Search results for "OXIDASE"

showing 10 items of 927 documents

Sjøgren's syndrome-associated oxidative stress and mitochondrial dysfunction: Prospects for chemoprevention trials

2012

An involvement of oxidative stress (OS) was found in recent studies of Sjøgren's syndrome (SS) that reported significant changes in protein oxidation, myeloperoxidase activity, TNF-α, nitrotyrosine, and GSH levels in plasma from SS patients. Excess levels of OS markers, as oxidative DNA damage and propanoyl-lysine, were reported in saliva from SS patients. Previous reports concurred with a role of OS in SS pathogenesis, by showing a decreased expression of antioxidant activities in conjunctival epithelial cells of SS patients and in parotid gland tissue samples from SS patients. A link between OS and mitochondrial dysfunction (MDF) is recognized both on the grounds of the established role o…

medicine.medical_specialtyDNA damageMitochondrionBiologyProtein oxidationmedicine.disease_causeChemopreventionBiochemistryPathogenesischemistry.chemical_compoundInternal medicinemedicineHumansSalivaPeroxidasechemistry.chemical_classificationReactive oxygen speciesTumor Necrosis Factor-alphaNitrotyrosineAutoantibodyGeneral MedicineGlutathioneMitochondriaOxidative StressSjogren's SyndromeEndocrinologychemistryTyrosineBiomarkersOxidative stressDNA DamageFree Radical Research
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Pathophysiology of polymorphonuclear leukocyte in arterial hypertension

2009

This review shows how polymorphonuclear leukocytes (PMNs) play a pivotal role in the development of the organ injury that is associated with arterial hypertension. Elevated white blood cell count and higher levels of PMNs activation are risk factors for arterial hypertension and cardiovascular disease. Spontaneously activated PMNs release proinflammatory factors and reactive oxygen species, which have negative effects on vascular tone and on their adhesion to the endothelium. The oxidative stress in hypertensive PMNs is revealed by increased NADPH-oxidase production and lipid peroxidation and by decreased cytosolic and mitochondrial superoxide dismutase concentrations. The overexpression of…

medicine.medical_specialtyEndotheliumNeutrophilsPhysiologyPolymorphonuclear leukocyte Hypertension oxidative stress adhesion moleculesmedicine.disease_causeProinflammatory cytokineSuperoxide dismutaseLipid peroxidationLeukocyte Countchemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansLeukocyte Rollingchemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxide Dismutasebusiness.industryCell adhesion moleculeNADPH OxidasesHematologymedicine.anatomical_structureEndocrinologychemistryCD18 AntigensHypertensionImmunologybiology.proteinLipid PeroxidationCardiology and Cardiovascular MedicinebusinessOxidative stressClinical Hemorheology and Microcirculation
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Sirolimus-Induced Vascular Dysfunction

2008

Objectives This study sought to analyze mechanisms that mediate vascular dysfunction induced by sirolimus. Background Despite excellent antirestenotic capacity, sirolimus-eluting stents have been found to trigger coronary endothelial dysfunction and impaired re-endothelialization. Methods To mimic the continuous sirolimus exposure of a stented vessel, Wistar rats underwent drug infusion with an osmotic pump for 7 days. Results Sirolimus treatment caused a marked degree of endothelial dysfunction as well as a desensitization of the vasculature to the endothelium-independent vasodilator nitroglycerin. Also, sirolimus stimulated intense transmural superoxide formation as detected by dihydroeth…

medicine.medical_specialtyEndotheliumVasodilationNitric oxidechemistry.chemical_compoundInternal medicinemedicinecardiovascular diseasesEndothelial dysfunctionNADPH oxidaseNicotinamidebiologybusiness.industrySuperoxideequipment and suppliesmedicine.diseasesurgical procedures operativemedicine.anatomical_structureEndocrinologychemistrySirolimuscardiovascular systembiology.proteinCardiology and Cardiovascular Medicinebusinessmedicine.drugJournal of the American College of Cardiology
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Dissociation of airway responsiveness and bronchoalveolar lavage (BAL) cell composition in sensitized guinea-pigs after daily inhalation of ovalbumin

1994

Summary. The association between inflammatory cell influx, cell activation status and change of airway responsiveness to acelylcholine (ACh) after daily inhalation of ovalbumin (OA) in sensitized guinea–pigs was investigated. Starting 3 weeks after sensitization (OA at 50mg/kg s.c. + i.p.) guinea–pigs were exposed daily to 2% OA (10min: undercover of 0.5Smg/kg mepyramine i.p. 15min before OA) for 2 weeks. Concentration–response curves (CRCs) for inhaled ACh were performed 24 h after the last OA–challenge and 24 h after another single OA–inhalation 1 week later. CRCs for inhaled ACh were neither affected 24 h after the last OA challenge (daily for two weeks) nor 24 h after another OA–inhalat…

medicine.medical_specialtyEosinophil PeroxidaseOvalbuminGuinea PigsImmunologyMepyramineBronchiLeukocyte CountInternal medicineAdministration InhalationmedicineAnimalsImmunology and AllergyRespiratory systemSensitizationPeroxidasemedicine.diagnostic_testbiologyInhalationbusiness.industryAcetylcholineOvalbuminmedicine.anatomical_structureBronchoalveolar lavageEndocrinologyPeroxidasesMethylprednisoloneImmunologybiology.proteinFemaleImmunizationBronchial HyperreactivitybusinessCell activationBronchoalveolar Lavage Fluidmedicine.drugClinical <html_ent glyph="@amp;" ascii="&"/> Experimental Allergy
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Statin-Induced Liver Injury Involves Cross-Talk between Cholesterol and Selenoprotein Biosynthetic Pathways

2009

Statins have become the mainstay of hypercholesterolemia treatment. Despite a seemingly clear rationale behind their use, the inhibition of HMG-CoA reductase, these compounds have been shown to elicit a variety of unanticipated and elusive effects and side effects in vivo. Among the most frequently noted side effects of statin treatment are elevations in liver enzymes. Here, we report our finding that atorvastatin, cerivastatin, and lovastatin at clinically common concentrations induce a selective, differential loss of selenoprotein expression in cultured human HepG2 hepatocytes. The primarily affected selenoprotein was glutathione peroxidase (GPx), whose biosynthesis, steady-state expressi…

medicine.medical_specialtyGPX1Thioredoxin-Disulfide ReductaseStatinPyridinesmedicine.drug_classAtorvastatinBiologyGPX4tert-ButylhydroperoxideCell Line TumorInternal medicineAtorvastatinmedicineHumansPyrrolesLovastatinSelenoproteinsPharmacologychemistry.chemical_classificationGlutathione Peroxidaseintegumentary systemCytotoxinsGlutathione peroxidaseCerivastatinIsoenzymesCholesterolEndocrinologychemistryHeptanoic AcidsHepatocytesMolecular MedicineLovastatinSelenoproteinHydroxymethylglutaryl-CoA Reductase InhibitorsReactive Oxygen SpeciesSignal Transductionmedicine.drugMolecular Pharmacology
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Neopterin, cellular adhesion molecules and myeolperoxidase in patients with stable and unstable angina pectoris

2011

Neopterin, cellular adhesion molecules and myeolperoxidase in patients with stable and unstable angina pectoris Recent data indicate that the serum level of neopterin, a marker of inflammation and immune modulator secreted by monocytes/macrophages, is elevated in patients with acute coronary syndrome (ACS) and seems to be a prognostic marker for major cardiovascular events. Soluble cellular adhesion molecules (sCAMs) and myeloperoxidase (MPO) levels are also related to ACS. The aim of the present study was to evaluate differences in serum levels of neopterin, sCAMs and MPO between coronary artery disease and metabolic syndrome (CAD-MetS) patients with stable and unstable angina pectoris (SA…

medicine.medical_specialtyGeneral interestSciencemetabolic syndromecellular adhesion moleculesCoronary artery diseasechemistry.chemical_compoundangina pectorisimmune system diseasesInternal medicinemedicineIn patientMultidisciplinarybiologyUnstable anginaCell adhesion moleculeQNeopterinmedicine.diseasemyeloperoxidaseneopterinchemistryMyeloperoxidasebiology.proteinCardiologyMetabolic syndromecoronary artery diseaseProceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences.
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Association of aMAOAgene variant with generalized anxiety disorder, but not with panic disorder or major depression

2001

This study was conducted to detect a possible association of a T941G single nucleotide polymorphism (SNP) in the monoamine oxidase A (MAOA) gene with generalized anxiety disorder (GAD), panic disorder (PD), or major depression (MD). Fifty GAD patients (34 females and 16 males), 38 PD patients (21 females and 17 males), and 108 MD patients (80 females and 28 males) were included. The comparison group consisted of 276 (132 females and 144 males) unrelated healthy individuals. The 941T allele was over-represented in patients suffering from GAD (chi(2) = 6.757; df = 1; P < 0.01, not corrected for multiple testing) when compared to healthy volunteers. No association was observed in MD or PD. Thi…

medicine.medical_specialtyGeneralized anxiety disorderbiologybusiness.industryPanic disorderPanicSingle-nucleotide polymorphismmedicine.diseaseCellular and Molecular NeurosciencePsychiatry and Mental healthInternal medicinemedicinebiology.proteinAnxietymedicine.symptomMonoamine oxidase AbusinessAllele frequencyGenetics (clinical)Anxiety disorderAmerican Journal of Medical Genetics Part B: Neuropsychiatric Genetics
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Progressive Endoplasmic Reticulum Stress Contributes to Hepatocarcinogenesis in Fatty Acyl-CoA Oxidase 1–Deficient Mice

2011

Fatty acyl-coenzyme A oxidase 1 (ACOX1) knockout (ACOX1(-/-)) mice manifest hepatic metabolic derangements that lead to the development of steatohepatitis, hepatocellular regeneration, spontaneous peroxisome proliferation, and hepatocellular carcinomas. Deficiency of ACOX1 results in unmetabolized substrates of this enzyme that function as biological ligands for peroxisome proliferator-activated receptor-α (PPARα) in liver. Here we demonstrate that sustained activation of PPARα in ACOX1(-/-) mouse liver by these ACOX1 substrates results in endoplasmic reticulum (ER) stress. Overexpression of transcriptional regulator p8 and its ER stress-related effectors such as the pseudokinase tribbles h…

medicine.medical_specialtyGenotypePeroxisome proliferator-activated receptorPeroxisome ProliferationMice TransgenicBiologyEndoplasmic ReticulumModels BiologicalPathology and Forensic MedicineMiceInternal medicinemedicineAnimalsHumansAcyl-CoA oxidasePPAR alphaTransgenesDNA Primerschemistry.chemical_classificationLiver cellEndoplasmic reticulumLiver NeoplasmsRegular ArticlePeroxisomemedicine.diseaseNeoplasm ProteinsCell biologyDNA-Binding ProteinsMice Inbred C57BLEndocrinologyGene Expression RegulationLiverchemistryHepatocytesUnfolded protein responseAcyl-CoA OxidaseSteatohepatitisThe American Journal of Pathology
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CRP-induced levels of oxidative stress are higher in brain than aortic endothelial cells

2010

C-reactive protein (CRP) has been demonstrated to induce blood-brain barrier disruption (BBB) involving NAD(P)H-oxidase dependent oxidative stress. It is unclear why CRP affects the BBB and not other vascular beds following stroke. Therefore we examined CRP receptor and NAD(P)H-oxidase expression levels in bovine brain- (BEC) and aortic endothelial cells. Dichlorodihydrofluorescein measurements revealed significantly higher CRP-induced reactive oxygen species (ROS) levels in BEC. Protein expression of the CRP-receptors CD16, CD32 and of the NAD(P)H-oxidase subunit p22phox were also significantly higher in BEC. In conclusion BEC show a higher vulnerability to CRP due to increased levels of C…

medicine.medical_specialtyImmunologyBlood–brain barriermedicine.disease_causeBiochemistryInternal medicinemedicineAnimalsImmunology and AllergyReceptorMolecular BiologyAortachemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyChemistryReceptors IgGBrainEndothelial CellsNADPH OxidasesHematologyOxidative StressC-Reactive Proteinmedicine.anatomical_structureEndocrinologyNAD(P)H oxidaseImmunologybiology.proteinCattleP22phoxNAD+ kinaseOxidative stressCytokine
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Role of cytokines and oxidative stress in the pathophysiology of acute pancreatitis: therapeutical implications.

2002

Abstract Severe acute pancreatitis causes a high incidence of mortality due to the systemic inflammatory response syndrome leading to multiple organ failure. At present, there is no treatment against severe acute pancreatitis, other than supportive critical care. The relationship between pancreatic injury and the uncontrolled systemic response is not completely understood. Nevertheless, experimental and clinical evidences have shown that pro-inflammatory cytokines and oxidative stress are critically involved in the development of local and systemic complications associated with severe acute pancreatitis. Serum levels of pro-inflammatory cytokines, such as TNF-alpha and IL-1beta, increase du…

medicine.medical_specialtyImmunologyInflammationmedicine.disease_causePentoxifyllinechemistry.chemical_compoundInternal medicinemedicineImmunology and AllergyHumansXanthine oxidasePharmacologyInflammationbusiness.industryPneumoniamedicine.diseaseSystemic inflammatory response syndromeOxidative StressEndocrinologymedicine.anatomical_structurechemistryPancreatitisImmunologyAcute DiseaseAcute pancreatitisCytokinesPancreatic injurymedicine.symptombusinessPancreasOxidative stressmedicine.drugCurrent drug targets. Inflammation and allergy
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