Search results for "Quinacrine"

showing 7 items of 7 documents

Exposure to gp120 of HIV-1 induces an increased release of arachidonic acid in rat primary neuronal cell culture followed by NMDA receptor-mediated n…

1995

After incubation of highly enriched neurons from rat cerebral cortex with the HIV-1 coat protein gp120 for 18 h, cells showed fragmentation of DNA at internucleosomal linkers followed by NMDA receptor-mediated neurotoxicity. We report that in response to exposure to gp120 cells react with an increased release of arachidonic acid (AA) via activation of phospholipase A2. This process was not inhibited by NMDA receptor antagonists. To investigate the role of AA on the sensitivity of the NMDA receptor towards its agonist, low concentrations of NMDA were co-administered with AA. This condition enhanced the NMDA-mediated cytotoxicity. Administration of mepacrine reduced cytotoxicity caused by gp1…

Agonistmedicine.drug_classNeurotoxinsPharmacologyHIV Envelope Protein gp120Receptors N-Methyl-D-Aspartatechemistry.chemical_compoundPhospholipase A2medicineAnimalsFragmentation (cell biology)Rats WistarCytotoxicityCells CulturedNeuronsArachidonic AcidbiologyCell DeathGeneral NeuroscienceNeurotoxicitymedicine.diseaseRatsnervous systemchemistryCell cultureQuinacrinebiology.proteinHIV-1NMDA receptorArachidonic acidDNA DamageThe European journal of neuroscience
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Molecular aspects of carcinogenesis. Part B

1989

Nitrogen mustards represent a major group of alkylating agents that are used in the chemotherapy of cancer. It is commonly accepted that they exert their cytotoxic effects by their ability to produce interstrand crosslinks in DNA. The main target site of the two identical alkylating moieties is the N-7 position of guanine. By a Maxam-Gilbert-type reaction it is possible to identify "hot spots" for alkylation by nitrogen mustards. Analysis of data obtained reveal the importance of the DNA context for efficient alkylation. For most of~ the compounds the highest reactivity is observed ila regions of G clusters, while in the neighbourhood of cytosine residues alkylation is reduced. As a consequ…

Cancer ResearchGuanineStereochemistrySubstituentGeneral MedicineAlkylationDNA sequencingchemistry.chemical_compoundUracil MustardQuinacrine MustardOncologychemistryCytosineDNAJournal of Cancer Research and Clinical Oncology
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A lytic mechanism based on soluble phospholypases A2 (sPLA2) and b-galactoside specific lectins is exerted by Ciona intestinalis (ascidian) unilocula…

2011

Abstract Hemocytes from the ascidian Ciona intestinalis exert in vitro Ca 2+ -dependent cytotoxic activity toward mammalian erythrocytes and K562 cells. To examine the lytic mechanism, hemocyte populations were separated (B1–B6 bands) through a Percoll discontinuous density gradient, the hemocyte cytotoxic activity (HCA) and the lytic activity of the hemocyte lysate supernatant (HLS) were assayed. In addition the separated hemocytes were cultured and the cell-free culture medium (CFM) assayed after 3 h culture. Results support that unilocular refractile hemocytes (URGs), enriched in B5, are cytotoxic. The B5-HLS contains lysins and the activity of B5-CFM shows that lysins can be released in…

HemocytesPhospholipase A2 Inhibitorsmedicine.medical_treatmentLysinDibucaineSettore BIO/05 - ZoologiaAquatic ScienceBiologyFucoseCell membranechemistry.chemical_compoundmedicineEnvironmental ChemistryAnimalsHumansCiona intestinalisLectins C-TypeEnzyme InhibitorsProteaseErythrocyte MembraneGeneral Medicinebiology.organism_classificationCytotoxicity Tests Immunologicbeta-GalactosidaseGalactosideCiona intestinalisPhospholipases A2medicine.anatomical_structurechemistryBiochemistryLytic cycleInvertebrate immunity Ciona intestinalis Hemocyte Cytotoxicity Soluble phospholipase A2 Rabbit erythrocyte K562QuinacrineCaspasesImmunologyMicroscopy Electron ScanningRabbitsK562 CellsPercoll
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Downregulation of nNOS and synthesis of PGs associated with endotoxin-induced delay in gastric emptying

2002

A single intraperitoneal injection of endotoxin (40 μg/kg) significantly delayed gastric emptying of a solid nutrient meal. Blockade of nitric oxide synthase (NOS) with 30 mg/kg ip N G-nitro-l-arginine methyl ester or 20 mg/kg ip 7-nitroindazole [neuronal NOS (nNOS) inhibitor] significantly delayed gastric emptying in control animals but failed to modify gastric emptying in endotoxin-treated rats. Administration of 2.5, 5, and 10 mg/kg ip N 6-iminoethyl-l-lysine [inducible NOS (iNOS) inhibitor] had no effect in either experimental group. Indomethacin (5 mg/kg sc), NS-398 (cyclooxygenase-2 inhibitor; 10 mg/kg ip), and dexamethasone (10 mg/kg sc) but not quinacrine (20 mg/kg ip) significantl…

MalePhysiologymedicine.medical_treatmentIndomethacinNitric Oxide Synthase Type IINitric Oxide Synthase Type IprostaglandinsRats Sprague-Dawleychemistry.chemical_compoundPyloric AntrumEnzyme InhibitorsAntrumSulfonamidesArachidonic AcidbiologyReverse Transcriptase Polymerase Chain ReactionStomachdigestive oral and skin physiologyGastroenterologyNitric oxide synthasemedicine.anatomical_structureNG-Nitroarginine Methyl EsterQuinacrinenutrient mealsantrum. pylorusmedicine.medical_specialtyIndazolesIntraperitoneal injectionNitric OxidePhospholipases ANitric oxidenitric oxidePhysiology (medical)Internal medicinemedicineAnimalsCyclooxygenase InhibitorsRNA MessengerNitrobenzenesHepatologyGastric emptyingPylorusdigestive system diseasesRatsEndotoxinsEndocrinologyPyloric AntrumchemistryGastric EmptyingFoodbiology.proteinProstaglandinsNitric Oxide Synthase
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Release of choline from rat brain under hypoxia: contribution from phospholipase A2 but not from phospholipase D

1993

Moderate hypoxia induced in rats by inhalation of 10% oxygen led to an increase of the concentration of free choline in the brain and caused a large net-release of choline from the brain into the venous blood as determined by the measurement of the arterio-venous difference. In hippocampal slices from rat brain, hypoxia increased the release of choline into the superfusion medium. The activity of phospholipase D, as measured by the formation of phosphatidylpropanol in the presence of propanol, was not stimulated under these conditions. However, the mobilization of choline was completely depressed by lowering extracellular calcium and by 0.1 mM mepacrine. We conclude that hypoxia leads to a …

Malemedicine.medical_specialtychemistry.chemical_elementIn Vitro TechniquesCalciumHippocampal formationHippocampusPhospholipases ACholinechemistry.chemical_compoundPhospholipase A2Internal medicinePhospholipase DmedicineExtracellularAnimalsCholineRats WistarHypoxia BrainMolecular BiologyPhospholipase AbiologyPhospholipase DGeneral NeuroscienceHypoxia (medical)RatsPerfusionPhospholipases A2EndocrinologychemistryQuinacrinebiology.proteinCalciumNeurology (clinical)medicine.symptomDevelopmental BiologyBrain Research
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The release of choline from phospholipids mediated by beta-adrenoceptor activation in isolated hearts.

1986

The resting efflux of choline into the perfusate (Tyrode's solution) of isolated hearts was equal to the rate, at which choline was liberated from phospholipid degradation (Lindmar et al. 1986). Infusion of isoprenaline (2 X 10(-7) mol/l), forskolin (1-3 X 10(-6) mol/l) or 3-isobutyl-1-methylxanthine (IBMX; 3 X 10(-4) mol/l) for 40 min markedly enhanced the efflux of choline. The increase was linear during the experimental period and, in the case of isoprenaline, was blocked by 3 X 10(-7) mol/l atenolol. In the guinea-pig heart, IBMX at a threshold concentration of 10(-4) mol/l shifted the concentration-response curve for the effect of forskolin on the efflux of choline to the left by one l…

medicine.medical_specialtyCarbacholIBMXGuinea PigsPhospholipidIn Vitro TechniquesCholinechemistry.chemical_compoundInternal medicineIsoprenaline1-Methyl-3-isobutylxanthineReceptors Adrenergic betamedicineCyclic AMPCholineAnimalsPhospholipidsCholinesterasePharmacologyForskolinbiologyMyocardiumColforsinGeneral MedicineMyocardial ContractionReceptors MuscarinicEndocrinologychemistryQuinacrinebiology.proteinCalciumChickensAcetylcholinemedicine.drugNaunyn-Schmiedeberg's archives of pharmacology
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Characterization of choline efflux from the perfused heart at rest and after muscarine receptor activation.

1986

The resting efflux of choline from perfused chicken hearts varied from 0.4 to 2.6 nmol/g min, but was constant for at least 80 min in the individual experiments. The rate of choline efflux was found to be equal to the rate of choline formation in the heart, which, from the following reasons, was essentially due to hydrolysis of choline phospholipids. Cardiac content of choline phospholipids (7,200 nmol/g) was much higher than that of acetylcholine (5.5 nmol/g). Resting release of acetylcholine was 0.016 nmol/g min and, after inhibition of cholinesterase, only about 0.1 nmol/g min. Resting efflux of choline was reduced by mepacrine, a phospholipase A2 inhibitor, by perfusion with a Ca2+-free…

medicine.medical_specialtyTime FactorsOleic AcidsIn Vitro TechniquesCholinechemistry.chemical_compoundInternal medicinemedicineCholineAnimalsMagnesiumPhospholipidsCholinesterasePharmacologyMuscarinebiologyMyocardiumGeneral MedicineIsolated heartMyocardial ContractionReceptors MuscarinicPerfusionEndocrinologychemistryParasympathomimeticsQuinacrinebiology.proteinCalciumEffluxCholine formationReceptor activationChickensAcetylcholinemedicine.drugOleic AcidNaunyn-Schmiedeberg's archives of pharmacology
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