Search results for "Reactive nitrogen specie"

showing 10 items of 67 documents

A novel form of ataxia oculomotor apraxia characterized by oxidative stress and apoptosis resistance

2007

Several different autosomal recessive genetic disorders characterized by ataxia with oculomotor apraxia (AOA) have been identified with the unifying feature of defective DNA damage recognition and/or repair. We describe here the characterization of a novel form of AOA showing increased sensitivity to agents that cause single-strand breaks (SSBs) in DNA but having no gross defect in the repair of these breaks. Evidence for the presence of residual SSBs in DNA was provided by dramatically increased levels of poly (ADP-ribose)polymerase (PARP-1) auto-poly (ADP-ribosyl)ation, the detection of increased levels of reactive oxygen/nitrogen species (ROS/RNS) and oxidative damage to DNA in the patie…

MaleMethylnitronitrosoguanidineProgrammed cell deathAtaxiaDNA RepairApraxiasDNA damageMitomycinBlotting WesternPoly (ADP-Ribose) Polymerase-1Apoptosismedicine.disease_causeAntioxidantschemistry.chemical_compoundRadiation IonizingmedicineHumansDNA Breaks Single-StrandedOculomotor apraxiaMolecular BiologyCells CulturedEtoposideMembrane Potential MitochondrialbiologyCytochrome cHydrogen PeroxideCell BiologyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicReactive Nitrogen SpeciesMolecular biologyOxidative StresschemistryApoptosisbiology.proteinAtaxiaCamptothecinFemalePoly(ADP-ribose) Polymerasesmedicine.symptomDNAOxidative stressDNA DamageCell Death & Differentiation
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Lymphocytic Mitochondrial Aconitase Activity is Reduced in Alzheimer's Disease and Mild Cognitive Impairment

2015

Background: Specific mechanisms behind the role of oxidative/nitrosative stress and mitochondrial dysfunction in Alzheimer's disease (AD) pathogenesis remain elusive. Mitochondrial aconitase (ACO2) is a Krebs cycle enzyme sensitive to free radicalmediated damage. Objective: We assessed activity and expression of ACO2 extracted from blood lymphocytes of subjects with AD, mild cognitive impairment (MCI), older adults with normal cognition (OCN, age >= 65 years), and younger adults with normal cognition (YCN, age < 65 years). Plasma levels and activities of antioxidants were also measured. Methods: Blood samples were collected from 28 subjects with AD, 22 with MCI, 21 OCN, and 19 YCN. ACO2 act…

MalePathologyantioxidantAntioxidantmedicine.medical_treatmentLymphocyteMitochondrionmedicine.disease_causePolymerase Chain ReactionPathogenesisVitamin Eoxidative stressLymphocytesaconitase (aconitate hydratase)Aconitate Hydratasereactive oxygen speciesGeneral NeuroscienceACO2General MedicineAlzheimer's diseasemitochondriaPsychiatry and Mental healthClinical Psychologyantioxidantsmedicine.anatomical_structureDisease ProgressionSettore MED/26 - NeurologiaFemaleAlzheimer diseaseAlzheimer's diseaseAzheimer diseasereactive nitrogen speciemedicine.medical_specialtyaconitase (aconitate hydratase); Alzheimer disease; antioxidants; free radicals; lymphocyte; mild cognitive impairment; mitochondria; oxidative stress; reactive nitrogen species; reactive oxygen speciesBlotting Westernfree radicalslymphocytemild cognitive impairmentInternal medicinemedicineHumansCognitive DysfunctionRNA MessengerAgedfree radicaloxidative strebusiness.industryVitamin EAconitasimedicine.diseasereactive nitrogen speciesEndocrinologyGeriatrics and GerontologyAlzheimer's disease; Aconitasi; oxidative stress; Aconitase (aconitate hydratase) Azheimer disease antioxidants free radicals lymphocyte mild cognitive impairment mitochondria oxidative stress reactive nitrogen species reactive oxygen speciesMental Status SchedulebusinessBiomarkersOxidative stressJournal of Alzheimer's Disease
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First Evidence for a Crosstalk Between Mitochondrial and NADPH Oxidase-Derived Reactive Oxygen Species in Nitroglycerin-Triggered Vascular Dysfunction

2008

Chronic nitroglycerin treatment results in development of nitrate tolerance associated with endothelial dysfunction (ED). We sought to clarify how mitochondria- and NADPH oxidase (Nox)-derived reactive oxygen species (ROS) contribute to nitrate tolerance and nitroglycerin-induced ED. Nitrate tolerance was induced by nitroglycerin infusion in male Wistar rats (100 microg/h/4 day) and in C57/Bl6, p47(phox/) and gp91(phox/) mice (50 microg/h/4 day). Protein and mRNA expression of Nox subunits were unaltered by chronic nitroglycerin treatment. Oxidative stress was determined in vascular rings and mitochondrial fractions of nitroglycerin-treated animals by L-012 enhanced chemiluminescence, revea…

MalePhysiologyVasodilator AgentsClinical BiochemistryMitochondrionPharmacologymedicine.disease_causeBiochemistryMitochondria HeartMiceNitroglycerinchemistry.chemical_compoundEthidiumAortaChromatography High Pressure LiquidHeart metabolismGeneral Environmental Sciencechemistry.chemical_classificationNADPH oxidasebiologyReverse Transcriptase Polymerase Chain ReactionReactive Nitrogen SpeciesBiochemistryCyclosporinecardiovascular systemcirculatory and respiratory physiologyBlotting WesternIn Vitro TechniquesTransfectionCell LineRotenonemedicineAnimalsHumansRNA MessengerRats WistarMolecular BiologyReactive oxygen speciesNADPH OxidasesCell BiologyRotenoneRatsMice Inbred C57BLchemistryMitochondrial permeability transition poreVasoconstrictionApocyninbiology.proteinGeneral Earth and Planetary SciencesReactive Oxygen SpeciesOxidative stressAntioxidants &amp; Redox Signaling
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Endothelial Dysfunction in Tristetraprolin-deficient Mice Is Not Caused by Enhanced Tumor Necrosis Factor-α Expression

2014

Cardiovascular events are important co-morbidities in patients with chronic inflammatory diseases like rheumatoid arthritis. Tristetraprolin (TTP) regulates pro-inflammatory processes through mRNA destabilization and therefore TTP-deficient mice (TTP(-/-) mice) develop a chronic inflammation resembling human rheumatoid arthritis. We used this mouse model to evaluate molecular signaling pathways contributing to the enhanced atherosclerotic risk in chronic inflammatory diseases. In the aorta of TTP(-/-) mice we observed elevated mRNA expression of known TTP targets like tumor necrosis factor-α (TNF-α) and macrophage inflammatory protein-1α, as well as of other pro-atherosclerotic mediators, l…

MaleVasculitismedicine.medical_specialtyMRNA destabilizationRNA StabilityTristetraprolinInflammationBiochemistryNitric oxideMicechemistry.chemical_compoundOrgan Culture TechniquesTristetraprolinhemic and lymphatic diseasesInternal medicinemedicineAnimalsEndothelial dysfunctionMolecular BiologyAortaReactive nitrogen speciesMice KnockoutMembrane GlycoproteinsNADPH oxidasebiologyTumor Necrosis Factor-alphaEndothelial CellsNADPH OxidasesMolecular Bases of DiseaseCell Biologyrespiratory systemAtherosclerosismedicine.diseaseReactive Nitrogen SpeciesMice Inbred C57BLOxidative StressCholesterolEndocrinologychemistryMice Inbred DBAChronic DiseaseNADPH Oxidase 2biology.proteinFemaleTumor necrosis factor alphamedicine.symptomReactive Oxygen SpeciesJournal of Biological Chemistry
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Hydralazine is a powerful inhibitor of peroxynitrite formation as a possible explanation for its beneficial effects on prognosis in patients with con…

2005

The hemodynamic and anti-ischemic effects of nitroglycerin (GTN) are rapidly blunted as a result of the development of nitrate tolerance. Hydralazine has been shown to prevent tolerance in experimental and clinical studies, all of which may be at least in part secondary to antioxidant properties of this compound. The antioxidant effects of hydralazine were tested in cell free systems, cultured smooth muscle cells, isolated mitochondria, and isolated vessels. Inhibitory effects on the formation of superoxide and/or peroxynitrite formation were tested using lucigenin and L-012 enhanced chemiluminescence as well as DHE-fluorescence. The peroxynitrite scavenging properties were also assessed by…

Malemedicine.medical_specialtyAntioxidantmedicine.medical_treatmentBiophysicsMitochondrionBiochemistryAntioxidantsMitochondrial ProteinsNitroglycerinchemistry.chemical_compoundPeroxynitrous AcidInternal medicinemedicineAnimalsHumansLucigeninRats WistarMolecular BiologyHeart FailureSuperoxideAldehyde Dehydrogenase MitochondrialMicrofilament ProteinsDrug ToleranceFree Radical ScavengersCell BiologyAldehyde DehydrogenaseHydralazineHydralazinePhosphoproteinsPrognosismedicine.diseaseReactive Nitrogen SpeciesMitochondriaRatsOxidative StressEndocrinologychemistryHeart failureIsosorbide dinitrateReactive Oxygen SpeciesCell Adhesion MoleculesPeroxynitritemedicine.drugBiochemical and Biophysical Research Communications
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17β-Estradiol Reduces Nitric Oxide Production in the Guinea Pig Cochlea

2013

Intense noise exposure and the application of ototoxic substances result in increased levels of reactive oxygen species (ROS) and reactive nitrogen species (RNS), such as nitric oxide (NO). In order to reduce the free NO concentration in the inner ear under pathological conditions, the use of natural cytoprotective substances such as 17β-estradiol is a promising therapeutic concept. In male guinea pigs the organ of Corti and the lateral wall were isolated from the cochlea and afterwards incubated for 6 h in cell-culture medium. 17β-Estradiol was adjusted in 2 concentrations to organ cultures of the right ears (12 animals per concentration). The left ears were used as controls. The NO produc…

Malemedicine.medical_specialtyEndocrinology Diabetes and MetabolismGuinea PigsClinical BiochemistryDown-RegulationBiologyNitric OxideCell morphologyOrgan cultureBiochemistryNitric oxidechemistry.chemical_compoundOrgan Culture TechniquesEndocrinologyInternal medicineotorhinolaryngologic diseasesmedicineAnimalsInner earCell ShapeNitritesCochleaReactive nitrogen specieschemistry.chemical_classificationReactive oxygen speciesEstradiolBiochemistry (medical)General MedicineCochleaUp-Regulationmedicine.anatomical_structureEndocrinologychemistryOrgan of Cortisense organsHormone and Metabolic Research
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Silibinin modulates lipid homeostasis and inhibits nuclear factor kappa B activation in experimental nonalcoholic steatohepatitis.

2012

Nonalcoholic steatohepatitis (NASH) is associated with increased liver-related mortality. Disturbances in hepatic lipid homeostasis trigger oxidative stress and inflammation (ie, lipotoxicity), leading to the progression of NASH. This study aimed at identifying whether silibinin may influence the molecular events of lipotoxicity in a mouse model of NASH. Eight-week-old db/db mice were fed a methionine-choline deficient (MCD) diet for 4 weeks and treated daily with silibinin (20 mg/kg intraperitoneally) or vehicle. Liver expression and enzyme activity of stearoyl-CoA desaturase-1 and acyl-CoA oxidase, and expression of liver fatty acid-binding protein were assessed. Hepatic levels of reactiv…

Malemedicine.medical_specialtyMice ObeseSilibininmedicine.disease_causeAntioxidantsTranslational Research BiomedicalMicechemistry.chemical_compoundMethionineNon-alcoholic Fatty Liver DiseasePhysiology (medical)Internal medicineNonalcoholic fatty liver diseasemedicineTBARSAnimalsHomeostasisNASH MCD Silibinin lipotoxicity.Reactive nitrogen speciesLiver injurychemistry.chemical_classificationReactive oxygen speciesAnti-Inflammatory Agents Non-SteroidalBiochemistry (medical)NF-kappa BPublic Health Environmental and Occupational HealthGeneral MedicineLipid Metabolismmedicine.diseaseCholine DeficiencyFatty LiverDisease Models AnimalOxidative StressEndocrinologyLiverchemistryLipotoxicitySilybinOxidative stressSilymarin
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Redox signaling (cross-talk) from and to mitochondria involves mitochondrial pores and reactive oxygen species

2010

This review highlights the important role of redox signaling between mitochondria and NADPH oxidases. Besides the definition and general importance of redox signaling, the cross-talk between mitochondrial and Nox-derived reactive oxygen species (ROS) is discussed on the basis of 4 different examples. In the first model, angiotensin-II is discussed as a trigger for NADPH oxidase activation with subsequent ROS-dependent opening of mitochondrial ATP-sensitive potassium channels leading to depolarization of mitochondrial membrane potential followed by mitochondrial ROS formation and respiratory dysfunction. This concept was supported by observations that ethidium bromide-induced mitochondrial d…

Mitochondrial ROSAgingPotassium ChannelsMyocytes Smooth MuscleBiophysicsIn Vitro TechniquesMitochondrionmedicine.disease_causeMitochondrial Membrane Transport ProteinsModels BiologicalMitochondrial apoptosis-induced channelBiochemistryPeroxynitritechemistry.chemical_compoundmedicineAnimalsHumansMitochondrionFeedback PhysiologicalNADPH oxidasebiologyNADPH oxidaseMitochondrial Permeability Transition PoreSuperoxideAngiotensin IINADPH OxidasesSuperoxideNitric oxideCell BiologyReactive Nitrogen SpeciesMitochondriaCell biologyOxidative StressOxidative protein modificationchemistryMitochondrial permeability transition poreRedox regulationNOX1Hypertensionbiology.proteinReactive Oxygen SpeciesOxidation-ReductionOxidative stressSignal TransductionBiochimica et Biophysica Acta (BBA) - Bioenergetics
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Nitric oxide synthase inhibition and oxidative stress in cardiovascular diseases: Possible therapeutic targets?

2013

International audience; Nitric oxide (• NO) is synthetized enzymatically from L-arginine (L-Arg) by three NO synthase isoforms, iNOS, eNOS and nNOS. The synthesis of NO is selectively inhibited by guanidino-substituted analogs of L-Arg or methylarginines such as asymmetric dimethylarginine (ADMA), which results from protein degradation in cells. Many disease states, including cardiovascular diseases and diabetes, are associated with increased plasma levels of ADMA. The N-terminal catalytic domain of these NOS isoforms binds the heme prosthetic group as well as the redox cofactor, tetrahydrobiopterin (BH 4) associated with a regulatory protein, calmodulin (CaM). The enzymatic activity of NOS…

NO inhibitorsfree radicals030204 cardiovascular system & hematologyProtein degradationPharmacologyNitric OxideNitric oxide03 medical and health scienceschemistry.chemical_compoundBH 40302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemcardiovascular diseaseEnosmedicineAnimalsHumansPharmacology (medical)Enzyme InhibitorsEndothelial dysfunctionReactive nitrogen species030304 developmental biologyPharmacologyNO synthases0303 health sciencesbiologyTetrahydrobiopterinbiology.organism_classificationmedicine.disease[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular system3. Good healthADMANitric oxide synthaseOxidative StresschemistryBiochemistryCardiovascular Diseasesbiology.proteinNitric Oxide SynthaseAsymmetric dimethylargininemedicine.drugPharmacology &amp; Therapeutics
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Redox signaling in acute pancreatitis

2015

Acute pancreatitis is an inflammatory process of the pancreatic gland that eventually may lead to a severe systemic inflammatory response. A key event in pancreatic damage is the intracellular activation of NF-κB and zymogens, involving also calcium, cathepsins, pH disorders, autophagy, and cell death, particularly necrosis. This review focuses on the new role of redox signaling in acute pancreatitis. Oxidative stress and redox status are involved in the onset of acute pancreatitis and also in the development of the systemic inflammatory response, being glutathione depletion, xanthine oxidase activation, and thiol oxidation in proteins critical features of the disease in the pancreas. On th…

NecrosisGSH reduced glutathioneSTAT3 signal transducer and activator of transcription 3ERK extracellular signal-regulated kinasesClinical BiochemistryCCK cholecystokininTRAFs TNF receptor associated factorsReview ArticleIκB kinasePharmacologymedicine.disease_causeBiochemistrySHP small heterodimer partnerSTIM1 stromal interaction molecule 1chemistry.chemical_compoundHATs histone acetyltransferasesMedicineASK1GCL glutamate cysteine ligaseTNF-α tumor necrosis factor alphaIKK IκB kinaseNOS nitric oxide synthaseAcute inflammationHIF hypoxia inducible factorlcsh:QH301-705.5NF-κB nuclear factor kappa BDAMPs damage-associated molecular pattern moleculeslcsh:R5-920biologyGSSG oxidized glutathioneNF-kappa BNLRs nucleotide-binding oligomerization domain (NOD) like receptorsTRADD tumor necrosis factor receptor type 1-associated DEATH domain proteinTRPC3 transient receptor potential channel 3VEGF vascular endothelial growth factorGlutathioneTNFR tumor necrosis factor receptorHMGB1 high-mobility group Box 1 proteinIP3R inositol 145-trisphosphate receptor type 3VCAM-1 Vascular Cell adhesion protein 1Acute DiseaseJNK c-Jun N-terminal kinaseAcute pancreatitisTLRs toll-like receptorsmedicine.symptomlcsh:Medicine (General)Oxidation-ReductionAP-1 activator protein-1Signal TransductionmRNA messenger ribonucleic acidHMGB1ASC apoptosis-associated speck-like protein containing a carboxy-terminal CARDRNS reactive nitrogen speciesPTPs protein tyrosine phosphatasesROS reactive oxygen speciesNADH nicotinamide adenine dinucleotidepHe extracellular pHFAEE fatty acid ethyl estersAP acute pancreatitisHumansXanthine oxidaseCBP CREB-binding proteinRyR endoplasmic reticulum membrane ryanodine receptorsMDA malondialdehydeNO nitric oxideXO xanthine oxidaseASK1 apoptosis signal-regulating kinase-1business.industryOrganic ChemistryAutophagyNADPH nicotinamide adenine dinucleotide phosphateHDACs histone deacetylasesmedicine.diseaseCARS compensatory anti-inflammatory response syndromeXDH xanthine dehydrogenaseIL interleukinIκB inhibitor of kappa BAcute pancreatitisETC Electron transport chainPancreatitisMKPs MAPK phosphatasesSAP severe acute pancreatitischemistrylcsh:Biology (General)DTT dithiothreitolOxidative stressNAC N-acetyl cysteineImmunologybiology.proteinCalciumLysosomesReactive Oxygen SpeciesbusinessMAPK mitogen-activated protein kinaseOxidative stressERCP endoscopic retrograde cholangiopancreatographyRedox Biology
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