deaths as estimated by the Lancet Commission on pollution and health as well as the World Health Organization. Ambient air pollution by particulate matter (PM) and ozone was found to be associated with an all-cause mortality rate of up to 9 million in the year 2015, with the majority being of cerebro- and cardiovascular nature (e.g. stroke and ischemic heart disease). Recent evidence suggests that exposure to airborne particles and gases contributes to and accelerates neurodegenerative diseases. Especially, airborne t…

0301 basic medicinePollutionmedia_common.quotation_subjectBiophysicsAir pollutionEnvironmental pollutionDiseasemedicine.disease_causeBiochemistry03 medical and health sciencesEnvironmental healthMedicineAnimalsHumansEnvironmental risk factorsNeurodegenerationMolecular Biologymedia_commonMitochondrial damage and dysfunctionAir Pollutants030102 biochemistry & molecular biologybusiness.industryMortality rateNeurodegenerationNeurodegenerative DiseasesParticulatesmedicine.diseaseCardiovascular diseaseMitochondriaOxidative Stress030104 developmental biologyCardiovascular DiseasesAmbient air pollution; Cardiovascular disease; Environmental risk factors; Mitochondrial damage and dysfunction; Neurodegeneration; Particulate matter; Air Pollutants; Animals; Cardiovascular Diseases; Humans; Mitochondria; Neurodegenerative Diseases; Oxidative Stress; Particulate MatterParticulate MatterAmbient air pollutionbusinessOxidative stress
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Rapid generation of hydrogen peroxide contributes to the complex cell death induction by the angucycline antibiotic landomycin E

2017

Landomycin E (LE) is an angucycline antibiotic produced by Streptomyces globisporus. Previously, we have shown a broad anticancer activity of LE which is, in contrast to the structurally related and clinically used anthracycline doxorubicin (Dx), only mildly affected by multidrug resistance-mediated drug efflux. In the present study, cellular and molecular mechanisms underlying the anticancer activity of landomycin E towards Jurkat T-cell leukemia cells were dissected focusing on the involvement of radical oxygen species (ROS). LE-induced apoptosis distinctly differed in several aspects from the one induced by Dx. Rapid generation of both extracellular and cell-derived hydrogen peroxide alr…

0301 basic medicinePoly (ADP-Ribose) Polymerase-1ApoptosisBiochemistryLandomycin EJurkat Cellschemistry.chemical_compoundSuperoxidesCaspaseCaspase-9chemistry.chemical_classificationCaspase 7Antibiotics AntineoplasticLeukemiabiologySuperoxideStreptomycesCaspase 9Respiratory burstMitochondriaBiochemistrySettore CHIM/03 - Chimica Generale E InorganicaReactive oxygen specieHumanJurkat CellCaspase 7Article03 medical and health sciencesPhysiology (medical)HumansReactive oxygen speciesAminoglycosideIntrinsic apoptosisApoptosiOxidative StreAnticancer drugHydrogen PeroxideMolecular biologyN-acetylcysteineSuperoxide radicalAcetylcysteineMulti-drug resistanceOxidative StressAminoglycosides030104 developmental biologychemistryStreptomyceApoptosisDoxorubicinbiology.proteinReactive Oxygen Species
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