Search results for "Active oxygen"

showing 10 items of 884 documents

Acidic Environment Leads to ROS-Induced MAPK Signaling in Cancer Cells

2011

Tumor micromilieu often shows pronounced acidosis forcing cells to adapt their phenotype towards enhanced tumorigenesis induced by altered cellular signalling and transcriptional regulation. In the presents study mechanisms and potential consequences of the crosstalk between extra- and intracellular pH (pH(e), pH(i)) and mitogen-activated-protein-kinases (ERK1/2, p38) was analyzed. Data were obtained mainly in AT1 R-3327 prostate carcinoma cells, but the principle importance was confirmed in 5 other cell types. Extracellular acidosis leads to a rapid and sustained decrease of pH(i) in parallel to p38 phosphorylation in all cell types and to ERK1/2 phosphorylation in 3 of 6 cell types. Furth…

Tumor PhysiologyIntracellular Spacelcsh:MedicineSignal transductionERK signaling cascadeMolecular cell biologyNeoplasmsBasic Cancer ResearchTumor MicroenvironmentSignaling in Cellular ProcessesPhosphorylationCyclic AMP Response Element-Binding ProteinCreb Signalinglcsh:ScienceCellular Stress ResponsesMultidisciplinaryKinaseMechanisms of Signal TransductionSignaling cascadesHydrogen-Ion ConcentrationProtein-Tyrosine KinasesCell biologyOncologyMedicinePhosphorylationMitogen-Activated Protein KinasesSodium-Potassium-Exchanging ATPaseIntracellularResearch ArticleCell SurvivalMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesIntracellular pHBiologyCREBModels BiologicalCell GrowthDogsCell Line TumorAnimalsHumansProtein Kinase InhibitorsBiologyPI3K/AKT/mTOR pathwaylcsh:RRatsEnzyme ActivationCancer cellbiology.proteinlcsh:QExtracellular SpaceReactive Oxygen SpeciesAcidsPLoS ONE
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Les microARN, une nouvelle voie de signalisation cellulaire empruntée par le resvératrol

2011

Les microARN (miARN), decouverts en 1993 dans le laboratoire de V. Ambros [1], ont d'abord ete identifies comme regulateurs du developpement chez Caenorhabditis elegans. Les recherches recentes confirment que ces petits ARN non codants simple-brins sont des elements de signalisation cellulaire fondamentaux dans la regulation de processus tels que le developpement, la differenciation ou la proliferation cellulaire. Ces ARN de 22 nucleotides en moyenne s'apparient de facon specifique a des ARN messagers cibles entrainant le blocage de leur traduction (en cas de complementarite parfaite) ou la degradation des transcrits (en cas de un ou quelques mesappariement[s]). Ils pourraient aussi reguler…

Tumor suppressor geneReactive oxygen species metabolismTumor cellsGeneral MedicineBiologymedicine.disease_causeMolecular biologyGeneral Biochemistry Genetics and Molecular BiologyNeoplasm geneticsGene expressionmicroRNAmedicineGene silencingCarcinogenesismédecine/sciences
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Reactive oxygen species activation of MAPK pathway results in VEGF upregulation as an undesired irradiation response

2013

Background Radioresistance limits the effectiveness of radiotherapy in head and neck squamous cell carcinoma. We previously demonstrated post-radiogenic mitogen-activated protein kinase (MAPK) pathway activation and vascular endothelial growth factor (VEGF) release resulting in reduced tumor cell response. Here, we examined the association of this mechanism with the induction of reactive oxygen species (ROS) under irradiation (IR). Methods Intracellular ROS after IR were measured. We modeled radiation-induced ROS by exposure of two SCC lines to H2O2 and evaluated the impact of irradiation and ROS on ERK phosphorylation by Western blot, immunohistochemistry, and ELISA. Results We found eleva…

Vascular Endothelial Growth Factor AMAPK/ERK pathwayCancer ResearchPathologymedicine.medical_specialtyMAP Kinase Signaling SystemBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyRadiation TolerancePathology and Forensic Medicinechemistry.chemical_compoundDownregulation and upregulationCell Line TumorNitrilesButadienesmedicineHumansEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesProtein kinase Achemistry.chemical_classificationReactive oxygen speciesHydrogen PeroxideImmunohistochemistryCytoprotectionUp-RegulationVascular endothelial growth factorVascular endothelial growth factor AOtorhinolaryngologychemistryCytoprotectionCarcinoma Squamous CellCancer researchPeriodonticsElectrophoresis Polyacrylamide GelOral SurgeryReactive Oxygen SpeciesIntracellularJournal of Oral Pathology & Medicine
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Anticancer therapy-induced vascular toxicity: VEGF inhibition and beyond

2017

Cardiotoxicity induced by chemotherapeutic agents and radiotherapy is a growing problem. In recent years, an increasing number of new drugs with targeted action have been designed. These molecules, such as monoclonal antibodies and tyrosine kinase inhibitors, can cause different type of toxicities compared to traditional chemotherapy. However, they can also cause cardiac complications such as heart failure, arterial hypertension, QT interval prolongation and arrhythmias. Currently, a field of intense research is the vascular toxicity induced by new biologic drugs, particularly those which inhibit vascular endothelial growth factor (VEGF) and its receptor (VEGF-R) and other tyrosine kinases.…

Vascular Endothelial Growth Factor APathologymedicine.medical_specialtyHeart Diseasesmedicine.medical_treatmentVascular toxicity VEGF cardiotoxicity new target therapy chemotherapy radiotherapy cardio-oncologyAntineoplastic Agents030204 cardiovascular system & hematologyQT intervalCardiooncology03 medical and health scienceschemistry.chemical_compoundCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Medicine (all); Cardiology and Cardiovascular Medicine0302 clinical medicineVascularReceptorsmedicineAnimalsHumansChemotherapyEndotheliumNew target therapyChemotherapyCardiotoxicityRadiotherapybusiness.industryVascular Endothelial Growth FactorMedicine (all)Cardiooncology; Vascular toxicity; New target therapyCardio-oncology; Cardiotoxicity; Chemotherapy; New target therapy; Radiotherapy; Vascular toxicity; VEGF; Animals; Antineoplastic Agents; Cardiotoxicity; Endothelium Vascular; Heart Diseases; Humans; Reactive Oxygen Species; Receptors Vascular Endothelial Growth Factor; Vascular Endothelial Growth Factor Amedicine.diseaseVEGFCardiotoxicityVascular endothelial growth factorRadiation therapyCardio-oncologyVascular endothelial growth factor AReceptors Vascular Endothelial Growth Factorchemistry030220 oncology & carcinogenesisHeart failureCancer researchEndothelium VascularVascular toxicityReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessTyrosine kinaseInternational Journal of Cardiology
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Oxidative stress in vascular disease: causes, defense mechanisms and potential therapies

2007

Endothelial cells control vascular homeostasis by generating paracrine factors that regulate vascular tone, inhibit platelet function, prevent adhesion of leukocytes, and limit proliferation of vascular smooth muscle. The dominant factor responsible for many of those effects is endothelium-derived nitric oxide (NO). Endothelial dysfunction characterized by enhanced inactivation or reduced synthesis of NO, alone or in combination, is seen in conjunction with risk factors for cardiovascular disease. Endothelial dysfunction can promote vasospasm, thrombosis, vascular inflammation, and proliferation of the intima. Vascular oxidative stress and increased production of reactive oxygen species con…

Vascular smooth muscleEndotheliumArteriosclerosisPharmacologyNitric Oxidemedicine.disease_causeAntioxidantsReceptor Angiotensin Type 1Superoxide dismutaseRisk FactorsmedicineHumansEndothelial dysfunctionchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologybusiness.industryAnticholesteremic AgentsGeneral Medicinemedicine.diseaseOxidative Stressmedicine.anatomical_structureMitochondrial respiratory chainchemistryImmunologybiology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesCardiology and Cardiovascular MedicinebusinessOxidative stressNature Clinical Practice Cardiovascular Medicine
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Organic Nitrate Therapy, Nitrate Tolerance, and Nitrate-Induced Endothelial Dysfunction: Emphasis on Redox Biology and Oxidative Stress

2015

Abstract Organic nitrates, such as nitroglycerin (GTN), isosorbide-5-mononitrate and isosorbide dinitrate, and pentaerithrityl tetranitrate (PETN), when given acutely, have potent vasodilator effects improving symptoms in patients with acute and chronic congestive heart failure, stable coronary artery disease, acute coronary syndromes, or arterial hypertension. The mechanisms underlying vasodilation include the release of •NO or a related compound in response to intracellular bioactivation (for GTN, the mitochondrial aldehyde dehydrogenase [ALDH-2]) and activation of the enzyme, soluble guanylyl cyclase. Increasing cyclic guanosine-3′,-5′-monophosphate (cGMP) levels lead to an activation of…

Vascular smooth musclePhysiologyVasodilator AgentsClinical BiochemistryVasodilationPharmacologymedicine.disease_causeBiochemistryCalcium in biologyComprehensive Invited ReviewmedicineAnimalsHumansEndothelial dysfunctionMolecular BiologyGeneral Environmental ScienceNitratesChemistryCell Biologymedicine.diseaseOxidative StressCardiovascular DiseasesGeneral Earth and Planetary SciencesEndothelium VascularIsosorbide dinitrateReactive Oxygen SpeciesSoluble guanylyl cyclaseOxidation-ReductionOxidative stressIntracellularmedicine.drugAntioxidants & Redox Signaling
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Pro-inflammatory effects of interleukin-17A on vascular smooth muscle cells involve NAD(P)H- oxidase derived reactive oxygen species.

2010

T cells are known for their contribution to the inflammatory element of atherosclerosis. Recently, it has been demonstrated that the Th17 derived cytokine IL-17 is involved in the pro-inflammatory response of vascular smooth muscle cells (VSMC). The aim of the present study was to examine whether reactive oxygen species (ROS) might be involved in this context. The effect of IL-17A on ROS generation was examined using the fluorescent dye 2′7′-dichlorodihydrofluorescein (H<sub>2</sub>DCF) in primary murine VSMC. IL-17A induced an increase in H<sub>2</sub>DCF fluorescence in VSMC, and this effect was blocked by the NAD(P)H-oxidase inhibitor apocynin and siRNA targeting …

Vascular smooth musclePhysiologymedicine.medical_treatmentAorta Thoracicmedicine.disease_causep38 Mitogen-Activated Protein KinasesMuscle Smooth Vascularchemistry.chemical_compoundMiceCell MovementmedicineAnimalsEnzyme InhibitorsRNA Small InterferingCells Culturedchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseMembrane GlycoproteinsbiologyInterleukin-17AcetophenonesNADPH OxidasesCell DifferentiationMolecular biologyMice Inbred C57BLOxidative StressCytokinechemistryBiochemistryNAD(P)H oxidaseNADPH Oxidase 4ApocyninNADPH Oxidase 2cardiovascular systembiology.proteinCytokinesNAD+ kinaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressJournal of vascular research
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Oral administration of vitamin C decreases muscle mitochondrial biogenesis and hampers training-induced adaptations in endurance performance

2008

Background Exercise practitioners often take vitamin C supplements because intense muscular contractile activity can result in oxidative stress, as indicated by altered muscle and blood glutathione concentrations and increases in protein, DNA, and lipid peroxidation. There is, however, considerable debate regarding the beneficial health effects of vitamin C supplementation. Objective This study was designed to study the effect of vitamin C on training efficiency in rats and in humans. Design The human study was double-blind and randomized. Fourteen men (27-36 y old) were trained for 8 wk. Five of the men were supplemented daily with an oral dose of 1 g vitamin C. In the animal study, 24 mal…

VitaminAdultMalemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentPeroxisome Proliferator-Activated ReceptorsMedicine (miscellaneous)Administration OralAscorbic AcidBiologymedicine.disease_causeAntioxidantsLipid peroxidationMitochondrial Proteinschemistry.chemical_compoundOxygen ConsumptionDouble-Blind MethodInternal medicinemedicineAnimalsHumansRats Wistarchemistry.chemical_classificationNutrition and DieteticsCross-Over StudiesVitamin CNuclear Respiratory Factor 1Glutathione peroxidaseAscorbic acidAdaptation PhysiologicalMitochondria MuscleRatsDNA-Binding ProteinsOxidative StressEndocrinologychemistryMitochondrial biogenesisDietary SupplementsPhysical EnduranceReactive Oxygen SpeciesOxidative stressTranscription Factors
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Vascular oxidative stress, nitric oxide and atherosclerosis.

2014

In the vascular wall, reactive oxygen species (ROS) are produced by several enzyme systems including NADPH oxidase, xanthine oxidase, uncoupled endothelial nitric oxide synthase (eNOS) and the mitochondrial electron transport chain. On the other hand, the vasculature is protected by antioxidant enzyme systems, including superoxide dismutases, catalase, glutathione peroxidases and paraoxonases, which detoxify ROS. Cardiovascular risk factors such as hypercholesterolemia, hypertension, and diabetes mellitus enhance ROS generation, resulting in oxidative stress. This leads to oxidative modification of lipoproteins and phospholipids, mechanisms that contribute to atherogenesis. In addition, oxi…

Xanthine OxidaseAntioxidantNitric Oxide Synthase Type IIImedicine.medical_treatmentMice TransgenicOxidative phosphorylationNitric Oxide Synthase Type Imedicine.disease_causeNitric OxideCardiovascular SystemAntioxidantsNitric oxideSuperoxide dismutasechemistry.chemical_compoundMiceSuperoxidesmedicineAnimalsHumansXanthine oxidasechemistry.chemical_classificationReactive oxygen speciesGlutathione PeroxidaseNADPH oxidasebiologyAryldialkylphosphataseSuperoxide DismutaseNADPH OxidasesAtherosclerosisCatalaseMitochondriaOxidative StresschemistryBiochemistrybiology.proteinCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressAtherosclerosis
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Sildenafil protects epithelial cell through the inhibition of xanthine oxidase and the impairment of ROS production

2009

Recent reports suggest that xanthine oxidase (XO), a modified form of the native xanthine dehydrogenase enzyme, plays an important role in various forms of ischemic and vascular injuries, inflammatory diseases, and chronic heart failure. The XO inhibitors allopurinol and its oxidation product oxypurinol held considerable promises in the treatment of these conditions both in experimental animals and in human clinical trials. More recently, an endothelium-based protective effect of sildenafil, a well-known type-5 phosphodiesterase inhibitor, has been reported in preconditioning prior to ischemia/reperfusion in healthy human subjects. Based on the structural similarities between allopurinol an…

Xanthine OxidasePurinonesEndotheliumCell SurvivalSildenafilIschemiaAllopurinolPharmacologyBiochemistryPiperazinesSildenafil CitrateStructure-Activity Relationshipchemistry.chemical_compoundSettore BIO/10 - BiochimicaTumor Cells CulturedmedicineHumansSulfonesXanthine oxidaseNADPH oxidasebiologybusiness.industryEpithelial CellsGeneral Medicinemedicine.diseasemedicine.anatomical_structurechemistryBiochemistryPurinesCell cultureSettore BIO/14 - Farmacologiabiology.proteinReactive Oxygen SpeciesZaprinastbusinessXanthine oxidase ROS production oxidative stress inhibition sildenafil zaprinast human mammary epithelial cellsmedicine.drugFree Radical Research
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