Search results for "Superoxide Dismutase-1"

showing 10 items of 22 documents

Does Metformin Protect Diabetic Patients from Oxidative Stress and Leukocyte-Endothelium Interactions?

2017

Since metformin can exert beneficial vascular effects, we aimed at studying its effect on reactive oxygen species (ROS) production, antioxidant enzyme expression, levels of adhesion molecules, and leukocyte-endothelium interactions in the leukocytes from type 2 diabetic (T2D) patients. The study was carried out in 72 T2D patients (41 of whom were treated with metformin for at least 12 months at a dose of 1700 mg per day), and in 40 sex- and age-matched control subjects. Leukocytes from T2D patients exhibited enhanced levels of mitochondrial ROS and decreased mRNA levels of glutathione peroxidase 1 (gpx1) and sirtuin 3 (sirt3) with respect to controls, whereas metformin was shown to revert t…

0301 basic medicineMitochondrial ROSMaleGPX1endocrine system diseasesPhysiologyClinical Biochemistry030204 cardiovascular system & hematologymedicine.disease_causeBiochemistry0302 clinical medicineSuperoxide Dismutase-1Glutathione Peroxidase GPX1Sirtuin 3LeukocytesGeneral Environmental Sciencechemistry.chemical_classificationbiologyMiddle AgedCatalaseIntercellular Adhesion Molecule-1MetforminMetforminP-SelectinCatalaseFemalemedicine.drugmedicine.medical_specialtySIRT3Superoxide dismutase03 medical and health sciencesInternal medicinemedicineCell AdhesionHumansHypoglycemic AgentsMolecular BiologyAgedReactive oxygen speciesGlutathione Peroxidasenutritional and metabolic diseasesEndothelial CellsCell BiologyOxidative Stress030104 developmental biologyEndocrinologychemistryDiabetes Mellitus Type 2biology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidantsredox signaling
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Antiproliferative Effect of Elastin-Derived Peptide VGVAPG on SH-SY5Y Neuroblastoma Cells

2019

Throughout the lifetime of humans, the amount of stem cells and the rate of cell proliferation continue to decrease. Reactive oxygen species (ROS) are one among the many factors that promote stem cell aging. Both a decrease in the level of stem cells and increase in ROS production can lead to the development of different neurodegenerative diseases. This study was conducted to determine how the VGVAPG peptide, liberated from elastin during the aging process and under pathological conditions, affects ROS production and activities of antioxidant enzymes in undifferentiated, proliferating SH-SY5Y cells. SH-SY5Y cells were maintained in Dulbecco’s modified Eagle’s medium/nutrient mixture F-12 su…

0301 basic medicineSH-SY5YProliferationEnzyme-Linked Immunosorbent AssayToxicologySH-SY5YReal-Time Polymerase Chain ReactionSuperoxide dismutase03 medical and health sciencesNeuroblastoma0302 clinical medicineSuperoxide Dismutase-1Cell Line TumorHumansCell Proliferationchemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidasebiologyDose-Response Relationship DrugCell growthGeneral NeuroscienceGlutathione peroxidaseROSCatalaseCell biologyElastin-derived peptidesElastinPPAR gamma030104 developmental biologyKi-67 AntigenchemistryVGVAPGbiology.proteinOriginal ArticleStem cellReactive Oxygen SpeciesElastinOligopeptides030217 neurology & neurosurgeryFetal bovine serumNeurotoxicity Research
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Anti-inflammatory and cognitive effects of interferon-β1a (IFNβ1a) in a rat model of Alzheimer’s disease

2018

Background: Aβ 1-42 peptide abnormal production is associated with the development and maintenance of neuroinflammation and oxidative stress in brains from Alzheimer disease (AD) patients. Suppression of neuroinflammation may then represent a suitable therapeutic target in AD. We evaluated the efficacy of IFNβ1a in attenuating cognitive impairment and inflammation in an animal model of AD. Methods: A rat model of AD was obtained by intra-hippocampal injection of Aβ 1-42 peptide (23 μg/2 μl). After 6 days, 3.6 μg of IFNβ1a was given subcutaneously (s.c.) for 12 days. Using the novel object recognition (NOR) test, we evaluated changes in cognitive function. Measurement of pro-inflammatory or …

0301 basic medicineTime Factorsmedicine.medical_treatmentHippocampusCell CountPharmacologymedicine.disease_causeHippocampuslcsh:RC346-429Superoxide Dismutase-10302 clinical medicineNeuroinflammationNF-kBMicrogliaGeneral NeuroscienceMicrofilament ProteinsROSPro-inflammatory cytokineIFNβ1amedicine.anatomical_structureCytokineNeurologyIL-10CytokinesFemalemedicine.symptomAlzheimer's diseaseInterferon beta-1aPro-inflammatory cytokinesImmunologyAβ 1-42InflammationProinflammatory cytokine03 medical and health sciencesCellular and Molecular NeuroscienceHippocampuAlzheimer DiseaseGlial Fibrillary Acidic ProteinmedicineAnimalsAβ1-42Rats WistarSODMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationInflammationAmyloid beta-PeptidesNeuroscience (all)Superoxide Dismutasebusiness.industryResearchCalcium-Binding ProteinsRecognition Psychologymedicine.diseasePeptide FragmentsRatsDisease Models Animal030104 developmental biologyLipid PeroxidationCognition DisordersReactive Oxygen Speciesbusiness030217 neurology & neurosurgeryOxidative stressJournal of Neuroinflammation
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Further evidence that D90A-SOD1 mutation is recessively inherited in ALS patients in Italy.

2008

Mutations in the Cu/Zn superoxide dismutase 1 (SOD1) gene have been reported to cause adult-onset autosomal dominant amyotrophic lateral sclerosis (FALS). In sporadic cases (SALS), de novo mutations in the SOD1 gene have occasionally been observed. All the SOD1 mutations are autosomal dominantly inherited with the exception of D90A. To date, in Italy, only two sporadic ALS cases carrying the D90A mutation have been reported in a homozygous state. We investigated for the presence of this mutation in 169 unrelated ALS patients from southern Italy. The genetic analysis revealed three ALS patients (1.8%) with mild phenotype carrying the homozygous D90A mutation.

AdultMaleGenotypeSOD1DNA Mutational AnalysisGenes RecessiveBiologyGenetic analysisSuperoxide dismutaseSuperoxide Dismutase-1GenotypemedicineHumansGenetic Predisposition to DiseaseAmyotrophic lateral sclerosisGeneDe novo mutationsAgedGeneticsSuperoxide DismutaseAmyotrophic Lateral SclerosisSOD1; SLA;General MedicineSOD1Middle Agedmedicine.diseaseMolecular biologyNeurologyItalyMutation (genetic algorithm)Mutationbiology.proteinFemaleNeurology (clinical)SLA
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Oxidative stress and antioxidant response in fibroblasts from Werner and Atypical Werner Syndromes

2014

Werner Syndrome (WS, ICD-10 E34.8, ORPHA902) and Atypical Werner Syndrome (AWS, ICD-10 E34.8, ORPHA79474) are very rare inherited syndromes characterized by premature aging. While approximately 90% of WS individuals have any of a range of mutations in theWRN gene, there exists a clinical subgroup in which the mutation occurs in the LMNA/C gene in heterozygosity. Although both syndromes exhibit an age-related pleiotropic phenotype, AWS manifests the onset of the disease during childhood, while major symptoms in WS appear between the ages of 20 and 30. To study the molecular mechanisms of progeroid diseases provides a useful insight into the normal aging process. Main changes found were the d…

AdultMalePremature agingAgingWerner Syndrome HelicaseAdolescentBiologymedicine.disease_causeAntioxidantsCell LineWerner Syndrome HelicaseLMNAProgeriaSuperoxide Dismutase-1antioxidant enzymesmedicineoxidative stressHumansRNA MessengerAtypical Werner syndromeChildeducationCell ProliferationWerner syndromeeducation.field_of_studyProgeriaAtypical Werner SyndromeRecQ Helicasespremature agingSuperoxide DismutaseAging PrematurethioredoxinglutaredoxinCell BiologyFibroblastsLamin Type Amedicine.diseaseGlutathioneMolecular biologyExodeoxyribonucleasesCase-Control StudiesMutationDNA damageFemaleWerner SyndromeThioredoxinOxidative stressResearch PaperAging
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Biological effects of inorganic arsenic on primary cultures of rat astrocytes

2010

It is well established that inorganic arsenic induces neurotoxic effects and neurological defects in humans and laboratory animals. The cellular and molecular mechanisms of its actions, however, remain elusive. Herein we report the effects of arsenite (NaAsO2) on primary cultures of rat astrocytes. Cells underwent induction of heat shock protein 70 only at the highest doses of inorganic arsenic (30 and 60 microM), suggesting a high threshold to respond to stress. We also investigated arsenic genotoxicity with the comet assay. Interestingly, although cells treated with 10 microM arsenite for 24 h maintained >70% viability, with respect to untreated cells, high DNA damage was already observed…

ArsenitesCell SurvivalDNA damagechemistry.chemical_elementBiologymedicine.disease_causeRats Sprague-Dawleychemistry.chemical_compoundSuperoxide Dismutase-1Settore BIO/10 - BiochimicaGeneticsmedicineAnimalsCell damageCells CulturedArsenicArseniteSuperoxide DismutaseGeneral Medicinemedicine.diseaseMolecular biologyCarcinogens EnvironmentalRatsHsp70Comet assaySettore BIO/18 - GeneticachemistryBiochemistryApoptosisAstrocytesComet Assayinorganic arsenic astrocytes cell damage DNA damage PIPPin.Reactive Oxygen SpeciesGenotoxicityDNA DamageInternational Journal of Molecular Medicine
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Exercise and Metformin Intervention Prevents Lipotoxicity-Induced Hepatocyte Apoptosis by Alleviating Oxidative and ER Stress and Activating the AMPK…

2022

Objective. Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes (T2DM) commonly coexist and act synergistically to drive adverse clinical outcomes. This study is aimed at investigating the effects of exercise intervention and oral hypoglycaemic drug of metformin (MET) alone or combined on hepatic lipid accumulation. To investigate if oxidative stress and endoplasmic reticulum stress (ERS) are involved in lipotoxicity-induced hepatocyte apoptosis in diabetic mice and whether exercise and/or MET alleviated oxidative stress or ERS-apoptosis by AMPK-Nrf2-HO-1 signaling pathway. Methods. Forty db/db mice with diabetes ( random   blood   glucose ≥ 250   mg / dL ) were randomly allocated i…

Blood GlucoseAgingArticle SubjectNF-E2-Related Factor 2metformiiniApoptosisAMP-Activated Protein KinasesBiochemistryAntioxidantsDiabetes Mellitus ExperimentalMiceohjelmoitunut solukuolemaSuperoxide Dismutase-1aineenvaihduntahäiriötAnimalsHypoglycemic AgentsHematoxylinoksidatiivinen stressibcl-2-Associated X ProteinCaspase 3Cell BiologyGeneral MedicineEndoplasmic Reticulum StressLipidsMetforminOxidative StressDiabetes Mellitus Type 2ei-alkoholiperäinen rasvamaksasairausHepatocyteslääkehoitoEosine Yellowish-(YS)koe-eläinmallitaikuistyypin diabetesSignal TransductionliikuntahoitoOxidative Medicine and Cellular Longevity
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The oxygen radicals involved in the toxicity induced by parthenolide in MDA-MB-231 cells

2014

It has been shown that the sesquiterpene lactone parthenolide lowers the viability of MDA-MB-231 breast cancer cells, in correlation with oxidative stress. The present report examined the different radical species produced during parthenolide treatment and their possible role in the toxicity caused by the drug. Time course experiments showed that in the first phase of treatment (0-8 h), and in particular in the first 3 h, parthenolide induced dichlorofluorescein (DCF) signal in a large percentage of cells, while dihydroethidium (DHE) signal was not stimulated. Since the effect on DCF signal was suppressed by apocynin and diphenyleneiodonium (DPI), two inhibitors of NADPH oxidase (NOX), we s…

Cancer Researchparthenolide oxygen radicals NADPH oxidase breast cancer cellsCell SurvivalBreast NeoplasmsSuperoxide dismutasechemistry.chemical_compoundSuperoxide Dismutase-1DichlorofluoresceinSuperoxidesCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidechemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideSuperoxide DismutaseAnti-Inflammatory Agents Non-SteroidalNADPH OxidasesGeneral MedicineHydrogen PeroxideMolecular biologyMitochondriaOncologychemistryApocyninbiology.proteinFemaleSesquiterpenesPeroxynitrite
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Heterodimer formation of wild-type and amyotrophic lateral sclerosis-causing mutant Cu/Zn-superoxide dismutase induces toxicity independent of protei…

2008

Recent studies provide evidence that wild-type Cu/Zn-superoxide dismutase (SOD1(hWT)) might be an important factor in mutant SOD1-mediated amyotrophic lateral sclerosis (ALS). In order to investigate its functional role in the pathogenesis of ALS, we designed fusion proteins of two SOD1 monomers linked by a polypeptide. We demonstrated that wild-type-like mutants, but not SOD1(G85R) homodimers, as well as mutant heterodimers including SOD1(G85R)-SOD1(hWT) display dismutase activity. Mutant homodimers showed an increased aggregation compared with the corresponding heterodimers in cell cultures and transgenic Caenorhabditis elegans, although SOD1(G85R) heterodimers are more toxic in functiona…

Cell SurvivalRecombinant Fusion Proteinsanimal diseasesSOD1MutantProtein aggregationAnimals Genetically ModifiedProtein CarbonylationSuperoxide dismutaseMicechemistry.chemical_compoundSuperoxide Dismutase-1Cell Line TumorGeneticsAnimalsHumansAmino Acid SequenceCaenorhabditis elegansMolecular BiologyGenetics (clinical)Motor NeuronsbiologySuperoxide DismutaseSuperoxideAmyotrophic Lateral SclerosisWild typenutritional and metabolic diseasesHydrogen PeroxideGeneral MedicineFusion proteinProtein Structure Tertiarynervous system diseasesCell biologyAmino Acid Substitutionnervous systemchemistryBiochemistrybiology.proteinDismutaseDimerizationHuman Molecular Genetics
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Wild-type Cu/Zn superoxide dismutase stabilizes mutant variants by heterodimerization

2014

Mutations in the gene encoding Cu/Zn superoxide dismutase (SOD1) are responsible for a subset of amyotrophic lateral sclerosis cases presumably by the acquisition of as yet unknown toxic properties. Additional overexpression of wild-type SOD1 in mutant SOD1 transgenic mice did not improve but rather accelerated the disease course. Recently, it was documented that the presence of wild-type SOD1 (SOD(WT)) reduced the aggregation propensity of mutant SOD1 by the formation of heterodimers between mutant and SOD1(WT) and that these heterodimers displayed at least a similar toxicity in cellular and animal models. In this study we investigated the biochemical and biophysical properties of obligate…

Genetically modified mouseanimal diseasesMutantSOD1HeterodimerizationPeptideBiologyProtein aggregationlcsh:RC321-571Superoxide Dismutase-1Humanslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryGenechemistry.chemical_classificationMisfoldingSuperoxide DismutaseWild typenutritional and metabolic diseasesSOD1Molecular biologynervous system diseasesHEK293 Cellsnervous systemNeurologychemistryBiochemistryDismutase activityMutationDismutaseProtein aggregationProtein MultimerizationMutant homodimersNeurobiology of Disease
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