Search results for "REDUCTASE"

showing 10 items of 798 documents

Reductive Drug Metabolism in Isolated Perfused Rat Liver under Restricted Oxygen Supply

1978

1. Hepatic azo and nitro reductase activities were studied in the perfused rat liver under normal and restricted oxygen supply. 2. Formation of sulphanilamide or p-aminobenzoic acid from neoprontosil or p-nitrobenzoic acid under aerobic conditions of liver perfusion was negligible, even at a reduced oxygen saturation of a pO2 of 300 mm Hg in the haemoglobinfree perfusion system. At a pO2 of 200 mm Hg reductase activities were almost maximal. 3. Conjugation of sulphanilamide (0-08 mM) was similar under aerobic and anaerobic conditions. Hepatic elimination of p-aminobenzoic acid (0-08 mM) showed an oxygen-dependent increase for 15 min after addition of substrate. 4. p-Nitroanisole demethylati…

Malemedicine.medical_specialtyTime FactorsHealth Toxicology and Mutagenesischemistry.chemical_elementIn Vitro TechniquesReductaseToxicologyBiochemistryOxygenInternal medicineRespirationmedicineAnimalsBilePyruvatesOxygen saturationDemethylationPharmacologyNitroanisole O-DemethylaseGeneral MedicineRatsOxygenEndocrinologyLiverPharmaceutical PreparationschemistryBiochemistryNitrobenzoatesLactatesAzo CompoundsOxidation-ReductionAnaerobic exercisePerfusionDrug metabolismXenobiotica
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Relation of markers of inflammation (C-reactive protein, fibrinogen, von Willebrand factor, and leukocyte count) and statin therapy to long-term mort…

2002

We evaluated a possible interaction between statins and inflammation in 1,246 patients with angiographically diagnosed coronary artery disease. Four different inflammatory markers were determined: high, sensitive C-reactive protein (hs-CRP) (p = 0.001), fibrinogen (p = 0.006), von Willebrand factor (p = 0.006), and leukocyte count (p = 0.03); these levels were significantly higher among the 88 patients who died of cardiac causes during follow-up (median 2.9 years) than among survivors. In a multivariate backward stepwise Cox regression mode, only hs-CRP was evaluated to be a significant predictor of death from coronary artery disease. This prediction was lost in statin-treated patients. Com…

Malemedicine.medical_specialtyTime FactorsStatinmedicine.drug_classCoronary Artery DiseaseCoronary AngiographyFibrinogenCoronary artery diseaseLeukocyte CountVon Willebrand factorPredictive Value of TestsRisk FactorsInternal medicinevon Willebrand FactormedicineHumansProspective StudiesRisk factorProspective cohort studyAgedProportional Hazards Modelsbiologybusiness.industryC-reactive proteinFibrinogenMiddle Agedmedicine.diseaseC-Reactive ProteinMultivariate Analysisbiology.proteinCardiologyFemaleHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicinebusinessAcute-Phase ProteinsFollow-Up Studiesmedicine.drugLipoproteinThe American Journal of Cardiology
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Delayed effects of ciprofibrate on rat liver peroxisomal properties and proto-oncogene expression.

1995

Peroxisome proliferators (PPs) are non-genotoxic carcinogens in rodents. Their reversible effects on rat liver have been studied with ciprofibrate and fenofibrate. We found that with the hypolipemic drug fenofibrate a pause of 28 days is sufficient for a return to normal status, whereas with the highly potent PP ciprofibrate, the stimulation of ACO mRNA levels remains after its withdrawal. We investigated the effects of the renewal of the treatment with PPs on other peroxisomal parameters and proto-oncogene expression using Wistar rats. Interestingly, c-myc expression was enhanced even upon drug withdrawal, and was more stimulated by the second exposure to ciprofibrate, while c-fos expressi…

Malemedicine.medical_specialtyTime FactorseducationStimulationMitochondria LiverBiologyBiochemistryMicrobodiesDrug withdrawalClofibric AcidFenofibrateInternal medicineProto-Oncogene ProteinsGene expressionmedicineAnimalsRats WistarCarcinogenPharmacologyFenofibrateOncogeneFibric AcidsPeroxisomemedicine.diseaseRatsEndocrinologyLiverMicrosomes LiverCiprofibrateAcyl-CoA OxidaseOxidoreductasesmedicine.drugBiochemical pharmacology
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Dexamethasone upregulates Nox1 expression in vascular smooth muscle cells.

2014

<b><i>Background/Aim:</i></b> It has been demonstrated that dexamethasone-induced hypertension can be prevented by the NADPH oxidase inhibitor apocynin. The effect of dexamethasone on NADPH oxidase, however, is unknown. The present study was conducted to investigate the effect of dexamethasone on the gene expression of Nox1, the major NADPH oxidase isoform in vascular smooth muscle cells. <b><i>Results:</i></b> Oral treatment of Wistar-Kyoto rats with dexamethasone (0.03 mg/kg/day) for 12 days led to an upregulation of Nox1 mRNA expression in the aorta. In cultured A7r5 rat aortic smooth muscle cells, dexamethasone increased Nox1 mRNA expressi…

Malemedicine.medical_specialtyVascular smooth muscleTime FactorsMyocytes Smooth Musclemedicine.disease_causeRats Inbred WKYDexamethasoneHistone DeacetylasesMuscle Smooth Vascularchemistry.chemical_compoundReceptors GlucocorticoidInternal medicinemedicineAnimalsNADH NADPH Oxidoreductasescardiovascular diseasesRNA MessengerGlucocorticoidsDexamethasoneAortaPharmacologychemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologyDose-Response Relationship DrugChemistryfungifood and beveragesGeneral MedicineRatsUp-RegulationEndocrinologyNOX1Gene Knockdown TechniquesApocynincardiovascular systembiology.proteinNADPH Oxidase 1Oxidative stresscirculatory and respiratory physiologymedicine.drugPharmacology
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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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Long-term outcomes after acute myocardial infarction in patients with familial hypercholesterolemia: The French registry of Acute ST-elevation and no…

2020

Patients with familial hypercholesterolemia (FH) are prone to develop acute myocardial infarction (AMI) at a younger age.The aim of the present study was to assess 5-year outcomes after AMI according to the presence of FH in a large multicenter cohort of patients.The French registry of Acute ST-elevation and non-ST-elevation Myocardial Infarction consists of nationwide surveys recruiting patients over a 1- to 2-month period every 5 years. Patients recruited in 2005 and 2010 were followed up to 5 years.Of 5147 patients discharged alive and in whom FH status could be assessed, 2.8% had probable/definite FH, using an adapted Dutch Lipid Clinic score. They were 12 years younger, on average, tha…

Malemedicine.medical_specialty[SDV]Life Sciences [q-bio]Endocrinology Diabetes and MetabolismFamilial hypercholesterolemia030204 cardiovascular system & hematologyCohort StudiesHyperlipoproteinemia Type II03 medical and health sciences0302 clinical medicineRisk FactorsInternal medicineSurveys and QuestionnairesInternal MedicinemedicineHumansIn patient030212 general & internal medicineMyocardial infarctionRegistriesNon-ST Elevated Myocardial InfarctionStrokeComputingMilieux_MISCELLANEOUSAgedNutrition and Dieteticsbusiness.industryST elevationHazard ratioMiddle Agedmedicine.diseasePrognosisConfidence interval3. Good healthCohortST Elevation Myocardial Infarction[SDV.SPEE]Life Sciences [q-bio]/Santé publique et épidémiologieFemaleFranceHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicinebusinessJournal of clinical lipidology
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New-Onset Diabetes and Statins: Throw the Bath Water Out, But, Please, Keep the Baby!

2015

Malemedicine.medical_specialtybusiness.industryEndocrinology Diabetes and MetabolismHypercholesterolemiamedicine.diseaseEndocrinologyEndocrinologyNew onset diabetesInternal medicineDiabetes MellitusmedicineHumansFemaleHydroxymethylglutaryl-CoA Reductase InhibitorsMetabolic syndromebusinessMetabolism
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The CO-releasing molecule CORM-2 is a novel regulator of the inflammatory process in osteoarthritic chondrocytes

2008

Previous work has shown that the CO-releasing molecule CORM-2 protects against cartilage degradation. The aim of this study was to examine whether CORM-2 can control the production of inflammatory mediators in osteoarthritic chondrocytes and determine the mechanisms involved.Primary cultures of chondrocytes from OA patients were stimulated with IL-1beta. The production of reactive oxygen species, nitrite, PGE(2), TNF-alpha and IL-1 receptor antagonist (IL-1Ra) were measured in the presence or absence of CORM-2. The expression of nitric oxide synthase-2 (NOS-2), cyclo-oxygenase-2 (COX-2) and microsomal PG E synthase-1 (mPGES-1) was followed by western blot and real-time PCR. Activation of nu…

Malemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IINitric Oxidemedicine.disease_causeDinoprostoneChondrocyteNitric oxidechemistry.chemical_compoundChondrocytesRheumatologyWestern blotInternal medicineOsteoarthritisOrganometallic CompoundsmedicineHumansPharmacology (medical)Cells CulturedAgedProstaglandin-E SynthasesAged 80 and overchemistry.chemical_classificationReactive oxygen speciesDose-Response Relationship Drugmedicine.diagnostic_testTumor Necrosis Factor-alphabusiness.industryNF-kappa BHypoxia-Inducible Factor 1 alpha SubunitReceptor antagonistMolecular biologyIntramolecular OxidoreductasesInterleukin 1 Receptor Antagonist ProteinEndocrinologymedicine.anatomical_structureCytokinechemistryCyclooxygenase 2PhosphorylationFemaleReactive Oxygen SpeciesbusinessOxidative stressRheumatology
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Rac1 GTPase, a multifunctional player in the regulation of genotoxic stress response

2013

The Ras-related C3 botulinum toxin substrate 1 (Rac1) belongs to the Ras-homologous (Rho) family of small GTPases, which transduce signals from the outside to the inside of a cell. Rac1 becomes activated upon ligand binding of a variety of receptors, including receptor tyrosine kinases and heterotrimeric G-protein-coupled receptors. After GTP loading by guanine exchange factors (GEFs), GTP-bound Rac1 engages numerous effector proteins, thereby eventually regulating cell motility and adhesion, cell cycle progression through G1, mitosis and meiosis, as well as cell death and metastasis.1 Besides, Rac1 adjusts cellular responses to genotoxic agents, such as UV light and alkylating agents, by r…

Malerac1 GTP-Binding Proteintopoisomerase IIAgingRHOADNA repairDNA damagep38 mitogen-activated protein kinasesApoptosisRAC1Editorials: Cell Cycle FeaturesDNA damage responseReceptor tyrosine kinasechemical carcinogenesisHistonesMiceTransforming Growth Factor betaRho GTPasesAnimalsMolecular BiologyTranscription factoranthracyclinesMice KnockoutbiologyKinaseNeuropeptidesConnective Tissue Growth FactorHMG-CoA reductase inhibitors (statins)Cell BiologyFibrosisgenotoxic stressActinsrac GTP-Binding ProteinsCell biologyOxidative Stressnormal tissue damageGene Expression RegulationLiverBiochemistryDoxorubicinGamma Raysbiology.proteinFemaleDNA DamageMutagensSignal TransductionDevelopmental BiologyCell Cycle
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Pharmacologic therapies in endometriosis: a systematic review

2012

To assess the literature on preclinical and clinical efficacy and safety data of pharmacologic groups proposed in the treatment of endometriosis, we performed a systematic review of publications from March 2002 to January 2012 via PubMed search. Additional relevant articles were identified from citations within these publications. A high number of medications were tested in preclinical models of endometriosis due to their theoretic capacity of disrupting important pathophysiologic pathways of the disease, such as inflammatory response, angiogenesis and cell survival, proliferation, migration, adhesion, and invasion. Tumor necrosis factor α-blockers, nuclear factor κB inhibitors, antiangioge…

Matrix metalloproteinase inhibitorAngiogenesisAnti-Inflammatory AgentsEndometriosisEndometriosisAngiogenesis InhibitorsPharmacologyp38 Mitogen-Activated Protein KinasesAntioxidantsEtanerceptmedicineAnimalsHumansHyaluronic AcidAdverse effectMelatoninTumor Necrosis Factor-alphabusiness.industryNF-kappa BObstetrics and Gynecologymedicine.diseaseMetforminReproductive MedicineEstrogen inhibitorFemaleHydroxymethylglutaryl-CoA Reductase InhibitorsEndostatinbusinessmedicine.drugFertility and Sterility
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