Search results for "NADPH oxidase"

showing 10 items of 135 documents

Reactive oxygen and ethylene are involved in the regulation of regurgitant-induced responses in bean plants.

2004

Summary Application of regurgitant from Leptinotarsa decemlineata Say on wound surfaces of one wounded leaf of intact bean ( Phaseolus vulgaris L.) plants resulted in activation of ethylene biosynthesis followed by an increase of both peroxidase and polyphenol oxidase activity. The aim of the present investigation was to study the source of increased oxidative enzyme activities in regurgitant-treated bean leaves and to determine if hydrogen peroxide and ethylene biosynthesis is responsible for regurgitant-induced amplification of wound responses in bean plants. As the regurgitant contained relative high activities of both peroxidase and polyphenol oxidase, there is a possibility that increa…

PhysiologyPlant SciencePolyphenol oxidaseSuperoxide dismutasechemistry.chemical_compoundPlant Growth RegulatorsOxidative enzymeAnimalsCycloheximideCatechol oxidasePlant DiseasesPhaseolusOxidase testNADPH oxidasebiologyTissue ExtractsImidazolesfood and beveragesAminooxyacetic AcidEthylenesAminooxyacetic acidColeopteraKineticschemistryBiochemistryPeroxidasesbiology.proteinReactive Oxygen SpeciesAgronomy and Crop ScienceCatechol OxidasePeroxidaseJournal of plant physiology
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Explaining the phenomenon of nitrate tolerance.

2005

During the last century, nitroglycerin has been the most commonly used antiischemic and antianginal agent. Unfortunately, after continuous application, its therapeutic efficacy rapidly vanishes. Neurohormonal activation of vasoconstrictor signals and intravascular volume expansion constitute early counter-regulatory responses (pseudotolerance), whereas long-term treatment induces intrinsic vascular changes, eg, a loss of nitrovasodilator-responsiveness (vascular tolerance). This is caused by increased vascular superoxide production and a supersensitivity to vasoconstrictors secondary to a tonic activation of protein kinase C. NADPH oxidase(s) and uncoupled endothelial nitric oxide synthase …

PhysiologyVasodilator AgentsPharmacologymedicine.disease_causeNitric OxideProstacyclin synthaseNitric oxidechemistry.chemical_compoundNitroglycerinSuperoxidesPeroxynitrous AcidmedicineCyclic GMP-Dependent Protein KinasesAnimalsHumansBiotransformationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyChemistrySuperoxidePhosphoric Diester HydrolasesAldehyde Dehydrogenase MitochondrialDrug ToleranceAldehyde DehydrogenaseCyclic Nucleotide Phosphodiesterases Type 1VasodilationOxidative StressBiochemistryVasoconstrictioncardiovascular systembiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseReactive Oxygen SpeciesPeroxynitriteOxidative stressSignal TransductionCirculation research
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Regulation of NADPH oxidase-mediated superoxide production by acetylation and deacetylation

2021

Oral treatment of apolipoprotein E-knockout (ApoE-KO) mice with the putative sirtuin 1 (SIRT1) activator resveratrol led to a reduction of nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity in the heart. In contrast, the SIRT1 inhibitor EX527 enhanced the superoxide production in isolated human polymorphonuclear granulocytes. In human monocytic THP-1 cells, phorbol ester-stimulated superoxide production was enhanced by inhibitors of histone deacetylases (HDACs; including quisinostat, trichostatin A (TSA), PCI34051, and tubastatin A) and decreased by inhibitors of histone acetyltransferases [such as garcinol, curcumin, and histone acetyltransferase (HAT) Inhibitor II]. Thes…

Physiologyresveratrolsirtuin 1histone acetyltransferaseSirtuinechemistry.chemical_compoundHistone deacetylasesSirtuin 1Physiology (medical)NADPH-OxidasemedicineQP1-981ddc:610Original ResearchacetylationAcetyltransferasenNADPH oxidasebiologyNADPH oxidaseSirtuin 1SuperoxideAcetylationHistone acetyltransferaseTrichostatin AchemistryBiochemistryHistone acetyltransferasesAcetylationResveratrolNADPH oxidaseshistone deacetylasebiology.proteinHistone deacetylaseDDC 610 / Medicine & healthNicotinamide adenine dinucleotide phosphateRac1medicine.drug
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Protective effect of apocynin in a mouse model of chemically-induced colitis.

2013

Apocynin, a constituent of Picrorhiza kurroa, successfully inhibits NADPH oxidase and shows promise as an anti-inflammatory drug. Now, we report anti-inflammatory effects of apocynin in an experimental colitis model induced by dextran sulfate sodium as well as the effects on the mediators involved in this process. Apocynin reduced the colitis induced in mice by administration of 5 % dextran sulfate sodium during 7 days. Mice were fed a control diet or a diet supplemented with 2 % of apocynin or 2 % of rutin. Sulfasalazine (50 mg/kg, p. o.) was used as a positive control. Treatment with apocynin and rutin ameliorated the course of colonic inflammation with results similar to those of the ref…

Picrorhiza kurroaRutinAnti-Inflammatory AgentsPharmaceutical ScienceNitric Oxide Synthase Type IIPharmacologyInflammatory bowel diseaseAnalytical Chemistrychemistry.chemical_compoundRutinMiceDrug DiscoveryPicrorhizaNADPH oxidasebiologyDextran SulfateColitisBiochemistrycardiovascular systemMolecular Medicinecirculatory and respiratory physiologymedicine.druginorganic chemicalsSTAT3 Transcription FactorColonNitric OxideDinoprostoneNitric oxideSulfasalazinemedicineAnimalscardiovascular diseasesColitisPharmacologyCyclooxygenase 2 Inhibitorsbusiness.industryPlant ExtractsOrganic ChemistryTranscription Factor RelAAcetophenonesmedicine.diseaseSulfasalazineDisease Models AnimalchemistryComplementary and alternative medicineCyclooxygenase 2Apocyninbiology.proteinbusinessPhytotherapyPlanta medica
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Antitumor effects of dehydroxymethylepoxyquinomicin, a novel nuclear factor-kappaB inhibitor, in human liver cancer cells are mediated through a reac…

2009

Activation of the nuclear transcription factor-kappa B (NF-kappa B) has been implicated in liver tumorigenesis. We evaluated the effects of a novel NF-kappa B inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), in two human liver cancer cell lines HA22T/VGH and HuH-6. DHMEQ treatment dose dependently decreased the DNA-binding capacity of the NF-kappa B p65 subunit, inhibited cell growth and proliferation, and increased apoptosis as shown by caspase activation, release of cytochrome c, poly(ADP-ribose) polymerase cleavage, and down-regulation of survivin. DHMEQ also induced a dose-dependent activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling, …

Programmed cell deathCarcinoma HepatocellularBIOLOGICAL-ACTIVITIESDrug Evaluation PreclinicalDown-RegulationAntineoplastic AgentsApoptosisBiologymedicine.disease_causeACTIVATIONchemistry.chemical_compoundHYDROGEN-PEROXIDEENDOPLASMIC-RETICULUM STRESSCell Line TumorSurvivinNADPH OXIDASEmedicineHumansOXIDATIVE STRESSProtein kinase AEndoplasmic Reticulum Chaperone BiPINDUCED APOPTOSISCell ProliferationPharmacologySettore MED/12 - GastroenterologiaDose-Response Relationship DrugUNFOLDED PROTEIN RESPONSECell growthCyclohexanonesINDUCTIONLiver NeoplasmsDEATHNF-kappa BCytochromes cMolecular biologyCell biologyEnzyme ActivationchemistryApoptosisCaspasesCancer cellBenzamidesSettore BIO/14 - FarmacologiaMolecular MedicineGrowth inhibitionMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesOxidative stressMolecular pharmacology
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Parthenolide induces caspase-independent and AIF-mediated cell death in human osteosarcoma and melanoma cells

2013

The mechanism of the cytotoxic effect exerted by parthenolide on tumor cells is not clearly defined today. This article shows that parthenolide stimulates in human osteosarcoma MG63 and melanoma SK-MEL-28 cells a mechanism of cell death, which is not prevented by z-VAD-fmk and other caspase inhibitors. In particular treatment with parthenolide rapidly stimulated (1-2 h) reactive oxygen species (ROS) generation by inducing activation of extracellular signal-regulated kinase 1/2 (ERK 1/2) and NADPH oxidase. This event caused depletion of thiol groups and glutathione, NF-κB inhibition, c-Jun N-terminal kinase (JNK) activation, cell detachment from the matrix, and cellular shrinkage. The increa…

Programmed cell deathMAP Kinase Signaling SystemPhysiologyClinical BiochemistryAmino Acid Chloromethyl Ketoneschemistry.chemical_compoundCell Line TumorSettore BIO/10 - BiochimicaHumansParthenolidePropidium iodideFragmentation (cell biology)MelanomaCaspaseOsteosarcomaCell DeathbiologyNF-kappa BApoptosis Inducing FactorNADPH OxidasesCell BiologyCaspase InhibitorsCell biologyGene Expression Regulation NeoplasticchemistryApoptosisCell cultureCaspasesbiology.proteinApoptosis-inducing factorReactive Oxygen SpeciesSesquiterpenesParthenolide caspase-independent cell death ROS AIFJournal of Cellular Physiology
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Zinc accelerates respiratory burst termination in human PMN

2021

The respiratory burst of phagocytes is essential for human survival. Innate immune defence against pathogens relies strongly on reactive oxygen species (ROS) production by the NADPH oxidase (NOX2). ROS kill pathogens while the translocation of electrons across the plasma membrane via NOX2 depolarizes the cell. Simultaneously, protons are released into the cytosol. Here, we compare freshly isolated human polymorphonuclear leukocytes (PMN) to the granulocytes-like cell line PLB 985. We are recording ROS production while inhibiting the charge compensating and pH regulating voltage-gated proton channel (HV1). The data suggests that human PMN and the PLB 985 generate ROS via a general mechanism,…

Programmed cell deathMedicine (General)PhagocyteQH301-705.5NeutrophilsClinical BiochemistryBiochemistryIon ChannelsFlow cytometryR5-920medicineHumansPhagocyte ; Zinc ; Zinkstoffwechsel ; pH ; H<sub>v</sub>1 ; ROSBiology (General)HV1Respiratory Burstchemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseInnate immune systembiologymedicine.diagnostic_testChemistrypHOrganic ChemistryNADPH OxidasesROSCell biologyRespiratory burstCytosolZincmedicine.anatomical_structurePhagocytebiology.proteinReactive Oxygen SpeciesResearch Paper
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Phytochemical indicaxanthin suppresses 7-ketocholesterol-induced THP-1 cell apoptosis by preventing cytosolic Ca(2+) increase and oxidative stress.

2012

7-Ketocholesterol (7-KC)-induced apoptosis of macrophages is considered a key event in the development of human atheromas. In the present study, the effect of indicaxanthin (Ind), a bioactive pigment from cactus pear fruit, on 7-KC-induced apoptosis of human monocyte/macrophage THP-1 cells was investigated. A pathophysiological condition was simulated by using amounts of 7-KC that can be reached in human atheromatous plaque. Ind was assayed within a micromolar concentration range, consistent with its plasma level after dietary supplementation with cactus pear fruit. Pro-apoptotic effects of 7-KC were assessed by cell cycle arrest, exposure of phosphatidylserine at the plasma membrane, varia…

Programmed cell deathPyridinesCellMedicine (miscellaneous)Apoptosismedicine.disease_causeMonocytesCell Linechemistry.chemical_compoundCytosolmedicineHumansSulfhydryl CompoundsKetocholesterolsNutrition and DieteticsChemistryPlant ExtractsMonocyteMacrophagesNF-kappa BNADPH OxidasesOpuntiaPhosphatidylserineAtherosclerosisPlaque AtheroscleroticCell biologyBetaxanthinsMitochondriaCytosolOxidative Stressmedicine.anatomical_structureApoptosisNADPH Oxidase 4FruitDietary SupplementsCalciumReactive Oxygen SpeciesIndicaxanthinOxidative stressPhytotherapyThe British journal of nutrition
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Neutrophil Extracellular Traps as a Drug Target to Counteract Chronic and Acute Inflammation

2019

Neutrophil extracellular traps (NET), extruded decondensated chromatin entangled with neutrophil proteases, have been first identified in neutrophils stimulated with bacteria or phorbol myristate acetate (PMA) via activation of NADPH oxidase and the generation of reactive oxygen species. Although the first findings demonstrated the beneficial role of NET formation by trapping the bacteria and limiting their dissemination, numerous studies in the recent decade revealed the multifunctional aspects of NET formation which manifests itself not only in the context of anti-microbial effect but also as a pathological trigger. Uncontrolled and exaggerated NET formation or inability to digest and rem…

ProteasesNeutrophilsPharmaceutical ScienceInflammationExtracellular TrapsmedicineHumansMolecular Targeted TherapyInflammationchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyNADPH OxidasesNeutrophil extracellular trapsChromatinCell biologyHistonechemistryAcute DiseaseChronic Diseasebiology.proteinSignal transductionmedicine.symptomReactive Oxygen SpeciesOxidation-ReductionSignal TransductionBiotechnologyCurrent Pharmaceutical Biotechnology
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Missense mutations of dual oxidase 2 (DUOX2) implicated in congenital hypothyroidism have impaired trafficking in cells reconstituted with DUOX2 matu…

2007

Abstract Dual oxidase 2 (DUOX2), a reduced NAD phosphate:O2 oxidoreductase flavoprotein, is a component of the thyrocyte H2O2 generator required for hormone synthesis at the apical plasma membrane. We recently identified a specific DUOX2 maturation factor (DUOXA2) that is necessary and sufficient for expression of functional DUOX2 in mammalian cell lines. We have now used a DUOXA2 reconstituted system to provide the first characterization of natural DUOX2 missense variants (Q36H, R376W, D506N) at the molecular level, analyzing their impact on H2O2 generation, trafficking, stability, folding, and DUOXA2 interaction. The Q36H and R376W mutations completely prevent routing of DUOX2 to the cell…

Protein FoldingMutantMutation MissenseBiologyEndoplasmic ReticulumCell membranesymbols.namesakeEndocrinologyMutant proteinPolysaccharidesCalnexinmedicineCongenital HypothyroidismAnimalsHumansMolecular BiologyCells CulturedFlavoproteinsOxidative foldingEndoplasmic reticulumCell MembraneMembrane ProteinsNADPH OxidasesDual oxidase 2General MedicineHydrogen PeroxideGolgi apparatusDual OxidasesRatsProtein Transportmedicine.anatomical_structureMannosyl-Glycoprotein Endo-beta-N-AcetylglucosaminidaseBiochemistrysymbolsOxidation-ReductionMolecular endocrinology (Baltimore, Md.)
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