Search results for "IRON CHELATOR"

showing 3 items of 3 documents

The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.

2019

Friedreich’s ataxia (FRDA) is a rare early-onset degenerative disease that affects both the central and peripheral nervous systems, and other extraneural tissues, mainly the heart and endocrine pancreas. This disorder progresses as a mixed sensory and cerebellar ataxia, primarily disturbing the proprioceptive pathways in the spinal cord, peripheral nerves and nuclei of the cerebellum. FRDA is an inherited disease with an autosomal recessive pattern caused by an insufficient amount of the nuclear-encoded mitochondrial protein frataxin, which is an essential and highly evolutionary conserved protein whose deficit results in iron metabolism dysregulation and mitochondrial dysfunction. The firs…

0301 basic medicineCerebellumAtaxiaFriedreich’s ataxiaReviewMitochondrionmedicine.disease_causelcsh:RC321-57103 medical and health sciencesiron0302 clinical medicineDegenerative diseasemedicineoxidative stresslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrychemistry.chemical_classificationReactive oxygen speciesfrataxinbiologyCerebellar ataxialipid deregulationGeneral Neurosciencemedicine.diseaseanimal modelsCell biology030104 developmental biologymedicine.anatomical_structurechemistryFrataxinbiology.proteiniron chelatorsmedicine.symptom030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in neuroscience
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''Effect of stroke on arginase expression and localization in the rat brain''

2013

Quirie, Aurore | Demougeot, C. Eline | Bertrand, Nathalie | Mossiat, Claude | Garnier, Philippe | Marie, Christine | Prigent-Tessier, Anne; International audience; ''Because arginase and nitric oxide (NO) synthases (NOS) compete to degrade l-arginine, arginase plays a crucial role in the modulation of NO production. Moreover, the arginase 1 isoform is a marker of M2 phenotype macrophages that play a key role in tissue remodeling and resolution of inflammation. While NO has been extensively investigated in ischemic stroke, the effect of stroke on the arginase pathway is unknown. The present study focuses on arginase expression/activity and localization before and after (1, 8, 15 and 30days) …

MaleGene Expressionchemistry.chemical_compound0302 clinical medicineNeurotrophic factorsMACROPHAGESIN-VIVONeuronsAXONAL REGENERATION0303 health sciencesGlial fibrillary acidic proteinGeneral NeuroscienceBrainGLIAL RESPONSESCerebral InfarctionStrokeNitric oxide synthaseArginasemedicine.anatomical_structureBiochemistry[ SCCO.NEUR ] Cognitive science/NeuroscienceARGININE METABOLISMmedicine.symptom2'-DIPYRIDYLmedicine.medical_specialtyCentral nervous systemIRON CHELATOR 2InflammationBiologyFOCAL ISCHEMIANitric oxideLesion03 medical and health sciencesInternal medicineGlial Fibrillary Acidic ProteinmedicineAnimalsRats WistarNITRIC-OXIDE SYNTHASE030304 developmental biologyArginaseCEREBRAL-ISCHEMIABrain-Derived Neurotrophic Factor[SCCO.NEUR]Cognitive science/NeuroscienceCENTRAL-NERVOUS-SYSTEM''NITRIC-OXIDE SYNTHASERatsEndocrinologychemistryAstrocytesbiology.proteinMACROPHAGES''030217 neurology & neurosurgery
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''Deferoxamine blocks death induced by glutathione depletion in PC 12 cells''

2013

Chouraqui, E. | Leon, A. | Repesse, Y. | Prigent-Tessier, A. | Bouhallab, S. | Bougle, D. | Marie, C. | Duval, D.; International audience; ''The purpose of the present work was to investigate the mechanisms by which glutathione depletion induced by treatment with buthionine sulfoximine (BSO) led within 24-30 h to PC 12 cells apoptosis. Our results showed that treatment by relatively low concentrations (10-30 mu M) of deferoxamine (DFx), a natural iron-specific chelator, almost completely shielded the cells from BSO-induced toxicity and that DFx still remained protective when added up to 9-12 h after BSO treatment. On the other hand, phosphopeptides derived from milk casein and known to carr…

Time FactorsIronApoptosisDeferoxaminePharmacologyIron Chelating AgentsToxicologymedicine.disease_causePC12 Cellschemistry.chemical_compoundOXIDATIVE-STRESSPARKINSONS-DISEASECaseinmedicineAnimalsHomeostasisButhionine sulfoximineButhionine SulfoximineNeuronsCELLULAR IRONDose-Response Relationship DrugbiologyChemistryGeneral NeuroscienceGlutathioneGlutathioneIRON CHELATORRatsDeferoxamineFerritinSYMPATHETIC NEURONSISCHEMIC-STROKEBiochemistryBRAIN IRONCELLULAR IRON''CytoprotectionApoptosisToxicity[ SCCO.NEUR ] Cognitive science/Neurosciencebiology.proteinSERUM DEPRIVATIONHEME OXYGENASE-1NEURODEGENERATIVE DISORDERSOxidative stress''OXIDATIVE-STRESSmedicine.drug
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