Search results for "Biopterin"

showing 10 items of 25 documents

Uncoupling of eNOS in Cardiovascular Disease

2017

Abstract Under physiological conditions, nitric oxide (NO) produced by the endothelial NO synthase (eNOS) represents a key vasoprotective factor. Under conditions of cardiovascular diseases, such as hypertension, diabetes, and atherosclerosis, eNOS may become uncoupled. Uncoupled eNOS generates superoxide at the expense of NO and contributes significantly to endothelial dysfunction and atherogenesis. Major mechanisms of eNOS uncoupling include depletion of tetrahydrobiopterin, an essential cofactor for the eNOS enzyme, and deficiency of l -arginine, the eNOS substrate, and/or eNOS S-glutathionylation. Reversal of eNOS uncoupling may represent a novel therapeutic strategy for the prevention …

0301 basic medicinemedicine.medical_specialtyArgininebiologySuperoxidebusiness.industryNitric Oxide Synthase Type IIITetrahydrobiopterin030204 cardiovascular system & hematologybiology.organism_classificationmedicine.diseaseVasoprotectiveNitric oxide03 medical and health scienceschemistry.chemical_compound030104 developmental biology0302 clinical medicineEndocrinologychemistryEnosInternal medicinemedicineEndothelial dysfunctionbusinessmedicine.drug
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Improved identification of heterozygotes for phenylketonuria using blood neopterin and biopterin

1993

A novel approach that combines information provided by the metabolism of pteridines and that of phenylalanine has been applied to the detection of heterozygotes for phenylketonuria. Phenylalanine, tyrosine, biopterin and neopterin have been measured in serum from normal controls and heterozygotes for classical phenylketonuria, before and after a phenylalanine oral load. Significant differences in neopterin and biopterin mean values in fasting serum and in the mean increase of biopterin induced by the phenylalanine load were found between groups. Inclusion of pteridine data in the discriminant analysis significantly improved the resolution of the classical phenylalanine loading test for the …

AdultMalemedicine.medical_specialtyPhenylalanineBiopterinPhenylalanineNeopterinchemistry.chemical_compoundPhenylketonuriasInternal medicineClassical phenylketonuriaGeneticsmedicineHumansTyrosineGenetics (clinical)ChemistryGenetic Carrier ScreeningNeopterinHeterozygote advantageTetrahydrobiopterinBiopterinEndocrinologyTyrosineFemalemedicine.drugPteridineJournal of Inherited Metabolic Disease
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Divergent in vivo and in vitro antileukemic activity of recombinant interferon beta in patients with chronic-phase chronic myelogenous leukemia

1993

It was the aim of this study to investigate the antileukemic activities of recombinant interferon beta (rIFN beta) in chronic-phase CML in vitro and in vivo. Nine patients in the early chronic-phase of CML were treated in a phase-II trial with escalating doses of rIFN beta. In parallel, antiproliferative and immunomodulatory activities of rIFN beta and rIFN alpha 2b were studied in vitro. rIFN beta exhibited a significantly higher antiproliferative activity on hematopoietic progenitor cells of CML patients in vitro than rIFN alpha 2b. In contrast, only very limited clinical antileukemic efficacy of rIFN beta was observed. None of the patients achieved a complete or partial hematologic respo…

AdultMalemedicine.medical_specialtymedicine.drug_classmedicine.medical_treatmentAlpha (ethology)Interferon alpha-2PharmacologyNeopterinIn vivoInternal medicineHumansMedicineBeta (finance)AgedHematologyDose-Response Relationship Drugbusiness.industryInterferon-alphaInterferon-betaHematologyGeneral MedicineImmunotherapyMiddle AgedReceptor antagonistmedicine.diseaseBiopterinRecombinant ProteinsCytokineGenesLeukemia Myeloid Chronic-PhaseImmunologyFemaleInterferonsbeta 2-MicroglobulinbusinessChronic myelogenous leukemiaAnnals of Hematology
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Differences in non-MHC restricted cytotoxic activities of human peripheral blood lymphocytes after transfusion with allogeneic leukocytes or platelet…

1990

Abstract MHC-unrestricted cytotoxic activity of peripheral blood lymphocytes (PBL) from 4–6 healthy donors was investigated before and after transfusion with allogeneic leukocytes or platelets. Natural killer and lectin-dependent cellular cytotoxicity (LDCC) of PBL was tested against K562 and Raji target cells in a 4-h and 16-h 51 Cr-release assay, respectively. After allotransfusion with leukocytes, we found increased cytotoxic activity of each donor's PBL against all the three targets on day 3 or 7. The highest non-specific cytotoxic activity was detected against the relatively NK resistant Raji target cells. The increase of cytotoxic activity was lowest against the LDCC target (PHA-treat…

Blood PlateletsCytotoxicity ImmunologicMaleImmunologyFluoroimmunoassaychemical and pharmacologic phenomenaHuman leukocyte antigenPlatelet TransfusionMajor histocompatibility complexNeopterinNatural killer cellImmune systemAntigenmedicineLeukocytesImmunology and AllergyCytotoxic T cellHumansPlateletBlood TransfusionLymphocytesCytotoxicitybiologyHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHematologyCytotoxicity Tests ImmunologicIntercellular Adhesion Molecule-1BiopterinKiller Cells NaturalLeukocyte Transfusionmedicine.anatomical_structureImmunologybiology.proteinInterleukin-2Immunizationbeta 2-MicroglobulinCell Adhesion MoleculesImmunobiology
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Identification of 5,6,7,8-tetrahydropterin and 5,6,7,8-tetrahydrobiopterin in Drosophila melanogaster.

1988

Summary Using reversed-phase high-performance liquid chromatography with electrochemical detection we have demonstrated the occurrence of 5,6,7,8-tetrahydropterin and 5,6,7,8-tetrahydrobiopterin in Drosophila melanogaster . The former is the first time that has been detected in vivo . The identification has been based on the retention times, hydrodinamic voltagrams and the differential concentration in three strains of Drosophila melanogaster . Compared to the wild type, the Punch 2 mutant has diminished levels of both pteridines, whereas Henna-recessive 3 lacks completely tetrahydropterin and has increased levels of tetrahydrobiopterin, as expected according to their biochemical lesions.

GeneticsbiologyMutantBiophysicsWild typeCell BiologyElectrochemical detectionTetrahydrobiopterinbiology.organism_classificationKidneyBiochemistryHigh-performance liquid chromatographyBiopterinPterinsRatsDrosophila melanogasterBiochemistryIn vivomedicineAnimalsDrosophila melanogasterMolecular BiologyChromatography High Pressure Liquidmedicine.drugBiochemical and biophysical research communications
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Evaluation of soluble CD 14 and neopterin as serum parameters of the inflammatory activity of pulmonary sarcoidosis.

1992

CD14 represents the most specific marker for monocytes/macrophages. It has been demonstrated in vitro that monocytes/macrophages lose this antigen upon activation. Results of studies investigating the expression of membrane-bound CD14 on the surface of monocytes/macrophages in sarcoidosis patients are controversial. To investigate whether the soluble form of CD14 reflects monocyte/macrophage activation in sarcoidosis, serum levels of soluble CD14 were determined concurrently with other serum markers of monocyte/macrophage activation (neopterin, angiotensin-converting enzyme) in 50 consecutive patients with bioptically confirmed sarcoidosis. The patients were allocated to three groups accord…

Lung Diseasesmedicine.medical_specialtySarcoidosisCD14CD4-CD8 RatioLipopolysaccharide ReceptorsAntigens Differentiation MyelomonocyticPeptidyl-Dipeptidase ANeopterinSensitivity and SpecificityMonocyteschemistry.chemical_compoundImmune systemAntigenAntigens CDInternal medicineDrug DiscoverymedicineMacrophageHumansGenetics (clinical)Inflammationmedicine.diagnostic_testMonocyteNeopterinGeneral MedicineMacrophage Activationmedicine.diseaseBiopterinBronchoalveolar lavageEndocrinologymedicine.anatomical_structurechemistrySolubilityImmunologyMolecular MedicineInterleukin-2SarcoidosisBronchoalveolar Lavage FluidBiomarkersThe Clinical investigator
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Redox Regulation of Dihydrofolate Reductase: Friend or Troublemaker?

2015

Oxidative stress is a hallmark of cardiovascular diseases1 and a major contributor to vascular dysfunction.2 On the basis on recent concepts, vascular oxidative stress is caused mainly by infiltrating inflammatory cells such as monocytes/macrophages or leucocytes,3,4 producing so-called kindling radicals that lead to the activation of secondary, vascular enzymatic sources of reactive oxygen species (mainly superoxide).2,5 A prominent example is the uncoupled nitric oxide (NO) synthase, which means that an NO-producing antiatherosclerotic enzyme is getting switched to a superoxide-producing proatherosclerotic enzyme.2 Molecular mechanisms causing endothelial NO synthase (eNOS) uncoupling or …

MaleNitric Oxide Synthase Type IIIAorta ThoracicOxidative phosphorylationBiologymedicine.disease_causeNitric OxideArticleNitric oxidechemistry.chemical_compoundEnosmedicineAnimalschemistry.chemical_classificationReactive oxygen speciesSuperoxideNitric Oxide Synthase Type IIIEndothelial CellsTetrahydrobiopterinbiology.organism_classificationTetrahydrofolate DehydrogenasechemistryBiochemistryCardiology and Cardiovascular MedicineOxidative stressmedicine.drugArteriosclerosis, thrombosis, and vascular biology
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Role of tetrahydrobiopterin in pulmonary vascular remodelling associated with pulmonary fibrosis

2013

[Background]: Pulmonary hypertension in idiopathic pulmonary fibrosis (IPF) is indicative of a poor prognosis. Recent evidence suggests that tetrahydrobiopterin (BH4), the cofactor of nitric oxide synthase (NOS), is involved in pulmonary hypertension and that pulmonary artery endothelial-to-mesenchymal transition (EnMT) may contribute to pulmonary fibrosis. However, the role of BH4 in pulmonary remodelling secondary to pulmonary fibrosis is unknown. This study examined the BH4 system in plasma and pulmonary arteries from patients with IPF as well as the antiremodelling and antifibrotic effects of the BH4 precursor sepiapterin in rat bleomycin-induced pulmonary fibrosis and in vitro EnMT mod…

MalePulmonary and Respiratory Medicinemedicine.medical_specialtySepiapterinPathologyNitric Oxide Synthase Type IIIHypertension PulmonaryPulmonary FibrosisNitric Oxide Synthase Type IIEnzyme-Linked Immunosorbent AssayPulmonary ArteryReal-Time Polymerase Chain ReactionEndothelial NOSchemistry.chemical_compoundIdiopathic pulmonary fibrosisInternal medicinemedicine.arteryPulmonary fibrosismedicineAnimalsHumansRats WistarGTP CyclohydrolaseSepiapterin reductaseChromatography High Pressure LiquidAgedbusiness.industryNitrotyrosineMiddle Agedmedicine.diseaseBiopterinImmunohistochemistryPulmonary hypertensionRatsAlcohol OxidoreductasesDisease Models AnimalEndocrinologychemistryPulmonary arteryTyrosineFemaleEndothelium Vascularbusiness
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Mechanisms underlying recoupling of eNOS by HMG-CoA reductase inhibition in a rat model of streptozotocin-induced diabetes mellitus

2007

Abstract Objective HMG-CoA reductase inhibitors have been shown to upregulate GTP cyclohydrolase I (GTPCH-I), the key enzyme for tetrahydrobiopterin de novo synthesis and to normalize tetrahydrobiopterin levels in hyperglycemic endothelial cells. We sought to determine whether in vivo treatment with the HMG-CoA reductase inhibitor atorvastatin is able to upregulate the GTPCH-I, to recouple eNOS and to normalize endothelial dysfunction in an experimental model of diabetes mellitus. Methods and results In male Wistar rats, diabetes was induced by streptozotocin (STZ, 60mg/kg). In STZ rats, atorvastatin feeding (20mg/kg/d, 7 weeks), normalized vascular dysfunction as analyzed by isometric tens…

Malemedicine.medical_specialtyNitric Oxide Synthase Type IIIGTP cyclohydrolase INitric Oxide Synthase Type IIReductaseArticleDiabetes Mellitus ExperimentalCytochrome P-450 Enzyme SystemEnosInternal medicineAtorvastatinmedicineAnimalsNADH NADPH OxidoreductasesPyrrolesRats WistarEndothelial dysfunctionGTP CyclohydrolaseNADPH oxidasebiologyStem CellsBody WeightMicrofilament ProteinsTetrahydrobiopterinPhosphoproteinsmedicine.diseasebiology.organism_classificationBiopterinRatsEnzyme ActivationIntramolecular OxidoreductasesVasodilationNitric oxide synthaseDisease Models AnimalOxidative StressTetrahydrofolate DehydrogenaseDiabetes Mellitus Type 1EndocrinologyHeptanoic AcidsHMG-CoA reductaseNADPH Oxidase 1biology.proteinEndothelium VascularHydroxymethylglutaryl-CoA Reductase InhibitorsCardiology and Cardiovascular MedicineCell Adhesion MoleculesDiabetic Angiopathiesmedicine.drugAtherosclerosis
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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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