Search results for "Active oxygen"

showing 10 items of 884 documents

MK801 blocks hypoxic blood-brain-barrier disruption and leukocyte adhesion.

2008

The aim of the present study was to examine the signaling pathways of hypoxia followed by reoxygenation (H/R)-induced disruption of the blood-brain-barrier (BBB) in a co-culture of astrocytes and brain endothelial cells (BEC) in vitro. We analyzed the possible stabilizing effect of MK801, a highly selective N-methyl-d-aspartate receptor (NMDAR) antagonist, on BBB integrity. Levels of reactive oxygen species (ROS), glutamate (Glut) release and monocyte adhesion were measured under normoxia and H/R. BBB integrity was monitored measuring the trans-endothelial electrical resistance (TEER). TEER values dropped under H/R conditions which was abolished by MK801. Glut release from astrocytes, but n…

Macrocyclic CompoundsSwineGlutamic AcidBiologyBlood–brain barrierchemistry.chemical_compoundmedicineExtracellularCell AdhesionElectric ImpedanceLeukocytesAnimalsEnzyme InhibitorsOxazolesCells Culturedchemistry.chemical_classificationReactive oxygen speciesRyanodine receptorRyanodineGeneral NeuroscienceEndoplasmic reticulumGlutamate receptorAcetophenonesBrainEndothelial CellsCell HypoxiaCoculture TechniquesCell biologyOxygenmedicine.anatomical_structurechemistryBlood-Brain BarrierAstrocytesApocyninCalciumNAD+ kinaseDizocilpine MaleateReactive Oxygen SpeciesExcitatory Amino Acid AntagonistsNeuroscience letters
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Oxidation Enhances Human Serum Albumin Thermal Stability and Changes the Routes of Amyloid Fibril Formation

2014

Oxidative damages are linked to several aging-related diseases and are among the chemical pathways determining protein degradation. Specifically, interplay of oxidative stress and protein aggregation is recognized to have a link to the loss of cellular function in pathologies like Alzheimer's and Parkinson's diseases. Interaction between protein and reactive oxygen species may indeed induce small changes in protein structure and lead to the inhibition/modification of protein aggregation process, potentially determining the formation of species with different inherent toxicity. Understanding the temperate relationship between these events can be of utmost importance in unraveling the molecul…

Macromolecular AssembliesProtein Foldinglcsh:MedicineProtein aggregationBiochemistryPhysical Chemistry01 natural sciencesProtein Structure SecondaryProtein structurePathologylcsh:Sciencechemistry.chemical_classification0303 health sciencesMultidisciplinarybiologyProtein StabilityChemistryPhysicsNeurodegenerationTemperatureNeurodegenerative DiseasesHuman serum albuminChemistryNeurologyBiochemistryMedicineOxidation-ReductionMolecular PathologyResearch Articlemedicine.drugAmyloidBiophysicsSerum albuminProtein degradation010402 general chemistry03 medical and health sciencesDiagnostic MedicinemedicineHumansProtein InteractionsBiologySerum Albumin030304 developmental biologyAmyloid Fluorescence Oxidation Protein aggregation Spectoscopy Light Scattering Serum AlbuminReactive oxygen specieslcsh:RProteinsHydrogen Peroxidemedicine.diseaseProtein tertiary structure0104 chemical sciencesKineticsbiology.proteinlcsh:QProtein MultimerizationGeneral Pathology
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Age-dependent allocation of carotenoids to coloration versus antioxidant defences.

2009

SUMMARYAging is commonly attributed to age-related changes in oxidative damage due to an increased production of reactive oxygen species (ROS) and a weakened efficacy of enzymatic antioxidants. These age-related changes might therefore modify the use of dietary antioxidants, including carotenoids. As carotenoids are closely associated with the expression of secondary sexual signals, the allocation of carotenoids to sexual signal versus antioxidant defences may vary with age. In this study, we explored how carotenoid-based ornament and antioxidant activity varied with age and how an inflammatory-induced oxidative burst affected ornament and antioxidant activity across a range of ages. Using …

Male0106 biological sciencesAntioxidantPhysiologymedicine.medical_treatmentPhysiologyAge dependent[ SDV.IMM.IA ] Life Sciences [q-bio]/Immunology/Adaptive immunology01 natural sciencesAntioxidantsCarotenoidComputingMilieux_MISCELLANEOUSchemistry.chemical_classification[SDV.EE]Life Sciences [q-bio]/Ecology environment0303 health scienceszebra finches[SDV.BID.EVO]Life Sciences [q-bio]/Biodiversity/Populations and Evolution [q-bio.PE]Beakfood and beveragesRespiratory burstAntioxidant capacityBeak[SDV.IMM.IA]Life Sciences [q-bio]/Immunology/Adaptive immunologyFemaleAquatic ScienceBiology010603 evolutionary biology[ SDV.EE ] Life Sciences [q-bio]/Ecology environmenthonesty03 medical and health sciencesBotanymedicineAnimalsMolecular BiologyEcology Evolution Behavior and Systematics030304 developmental biologyReactive oxygen species[ SDE.BE ] Environmental Sciences/Biodiversity and Ecologyallocation strategiesagingPigments Biologicalbiology.organism_classificationCarotenoidschemistryInsect ScienceAnimal Science and ZoologyFinches[SDE.BE]Environmental Sciences/Biodiversity and EcologysignalTaeniopygia
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G6PD protects from oxidative damage and improves healthspan in mice

2016

S.N.-P. and P.J.F.-M. have been funded by the Spanish Association Against Cancer(aecc). Work in the laboratory of M.S. is funded by the CNIO and by grants from the Spanish Ministry of Economy co-funded by the European Regional Development Fund(SAF project), the European Research Council (ERC Advanced Grant), the Regional Government of Madrid co-funded by the European Social Fund (ReCaRe project), the European Union (RISK-IR project), the Botin Foundation and Banco Santander(Santander Universities Global Division), the Ramon Areces Foundation, and the AXA Foundation. Work in the laboratory of J.V. was supported by grants SAF2013-44663-R,from the Spanish Ministry of Education and Science (MEC…

Male0301 basic medicineAgingCellGeneral Physics and AstronomyDehydrogenaseEndogenymedicine.disease_causestressMicehemic and lymphatic diseasesratmécanismegenesreactive oxygen specieschemistry.chemical_classificationMultidisciplinary[SDV.BA]Life Sciences [q-bio]/Animal biologyQvieillissementCell biologymedicine.anatomical_structureanimal transgéniqueFemaleGenetically modified mouse[SDV.OT]Life Sciences [q-bio]/Other [q-bio.OT]congenital hereditary and neonatal diseases and abnormalitiesScienceTransgeneLongevityMice TransgenicGlucosephosphate DehydrogenaseBiologyGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesparasitic diseasesmedicineAnimalsHumansReactive oxygen speciesgènenutritional and metabolic diseasesGeneral ChemistrycellMolecular biologytransgenic mouseOxidative Stress030104 developmental biologymechanistic theorychemistryageingenzyme antioxydanteAgeingespèce reactive de l'oxygènecelluleReactive Oxygen SpeciesNADPOxidative stressNature Communications
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Dual disruption of aldehyde dehydrogenases 1 and 3 promotes functional changes in the glutathione redox system and enhances chemosensitivity in nonsm…

2020

AbstractAldehyde dehydrogenases (ALDHs) are multifunctional enzymes that oxidize diverse endogenous and exogenous aldehydes. We conducted a meta-analysis based on The Cancer Genome Atlas and Gene Expression Omnibus data and detected genetic alterations in ALDH1A1, ALDH1A3, or ALDH3A1, 86% of which were gene amplification or mRNA upregulation, in 31% of nonsmall cell lung cancers (NSCLCs). The expression of these isoenzymes impacted chemoresistance and shortened survival times in patients. We hypothesized that these enzymes provide an oxidative advantage for the persistence of NSCLC. To test this hypothesis, we used genetic and pharmacological approaches with DIMATE, an irreversible inhibito…

Male0301 basic medicineCancer ResearchLung NeoplasmsCell- och molekylärbiologiCellAldehyde dehydrogenaseKaplan-Meier EstimateMicechemistry.chemical_compound0302 clinical medicineCarcinoma Non-Small-Cell LungAntineoplastic Combined Chemotherapy ProtocolsCytotoxicityMiddle AgedAldehyde OxidoreductasesGlutathioneCancer metabolismUp-Regulation3. Good healthCancer therapeutic resistancemedicine.anatomical_structureAlkynes030220 oncology & carcinogenesisFemale[SDV.CAN]Life Sciences [q-bio]/CancerBiologyIsozymeAldehyde Dehydrogenase 1 FamilyArticle03 medical and health sciencesTargeted therapiesDownregulation and upregulationCell Line TumorGeneticsmedicineAnimalsHumansSulfhydryl CompoundsLung cancerMolecular BiologyAgedCancer och onkologiGene AmplificationRetinal DehydrogenaseGlutathioneAldehyde Dehydrogenasemedicine.diseaseXenograft Model Antitumor AssaysALDH1A1030104 developmental biologychemistryDrug Resistance NeoplasmCancer and Oncologybiology.proteinCancer researchCisplatinReactive Oxygen SpeciesCell and Molecular Biologynonsmall cell lung cancer
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The Effectiveness of Glutathione Redox Status as a Possible Tumor Marker in Colorectal Cancer

2021

The role of oxidative stress (OS) in cancer is a matter of great interest due to the implication of reactive oxygen species (ROS) and their oxidation products in the initiation of tumorigenesis, its progression, and metastatic dissemination. Great efforts have been made to identify the mechanisms of ROS-induced carcinogenesis

Male0301 basic medicineColorectal cancermedicine.disease_causechemistry.chemical_compound0302 clinical medicineoxidative stressBiology (General)Spectroscopychemistry.chemical_classificationChemistryGeneral MedicineMiddle AgedGlutathioneComputer Science ApplicationsChemistrytumor markers030220 oncology & carcinogenesisFemaleGSSGColorectal NeoplasmsGSH redox stateOxidation-ReductionQH301-705.5colorectal cancerRedoxArticleCatalysisInorganic Chemistry03 medical and health sciencesBiomarkers TumorGSHmedicineHumansPhysical and Theoretical ChemistryQD1-999Molecular BiologyAgedGSSG/GSH redox stateTumor markerReactive oxygen speciesOrganic ChemistryCancerGlutathionemedicine.disease030104 developmental biologyCase-Control StudiesCancer researchReactive Oxygen SpeciesCarcinogenesisOxidative stressInternational Journal of Molecular Sciences
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Moderate weight loss attenuates chronic endoplasmic reticulum stress and mitochondrial dysfunction in human obesity

2018

Abstract Objective In obese patients undergoing caloric restriction, there are several potential mechanisms involved in the improvement of metabolic outcomes. The present study further explores whether caloric restriction can modulate endoplasmic reticulum (ER) stress and mitochondrial function, as both are known to be mechanisms underlying inflammation and insulin resistance (IR) during obesity. Methods A total of 64 obese patients with BMI ≥35 kg/m2 underwent a dietary program consisting of 6 weeks of a very-low-calorie diet followed by 18 weeks of low-calorie diet. We evaluated changes in the metabolic and inflammatory markers -TNFα, hsCRP, complement component 3 (C3c), and retinol bindi…

Male0301 basic medicineGPX1MitochondrionSystemic inflammationmedicine.disease_causeGlutathione Peroxidase GPX10302 clinical medicineSirtuin 1Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsMembrane Potential MitochondrialbiologyComplement C3Middle AgedEndoplasmic Reticulum StressMitochondriaC-Reactive ProteinFemalemedicine.symptomAdultmedicine.medical_specialty030209 endocrinology & metabolism03 medical and health sciencesInsulin resistanceInternal medicineWeight LossmedicineHumansObesityMolecular BiologyCaloric RestrictionInflammationGlutathione PeroxidaseRetinol binding protein 4Tumor Necrosis Factor-alphabusiness.industryEndoplasmic reticulumCell Biologymedicine.disease030104 developmental biologyEndocrinologySpainbiology.proteinUnfolded protein responseInsulin ResistanceReactive Oxygen SpeciesbusinessRetinol-Binding Proteins PlasmaOxidative stressMolecular Metabolism
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Aged Mice Devoid of the M3 Muscarinic Acetylcholine Receptor Develop Mild Dry Eye Disease

2021

The parasympathetic nervous system is critically involved in the regulation of tear secretion by activating muscarinic acetylcholine receptors. Hence, various animal models targeting parasympathetic signaling have been developed to induce dry eye disease (DED). However, the muscarinic receptor subtype (M1–M5) mediating tear secretion remains to be determined. This study was conducted to test the hypothesis that the M3 receptor subtype regulates tear secretion and to evaluate the ocular surface phenotype of mice with targeted disruption of the M3 receptor (M3R−/−). The experimental techniques included quantification of tear production, fluorescein staining of the ocular surface, environmenta…

Male0301 basic medicineM3medicine.disease_causeMiceM<sub>3</sub>0302 clinical medicineMuscarinic acetylcholine receptorTear secretionBiology (General)SpectroscopyCorneal epitheliumMice Knockouttear secretionChemistryEpithelium CornealMuscarinic acetylcholine receptor M3General Medicinedry eye diseaseComputer Science ApplicationsChemistrymedicine.anatomical_structureDry Eye SyndromesGoblet CellsConjunctivamedicine.medical_specialtyConjunctivaQH301-705.5ArticleCatalysisProinflammatory cytokineInorganic Chemistry03 medical and health sciencesmuscarinic receptorInternal medicinecorneamedicineAnimalsPhysical and Theoretical ChemistryQD1-999Molecular BiologyReceptor Muscarinic M3Goblet cellOrganic Chemistryeye diseasesMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologyTears030221 ophthalmology & optometrysense organsReactive Oxygen SpeciesOxidative stressInternational Journal of Molecular Sciences
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Malnutrition impairs mitochondrial function and leukocyte activation

2019

Abstract Background The aim of this study was to evaluate markers of inflammation, oxidative stress and endothelial function in a disease-related malnutrition (DRM) outpatient population. Methods For this cross-sectional study, a total of 83 subjects were included and clustered in 3 groups: 34 with normonutrition (NN), 21 with DRM without inflammation (DRM-I) and 28 with DRM and inflammation (DRM + I). Nutritional diagnosis was conducted for all subjects according to ASPEN. Biochemical parameters, proinflammatory cytokines, reactive oxygen species production, glutathione, mitochondrial membrane potential, oxygen consumption, adhesion molecules and leukocyte-endothelium interactions were eva…

Male0301 basic medicineMedicine (miscellaneous)Mitochondrionmedicine.disease_causechemistry.chemical_compound0302 clinical medicineLeukocytesDisease-related malnutrition030212 general & internal medicineEndothelial dysfunctionlcsh:RC620-627Membrane Potential Mitochondrialchemistry.chemical_classificationeducation.field_of_studyNutrition and DieteticsMiddle AgedGlutathioneMitochondrialcsh:Nutritional diseases. Deficiency diseasesCytokinesFemalelcsh:Nutrition. Foods and food supplymedicine.medical_specialtyPopulationlcsh:TX341-641Proinflammatory cytokine03 medical and health sciencesInternal medicineCell AdhesionmedicineHumanseducationOutpatient populationAgedInflammationReactive oxygen species030109 nutrition & dieteticsbusiness.industryResearchMalnutritionEndothelial functionGlutathionemedicine.diseaseOxygenCross-Sectional StudiesEndocrinologychemistrySpainTransferrinOxidative stressReactive Oxygen SpeciesbusinessOxidative stressNutrition Journal
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Investigating and re-evaluating the role of glycogen synthase kinase 3 beta kinase as a molecular target for cardioprotection by using novel pharmaco…

2019

Aims Glycogen synthase kinase 3 beta (GSK3β) link with the mitochondrial Permeability Transition Pore (mPTP) in cardioprotection is debated. We investigated the role of GSK3β in ischaemia (I)/reperfusion (R) injury using pharmacological tools. Methods and results Infarct size using the GSK3β inhibitor BIO (6-bromoindirubin-3'-oxime) and several novel analogues (MLS2776-MLS2779) was determined in anaesthetized rabbits and mice. In myocardial tissue GSK3β inhibition and the specificity of the compounds was tested. The mechanism of protection focused on autophagy-related proteins. GSK3β localization was determined in subsarcolemmal (SSM) and interfibrillar mitochondria (IFM) isolated from Lang…

Male0301 basic medicinePhysiologyMyocardial InfarctionAutophagy-Related ProteinsMyocardial Reperfusion Injury030204 cardiovascular system & hematologyMitochondrionPharmacologyMitochondrial Membrane Transport ProteinsMitochondria HeartStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineReperfusion therapyPhysiology (medical)AnimalsMyocytes CardiacProtein Kinase InhibitorsGSK3BMice Knockoutchemistry.chemical_classificationCardioprotectionReactive oxygen speciesGlycogen Synthase Kinase 3 betaMolecular StructureMitochondrial Permeability Transition PoreChemistryKinaseMPTPIsolated Heart PreparationMice Inbred C57BLDisease Models Animal030104 developmental biologyMitochondrial permeability transition poreFemaleRabbitsCardiology and Cardiovascular MedicineCyclophilin DSignal TransductionCardiovascular Research
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