Search results for "Oxidoreductases"

showing 10 items of 230 documents

Diabetes, oxidative stress and therapeutic strategies.

2014

Abstract Background Diabetes has emerged as a major threat to health worldwide. Scope of Review The exact mechanisms underlying the disease are unknown; however, there is growing evidence that excess generation of reactive oxygen species (ROS), largely due to hyperglycemia, causes oxidative stress in a variety of tissues. Oxidative stress results from either an increase in free radical production, or a decrease in endogenous antioxidant defenses, or both. ROS and reactive nitrogen species (RNS) are products of cellular metabolism and are well recognized for their dual role as both deleterious and beneficial species. In type 2 diabetic patients, oxidative stress is closely associated with ch…

medicine.medical_specialtyAntioxidantEndogenous Factorsmedicine.medical_treatmentBiophysicsInflammationEndogeny030204 cardiovascular system & hematologyBiologyPharmacologymedicine.disease_causeBiochemistryAntioxidants03 medical and health scienceschemistry.chemical_compound0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicineDiabetes mellitusmedicineDiabetes MellitusHumansMolecular BiologyReactive nitrogen speciesComputingMilieux_MISCELLANEOUS030304 developmental biologychemistry.chemical_classification0303 health sciencesReactive oxygen speciesmedicine.disease3. Good health[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemOxidative StressEndocrinologychemistrymedicine.symptomOxidoreductasesReactive Oxygen SpeciesOxidative stressBiochimica et biophysica acta
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Anti-androgens for the treatment of hirsutism.

2002

Many alternatives exist for treating hirsutism. Based on an analysis of scientific literature and on the experiences of the author, the most common anti-androgen agents are discussed in this review. Androgen receptor blockers (cyproterone acetate, flutamide and spironolactone), 5 alpha-reductase inhibitors (finasteride) and androgen-suppressing agents (gonadotrophin-releasing hormone [GnRH] agonists, oestroprogestins, corticosteroids and insulin-sensitising agents) are evaluated and compared. The importance of diagnosis in choosing the most appropriate anti-androgen treatment is also discussed.

medicine.medical_specialtyCholestenone 5 alpha-ReductaseHirsutismAnti-Androgenurologic and male genital diseasesFlutamideGonadotropin-Releasing Hormonechemistry.chemical_compoundInternal medicineAndrogen Receptor AntagonistsMedicineHumansPharmacology (medical)Androgen Receptor AntagonistshirsutismPharmacologybusiness.industryCyproterone acetateAndrogen AntagonistsGeneral Medicinemedicine.diseaseAndrogen receptorEndocrinologyTreatment OutcomechemistrySpironolactoneFinasterideAndrogensFemalebusinessOxidoreductasesExpert opinion on investigational drugs
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Retinoid receptors and vitamin A deficiency: differential patterns of transcription during early avian development and the rapid induction of RARs by…

2003

The functional links of specific retinoid receptors to early developmental events in the avian embryo are not known. Before such studies are undertaken, knowledge is required of the spatiotemporal expression patterns of the receptor genes and their regulation by endogenous retinoic acid levels during the early stages of development. Here, we report the expression patterns of mRNAs for RARalpha, RARalpha2, RARbeta2, RARgamma, RARgamma2, RXRalpha, and RARgamma from neurulation to HH10 in the normal and vitamin A-deficient (VAD) quail embryo. The transcripts for all retinoid receptors are detectable at HH5, except for RXRgamma, which is detected at the beginning of HH6. At the 4/5 somite stage…

medicine.medical_specialtyEmbryo Nonmammaliananimal structuresTranscription GeneticReceptors Retinoic Acidmedicine.drug_classRetinoic acidRetinoid receptorTretinoinCoturnixRetinoid X receptorBiologyMicechemistry.chemical_compoundInternal medicinemedicineAnimalsRetinoidReceptorFetal DeathMolecular BiologyRetinoid X receptor alphaVitamin A DeficiencyRetinoic Acid Receptor alphaGene Expression Regulation DevelopmentalRetinal DehydrogenaseCell BiologyRetinoid X receptor gammaAldehyde OxidoreductasesCell biologyRetinoid X ReceptorsEndocrinologychemistryRetinoid X receptor betaTranscription FactorsDevelopmental BiologyDevelopmental Biology
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Increase by NO synthase inhibitors of acetylcholine release from guinea-pig myenteric plexus

1994

The effects of nitric oxide (NO) synthase inhibitors on the electrically evoked release of [3H]acetylcholine were studied in guinea-pig myenteric plexus preparations preincubated with [3H]choline. NG-monomethyl-L-arginine (EC50 5.3 mumol l-1) and NG-nitro-L-arginine (EC50 1.3 mumol l-1) concentration-dependently increased the evoked release of [3H]acetylcholine without affecting the basal outflow. The facilitatory effect of NG-mono-methyl-L-arginine was prevented by L-arginine but not by D-arginine. The results suggest that endogenous NO inhibits the depolarisation-evoked release of acetylcholine.

medicine.medical_specialtyGuinea PigsMyenteric PlexusArginineNitric OxideNitroarginineNitric oxideGuinea pigchemistry.chemical_compoundInternal medicinemedicineAnimalsCholineEvoked PotentialsMyenteric plexusPharmacologyomega-N-MethylargininebiologyMuscle SmoothGeneral MedicineAcetylcholineElectric StimulationNitric oxide synthaseEndocrinologychemistryEnzyme inhibitorbiology.proteinLiberationAmino Acid OxidoreductasesNitric Oxide SynthaseAcetylcholinemedicine.drugNaunyn-Schmiedeberg's Archives of Pharmacology
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NADPH Oxidase Accounts for Enhanced Superoxide Production and Impaired Endothelium-Dependent Smooth Muscle Relaxation in BKβ1 −/− Mice

2006

Objective— Nitric oxide (NO)-induced vasorelaxation involves activation of large conductance Ca 2+ -activated K + channels (BK). A regulatory BKβ1 subunit confers Ca 2+ , voltage, and NO/cGMP sensitivity to the BK channel. We investigated whether endothelial function and NO/cGMP signaling is affected by a deletion of the β1-subunit. Methods and Results— Vascular superoxide in BKβ1 −/− was measured using the fluorescent dye hydroethidine and lucigenin-enhanced chemiluminescence. Vascular NO formation was analyzed using electron paramagnetic resonance (EPR), expression of NADPH oxidase subunits, the endothelial NO synthase (eNOS), the soluble guanylyl cyclase (sGC), as well as the activity a…

medicine.medical_specialtyNitric Oxide Synthase Type IIIEndotheliumAorta ThoracicNitric OxideMuscle Smooth VascularNitric oxideMicechemistry.chemical_compoundSuperoxidesInternal medicineCyclic GMP-Dependent Protein KinasesmedicineAnimalsHumansProtein IsoformsNADH NADPH OxidoreductasesLarge-Conductance Calcium-Activated Potassium ChannelsMice KnockoutNADPH oxidasebiologySuperoxideMicrofilament ProteinsNADPH OxidasesPhosphoproteinsMolecular biologyVasodilationEndocrinologymedicine.anatomical_structurechemistryGuanylate CyclaseNAD(P)H oxidaseNOX1ApocyninNADPH Oxidase 1biology.proteinEndothelium VascularCardiology and Cardiovascular MedicineSoluble guanylyl cyclaseCell Adhesion MoleculesSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Progestogens reduce thromboxane production by cultured human endothelial cells.

2011

Objectives Progestogens have been poorly studied concerning their roles in endothelial physiology. Prostanoids are vasoactive compounds, such as thromboxane A2, a potent vasoconstrictor, and prostacyclin, a vasodilator. We examined the effects of two progestogens used clinically, progesterone and medroxyprogesterone acetate, on thromboxane A2 production by cultured human umbilical vein endothelial cells (HUVEC) and investigated the role of progesterone receptors and the enzymes involved in production of thromboxane A2 and prostacyclin. Methods Cells were exposed to 1‐100 nmol/l of either progesterone or medroxyprogesterone acetate, and thromboxane A2 production was measured in culture mediu…

medicine.medical_specialtyUmbilical VeinsAntineoplastic Agents HormonalThromboxaneBlotting WesternGene ExpressionProstacyclinMedroxyprogesterone AcetatePolymerase Chain ReactionProstacyclin synthaseThromboxane receptorThromboxane ProductionThromboxane A2chemistry.chemical_compoundThromboxane A2Hormone AntagonistsCytochrome P-450 Enzyme SystemInternal medicineProgesterone receptorMedicineHumansCyclooxygenase InhibitorsRNA MessengerCells CulturedProgesteronebiologyDose-Response Relationship Drugbusiness.industryObstetrics and GynecologyEndothelial CellsGeneral MedicineIntramolecular OxidoreductasesThromboxane B2MifepristoneEndocrinologychemistrycardiovascular systembiology.proteinPyrazolesThromboxane-A synthaseThromboxane-A SynthaseProgestinsbusinessmedicine.drugClimacteric : the journal of the International Menopause Society
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Vasoactive intestinal peptide stimulation of cyclic guanosine monophosphate formation: further evidence for a role of nitric oxide synthase and cytos…

1993

In the rat pineal gland vasoactive intestinal peptide (VIP) and beta-adrenergic agonists stimulate cyclic guanosine monophosphate (cGMP) formation and their action is amplified by alpha 1-adrenergic agonists. Since beta-adrenergic stimulation of cGMP is suggested to involve activation of nitric oxide (NO) synthase and NO-mediated activation of cytosolic guanylate cyclase (GC), we investigated the effects of the NO synthase inhibitor N-monomethyl-L-arginine (L-NMMA) and of the cytosolic GC inhibitor methylene blue (MB) on VIP receptor-stimulated cGMP formation. Both L-NMMA and MB depressed VIP-induced cGMP formation as well as alpha 1-adrenergic potentiation of VIP-stimulated cGMP formation …

medicine.medical_specialtyVasoactive intestinal peptideArgininePineal GlandPinealocyteNitric oxidechemistry.chemical_compoundPhenylephrineEndocrinologyCytosolInternal medicinemedicineAnimalsCyclic guanosine monophosphateCyclic GMPomega-N-MethylarginineATP synthasebiologyDrug SynergismRatsNitric oxide synthaseMethylene BlueEndocrinologychemistryGuanylate CyclaseSecond messenger systembiology.proteinOmega-N-MethylarginineAmino Acid OxidoreductasesNitric Oxide Synthasehormones hormone substitutes and hormone antagonistsVasoactive Intestinal PeptideEndocrinology
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α-HYDROXYBUTYRIC DEHYDROGENASE IN THE DIAGNOSIS OF MYOCARDIAL INFARCTION

1962

medicine.medical_specialtybusiness.industryMyocardial InfarctionElectrocardiography in myocardial infarctionDehydrogenaseGeneral Medicinemedicine.diseaseCardiovascular DiseasesInternal medicinemedicineCardiologyHumansMyocardial infarctionOxidoreductasesbusinessAgedThe Lancet
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Physical inactivity increases oxidative stress, endothelial dysfunction, and atherosclerosis.

2005

Objective— Sedentary lifestyle is associated with increased cardiovascular events. The underlying molecular mechanisms are incompletely understood. Reactive oxygen species (ROS) contribute to endothelial dysfunction and atherosclerosis. An important source of vascular ROS is the NADPH oxidase. Methods and Results— C57BL6 mice were subjected to regular housing (physical inactivity) or voluntary training on running wheels (6 weeks). Inactivity increased vascular lipid peroxidation to 148±9% and upregulated superoxide release to 176±17% (L-012 chemiluminescence) and 188±29% (cytochrome C reduction assay), respectively. ROS production was predominantly increased in the endothelium and the medi…

rac1 GTP-Binding Proteinmedicine.medical_specialtyEndotheliumNitric Oxide Synthase Type IIIArteriosclerosisNitric Oxide Synthase Type IIBiologymedicine.disease_causechemistry.chemical_compoundMiceApolipoproteins EInternal medicinePhysical Conditioning AnimalmedicineAnimalsNADH NADPH OxidoreductasesRNA MessengerEndothelial dysfunctionLife Stylechemistry.chemical_classificationReactive oxygen speciesNADPH oxidaseSuperoxideNeuropeptidesNADPH Oxidase 1NADPH Oxidasesmedicine.diseasePhosphoproteinsMice Mutant Strainsrac GTP-Binding ProteinsMice Inbred C57BLVasodilationOxidative Stressmedicine.anatomical_structureEndocrinologychemistryNOX1biology.proteinNADPH Oxidase 1Endothelium VascularNitric Oxide SynthaseCardiology and Cardiovascular MedicineReactive Oxygen SpeciesOxidative stressArteriosclerosis, thrombosis, and vascular biology
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Protein tyrosine nitration and thiol oxidation by peroxynitrite-strategies to prevent these oxidative modifications.

2013

The reaction product of nitric oxide and superoxide, peroxynitrite, is a potent biological oxidant. The most important oxidative protein modifications described for peroxynitrite are cysteine-thiol oxidation and tyrosine nitration. We have previously demonstrated that intrinsic heme-thiolate (P450)-dependent enzymatic catalysis increases the nitration of tyrosine 430 in prostacyclin synthase and results in loss of activity which contributes to endothelial dysfunction. We here report the sensitive peroxynitrite-dependent nitration of an over-expressed and partially purified human prostacyclin synthase (3.3 μM) with an EC50 value of 5 μM. Microsomal thiols in these preparations effectively co…

thiol oxidationprotein tyrosine nitrationlcsh:Chemistrychemistry.chemical_compoundCytochrome P-450 Enzyme SystemSf9 CellsTyrosinelcsh:QH301-705.5Spectroscopychemistry.chemical_classification0303 health sciencesbiologySuperoxide030302 biochemistry & molecular biologyGeneral MedicineComputer Science ApplicationsIntramolecular OxidoreductasesBiochemistryThiolprostacyclin synthasesuperoxideOxidation-ReductionPeroxynitriteOxidative phosphorylationSpodopteraCatalysisArticleperoxynitriteNitric oxideProstacyclin synthaseInorganic Chemistry03 medical and health sciencesnitric oxideddc:570NitrationPeroxynitrous AcidAnimalsHumansSulfhydryl CompoundsPhysical and Theoretical ChemistryMolecular Biology030304 developmental biologyOrganic Chemistrynitric oxide; superoxide; peroxynitrite; protein tyrosine nitration; thiol oxidation; peroxynitrite scavengers; prostacyclin synthasechemistrylcsh:Biology (General)lcsh:QD1-999biology.proteinTyrosineCattleperoxynitrite scavengersProtein Processing Post-TranslationalInternational journal of molecular sciences
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