Search results for "Superoxides"

showing 10 items of 91 documents

Pregnenolone sulfate, a naturally occurring excitotoxin involved in delayed retinal cell death.

2002

The present study was designed to investigate the neurosteroid pregnenolone sulfate (PS), known for its ability to modulate NMDA receptors and interfere with acute excitotoxicity, in delayed retinal cell death. Three hours after exposure of the isolated and intact retina to a 30-min PS pulse, DNA fragmentation as assessed by genomic DNA gel electrophoresis and a modified in situ terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end-labeling (TUNEL) method appeared concurrently with an increase in superoxide dismutase (SOD) activity and thiobarbituric acid-reactive substances (TBARS) levels. At 7 h, the increased amount of DNA laddering was accompanied by a higher number of TUN…

Malemedicine.medical_specialtyNeurotoxinsExcitotoxicityApoptosisDNA FragmentationDNA ladderingBiologymedicine.disease_causeBiochemistryReceptors N-Methyl-D-AspartateThiobarbituric Acid Reactive SubstancesRetinaCellular and Molecular Neurosciencechemistry.chemical_compoundAdjuvants ImmunologicSuperoxidesInternal medicinemedicineTBARSIn Situ Nick-End LabelingAnimalsCycloheximideRats WistarProgesteroneProtein Synthesis InhibitorsTUNEL assayEstradiolL-Lactate DehydrogenaseDehydroepiandrosterone SulfateSuperoxide DismutaseRatsEndocrinologychemistryApoptosisPregnenolonePregnenoloneDNA fragmentationLipid PeroxidationPregnenolone sulfateReactive Oxygen Speciesmedicine.drugJournal of neurochemistry
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Chronic Therapy With Isosorbide-5-Mononitrate Causes Endothelial Dysfunction, Oxidative Stress and a Marked Increase in Vascular Endothelin-1 Express…

2011

Aims Isosorbide-5-mononitrate (ISMN) is one of the most frequently used compounds in the treatment of coronary artery disease predominantly in the USA. However, ISMN was reported to induce endothelial dysfunction, which was corrected by vitamin C pointing to a crucial role of reactive oxygen species (ROS) in causing this phenomenon. We sought to elucidate the mechanism how ISMN causes endothelial dysfunction and oxidative stress in vascular tissue. Methods and results Male Wistar rats ( n = 69 in total) were treated with ISMN (75 mg/kg/day) or placebo for 7 days. Endothelin (ET) expression was determined by immunohistochemistry in aortic sections. Isosorbide-5-mononitrate infusion caused si…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIIsosorbide DinitratePharmacologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesEnosInternal medicinePhysiology (medical)medicineAnimalsNitric Oxide DonorsEnzyme InhibitorsRats WistarEndothelial dysfunctionCyclic GMPAortaMice KnockoutNADPH oxidaseEndothelin-1biologybusiness.industryNADPH Oxidasesmedicine.diseasebiology.organism_classificationEndothelin 1BosentanRatsNitric oxide synthaseEndothelial stem cellOxidative StressNG-Nitroarginine Methyl EsterEndocrinologychemistryApocyninbiology.proteinEndothelium VascularCardiology and Cardiovascular MedicineEndothelin receptorbusinessOxidative stressSignal Transductionmedicine.drugFree Radical Biology and Medicine
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Resveratrol Reverses Endothelial Nitric-Oxide Synthase Uncoupling in Apolipoprotein E Knockout Mice

2010

A crucial cause of the decreased bioactivity of nitric oxide (NO) in cardiovascular diseases is the uncoupling of the endothelial NO synthase (eNOS) caused by the oxidative stress-mediated deficiency of the NOS cofactor tetrahydrobiopterin (BH(4)). The reversal of eNOS uncoupling might represent a novel therapeutic approach. The treatment of apolipoprotein E knockout (ApoE-KO) mice with resveratrol resulted in the up-regulation of superoxide dismutase (SOD) isoforms (SOD1-SOD3), glutathione peroxidase 1 (GPx1), and catalase and the down-regulation of NADPH oxidases NOX2 and NOX4 in the hearts of ApoE-KO mice. This was associated with reductions in superoxide, 3-nitrotyrosine, and malondiald…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIISOD3SOD2ResveratrolAntioxidantsSuperoxide dismutaseMicechemistry.chemical_compoundApolipoproteins ESuperoxidesEnosMalondialdehydeInternal medicineStilbenesmedicineAnimalsGTP CyclohydrolaseMice KnockoutPharmacologychemistry.chemical_classificationReactive oxygen speciesbiologyReverse Transcriptase Polymerase Chain ReactionSuperoxide DismutaseChemistrySuperoxideMyocardiumTetrahydrobiopterinbiology.organism_classificationBiopterinIsoenzymesOxidative StressEndocrinologyBiochemistryResveratrolbiology.proteinRNATyrosineMolecular Medicinemedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Acute ammonia intoxication induces an NMDA receptor-mediated increase in poly(ADP-ribose) polymerase level and NAD+ metabolism in nuclei of rat brain…

2004

Acute ammonia toxicity is mediated by excessive activation of NMDA receptors. Activation of NMDA receptors leads to activation of poly(ADP-ribose) polymerase (PARP) which mediates NMDA excitotoxicity. PARP is activated following DNA damage and may lead to cell death via NAD+ and ATP depletion. The aim of the present work was to assess whether acute ammonia intoxication in vivo leads to increased PARP in brain cells nuclei and to altered NAD+ and superoxide metabolism and the contribution of NMDA receptors to these alterations. Acute ammonia intoxication increases PARP content twofold in brain cells nuclei.NAD+ content decreased by 55% in rats injected with ammonia. This was not due to decre…

Malemedicine.medical_specialtyPoly ADP ribose polymeraseExcitotoxicityBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundNAD+ NucleosidaseAmide SynthasesAmmoniaSuperoxidesInternal medicinemedicineAnimalsNeurotoxinRats WistarReceptorBrain ChemistryCell NucleusProtein Synthesis InhibitorsSuperoxideNAD+ ADP-RibosyltransferaseBrainProteinsNADMolecular biologyRatsEndocrinologychemistryTyrosineNMDA receptorNAD+ kinasePoly(ADP-ribose) PolymerasesJournal of Neurochemistry
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Differential effects of diabetes on the expression of the gp91phox homologues nox1 and nox4.

2004

The nox2-dependent NADPH oxidase was shown to be a major superoxide source in vascular disease, including diabetes. Smooth muscle cells of large arteries lack the phagocytic gp91phox subunit of the enzyme; however, two homologues have been identified in these cells, nox1 and nox4. It remained to be established whether also increases in protein levels of the nonphagocytic NADPH oxidase contribute to increased superoxide formation in diabetic vessels. To investigate changes in the expression of these homologues, we measured their expression in aortic vessels of type I diabetic rats. Eight weeks after streptozotocin treatment, we found a doubling in nox1 protein expression, while the expressio…

Malemedicine.medical_specialtyXanthine OxidaseVasodilator AgentsBlotting WesternFluorescent Antibody TechniqueNitric OxideBiochemistryNitric oxideDiabetes Mellitus Experimentalchemistry.chemical_compoundNitroglycerinSuperoxidesPhysiology (medical)Internal medicinemedicineAnimalsNADH NADPH OxidoreductasesRats WistarXanthine oxidaseAortaNADPH oxidasebiologySuperoxideMyocardiumMicrofilament ProteinsElectron Spin Resonance SpectroscopyNOX4NADPH Oxidase 1Endothelial CellsNADPH OxidasesPhosphoproteinsImmunohistochemistryAcetylcholineRatsNitric oxide synthaseEndocrinologychemistryNADPH Oxidase 4NOX1cardiovascular systembiology.proteinNADPH Oxidase 1Nitric Oxide SynthaseCell Adhesion MoleculesFree radical biologymedicine
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Nebivolol inhibits superoxide formation by NADPH oxidase and endothelial dysfunction in angiotensin II-treated rats.

2006

Nebivolol is a β 1 -receptor antagonist with vasodilator and antioxidant properties. Because the vascular NADPH oxidase is an important superoxide source, we studied the effect of nebivolol on endothelial function and NADPH oxidase activity and expression in the well-characterized model of angiotensin II–induced hypertension. Angiotensin II infusion (1 mg/kg per day for 7 days) caused endothelial dysfunction in male Wistar rats and increased vascular superoxide as detected by lucigenin-derived chemiluminescence, as well as dihydroethidine staining. Vascular NADPH oxidase activity, as well as expression at the mRNA and protein level, were markedly upregulated, as well as NOS III uncoupled, …

Malerac1 GTP-Binding Proteinmedicine.medical_specialtyLuminescenceEndotheliumNitric Oxide Synthase Type IIIAdrenergic beta-AntagonistsNitric OxideFluorescenceCell LineNebivololchemistry.chemical_compoundHemoglobinsSuperoxidesInternal medicineInternal MedicinemedicineAnimalsHumansBenzopyransRats WistarCyclic GMPNitritesOxidase testNADPH oxidaseLuminescent AgentsbiologyChemistrySuperoxideAngiotensin IIMyocardiumNADPH OxidasesDicarbethoxydihydrocollidinePhosphoproteinsAngiotensin IINebivololRatsNitric oxide synthasemedicine.anatomical_structureEndocrinologyEthanolaminesNOX1biology.proteinAcridinesBlood VesselsLuminolEndothelium Vascularmedicine.drugSignal TransductionHypertension (Dallas, Tex. : 1979)
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Influence of cadmium on the morphology and functionality of haemocytes in the compound ascidian Botryllus schlosseri

2013

In order to get insights into the effects of cadmium (Cd) on cell morphology and functions, we exposed haemocytes of the colonial ascidian Botryllus schlosseri to sub-lethal concentrations of CdCl(2). Results indicate that Cd hampers haemocyte spreading and phagocytosis in a dose-dependent way, through the alteration of the actin cytoskeleton. In addition, the metal decreases the stability of the internal membranes, as revealed by the Neutral Red assay. The fraction of cells showing positivity for the lysosomal enzyme acid phosphatase is also reduced in the presence of Cd, whereas the number of cells responsive to the Annexin-V assay and showing chromatin condensation increases, suggesting …

Neutral redHemocytesAscidiansPhysiologyCell SurvivalHealth Toxicology and MutagenesisPhagocytosisApoptosisBotryllus schlosseriToxicologyCell morphologyBiochemistrychemistry.chemical_compoundPhagocytosisSuperoxidesCell AdhesionAnimalsUrochordataBotryllus sp.; Ascidians; Haemocytes; Toxicity; CadmiumHaemocytesbiologyCell DeathToxicitySuperoxideCell MembraneAcid phosphataseCell BiologyGeneral MedicineAnatomyActin cytoskeletonbiology.organism_classificationChromatinPhosphoric Monoester HydrolasesCell biologyActin CytoskeletonOxidative StresschemistryBotryllus spApoptosisbiology.proteinMetallothioneinLysosomesOxidation-ReductionCadmium
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Heparin–polynitroxides: Synthesis and preliminary evaluation as cardiovascular EPR/MR imaging probes and extracellular space-targeted antioxidants

2011

We report here the synthesis of heparin-polynitroxide derivatives (HPNs) in which nitroxide moieties are linked either to uronic acid or glycosamine residues of the heparin macromolecule. HPNs have low anticoagulant activity, possess superoxide scavenging properties, bind to the vascular endothelium/extra-cellular matrix and can be detected by EPR and MRI techniques. As the vascular wall-targeted redox-active paramagnetic compounds, HPNs may have both diagnostic (molecular MRI) and therapeutic (ecSOD mimics) applications.

Nitroxide mediated radical polymerizationmedicine.drug_mechanism_of_actionFactor Xa InhibitorUronic acidAntioxidantslaw.inventionchemistry.chemical_compoundSuperoxideslawDrug DiscoverymedicineExtracellularHumansElectron paramagnetic resonancePharmacologyHeparinSuperoxideOrganic ChemistryElectron Spin Resonance SpectroscopyAnticoagulantsHexosaminesGeneral MedicineHeparinMagnetic Resonance ImagingExtracellular MatrixUronic AcidschemistryBiochemistryMolecular ProbesFactor XaNitrogen OxidesPartial Thromboplastin TimeEndothelium VascularFactor Xa Inhibitorsmedicine.drugMacromoleculeEuropean Journal of Medicinal Chemistry
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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 tumour cell sensitivity to TNF-induced oxidative stress and cytotoxicity: Role of glutathione

1998

Glutathione (GSH) and the rate of cellular proliferation determine tumour cell sensitivity to tumour necrosis factor (TNF). Buthionine sulphoximine (BSO), a selective inhibitor of GSH synthesis, inhibits tumour growth and increases recombinant human TNF (rhTNF)-alpha cytoxicity in vitro. Administration of sublethal doses of rhTNF-alpha to Ehrlich ascites-tumour (EAT)-bearing mice induces oxidative stress (as measured by increases in intracellular peroxide levels, O2.- generation and mitochondrial GSSG). ATP-induced selective GSH depletion, when combined with rhTNF-alpha administration, affords a 61% inhibition of tumour growth and results in a significant extent of host survival. Administra…

Programmed cell deathCell SurvivalClinical BiochemistryMitochondrionPharmacologyBiologymedicine.disease_causeBiochemistryMicechemistry.chemical_compoundSuperoxidesmedicineAnimalsHumansCarcinoma Ehrlich TumorGlutathione DisulfideTumor Necrosis Factor-alphaGeneral MedicineGlutathioneGlutathioneRecombinant ProteinsOxidative StresschemistryBiochemistryCancer cellMolecular MedicineGlutathione disulfideTumor necrosis factor alphaOxidative stressIntracellularBioFactors
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