Search results for "Ribose"

showing 10 items of 103 documents

Early mitochondrial dysfunction, superoxide anion production, and DNA degradation are associated with non-apoptotic death of human airway epithelial …

2002

It has been shown that bacterial exoproducts may induce airway epithelium injury. During the epithelial repair process, the respiratory epithelial cells no more establish tight junctional intercellular complexes and may be particularly susceptible to bacterial virulence factors. In this study, we analyzed the effect of Pseudomonas aeruginosa exotoxin A (ETA) at different periods of time and concentrations on 16 HBE 14o(-) human bronchial epithelial cells in culture conditions inducing a phenotype of repairing cells. ETA treatment for 24 and 48 h led to the killing of 40.0 +/- 5.7% and 79.0 +/- 1.4% of the cells, respectively, as determined by the dimethylthiazole 2,5 diphenyl tetrazolium br…

MESH: Cell DeathMESH: ADP Ribose TransferasesMESH : DNAClinical BiochemistryCellApoptosisMESH : Dose-Response Relationship DrugMitochondrion[SDV.MHEP.PSR]Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMembrane PotentialsMESH: Dose-Response Relationship Drugchemistry.chemical_compoundSuperoxidesMESH: Intracellular MembraneMESH : DNA FragmentationRespiratory systemEnzyme InhibitorsCells CulturedADP Ribose TransferasesMESH : Cell SurvivalCell DeathSuperoxideMESH: DNAMESH: BronchiCaspase InhibitorsMESH : BronchiMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Cell SurvivalMESH: Enzyme InhibitorsMESH: Epithelial CellsMESH : ADP Ribose TransferasesIntracellularMESH: Cells CulturedPulmonary and Respiratory MedicineProgrammed cell deathCell SurvivalVirulence FactorsBacterial ToxinsExotoxinsBronchiDNA FragmentationRespiratory MucosaBiologyMicrobiologyNecrosisNasal PolypsMESH : Cells CulturedmedicineHumansMESH: DNA FragmentationMESH : Intracellular MembraneMolecular BiologyMESH : Enzyme InhibitorsMESH: HumansMESH: CaspasesDose-Response Relationship DrugMESH: ApoptosisMESH : HumansEpithelial CellsCell BiologyDNAIntracellular MembranesMESH: ExotoxinschemistryMESH: Bacterial ToxinsApoptosisMESH : ExotoxinsMESH : Cell DeathMESH : Bacterial ToxinsRespiratory epithelium[SDV.MHEP.PSR] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tractMESH : CaspasesMESH : Apoptosis[ SDV.MHEP.PSR ] Life Sciences [q-bio]/Human health and pathology/Pulmonology and respiratory tract
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Deletion of 11q in Neuroblastomas Drives Sensitivity to PARP Inhibition

2017

AbstractPurpose: Despite advances in multimodal therapy, neuroblastomas with hemizygous deletion in chromosome 11q (20%–30%) undergo consecutive recurrences with poor outcome. We hypothesized that patients with 11q-loss may share a druggable molecular target(s) that can be exploited for a precision medicine strategy to improve treatment outcome.Experimental Design: SNP arrays were combined with next-generation sequencing (NGS) to precisely define the deleted region in 17 primary 11q-loss neuroblastomas and identify allelic variants in genes relevant for neuroblastoma etiology. We assessed PARP inhibitor olaparib in combination with other chemotherapy medications using both in vitro and in v…

Male0301 basic medicineCancer ResearchDNA repairAntineoplastic AgentsAtaxia Telangiectasia Mutated ProteinsKaplan-Meier EstimatePoly(ADP-ribose) Polymerase InhibitorsBiologyModels BiologicalPolymorphism Single NucleotideImmunophenotypingOlaparibNeuroblastoma03 medical and health scienceschemistry.chemical_compound0302 clinical medicineRecurrenceCell Line TumorNeuroblastomaBiomarkers TumormedicineAnimalsHumansAllelesNeoplasm StagingCisplatinTemozolomideChromosomes Human Pair 11High-Throughput Nucleotide SequencingCancerDrug SynergismPrognosismedicine.diseaseXenograft Model Antitumor AssaysMolecular biologyDisease Models Animal030104 developmental biologyOncologychemistryDrug Resistance Neoplasm030220 oncology & carcinogenesisPARP inhibitorCancer researchFemaleChromosome DeletionHaploinsufficiencyBiomarkersmedicine.drugClinical Cancer Research
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Pyrrolotetrazinones deazaanalogues of temozolomide induce apoptosis in Jurkat cell line: involvement of tubulin polymerization inhibition.

2009

Pyrrolotetrazinones are a new class of azolotetrazinones endowed with a high, remarkable antiproliferative activity in human tumor cultured cells. They hold the deaza skeleton of the antitumor drug temozolomide, although preliminary investigations indicated a different mechanism of action. To understand their mechanism(s) of action along with their target at molecular level, four derivatives were selected on the basis of their activity on a panel of human tumor cell lines and they were investigated in depth in a T leukemia cell line (Jurkat). Flow cytometric analysis of cell cycle after treatment with pyrrolotetrazinones has demonstrated that they were able to induce an arrest of the cell c…

MaleCancer ResearchProgrammed cell deathCarcinoma HepatocellularCell SurvivalCellGene ExpressionAntineoplastic AgentsApoptosisPhosphatidylserinesBiologyToxicologyJurkat cellsMicrotubulesMicrotubule polymerizationJurkat CellsMiceTubulinCell Line TumormedicineTemozolomideAnimalsHumansPharmacology (medical)Cell Proliferationbcl-2-Associated X ProteinPharmacologyMembrane Potential MitochondrialMice Inbred BALB CCaspase 3Cell CycleCell MembraneCell cycleSettore CHIM/08 - Chimica FarmaceuticaTubulin ModulatorsCell biologyMitochondriaDacarbazinemedicine.anatomical_structureOncologyMechanism of actionBiochemistryProto-Oncogene Proteins c-bcl-2ApoptosisCell culturemedicine.symptomPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesPyrrolotetrazinoneCancer chemotherapy and pharmacology
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POLE, POLD1, and NTHL1: the last but not the least hereditary cancer-predisposing genes

2021

POLE, POLD1, and NTHL1 are involved in DNA replication and have recently been recognized as hereditary cancer-predisposing genes, because their alterations are associated with colorectal cancer and other tumors. POLE/POLD1-associated syndrome shows an autosomal dominant inheritance, whereas NTHL1-associated syndrome follows an autosomal recessive pattern. Although the prevalence of germline monoallelic POLE/POLD1 and biallelic NTHL1 pathogenic variants is low, they determine different phenotypes with a broad tumor spectrum overlapping that of other hereditary conditions like Lynch Syndrome or Familial Adenomatous Polyposis. Endometrial and breast cancers, and probably ovarian and brain tumo…

MaleCancer ResearchSettore MED/06 - Oncologia MedicaColorectal cancerBiologymedicine.disease_causeGermlineFamilial adenomatous polyposisDeoxyribonuclease (Pyrimidine Dimer)Breast cancerNeoplasmsGeneticsmedicineHumansGenetic Predisposition to DiseasePoly-ADP-Ribose Binding ProteinsMolecular BiologyDNA Polymerase IIIGenetic testingMutationPOLD1medicine.diagnostic_testDNA Polymerase IIDNAmedicine.diseaseLynch syndromePOLE POLD1 and NTHL1Lynch SyndromeCancer researchFemaleOncogene
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A novel form of ataxia oculomotor apraxia characterized by oxidative stress and apoptosis resistance

2007

Several different autosomal recessive genetic disorders characterized by ataxia with oculomotor apraxia (AOA) have been identified with the unifying feature of defective DNA damage recognition and/or repair. We describe here the characterization of a novel form of AOA showing increased sensitivity to agents that cause single-strand breaks (SSBs) in DNA but having no gross defect in the repair of these breaks. Evidence for the presence of residual SSBs in DNA was provided by dramatically increased levels of poly (ADP-ribose)polymerase (PARP-1) auto-poly (ADP-ribosyl)ation, the detection of increased levels of reactive oxygen/nitrogen species (ROS/RNS) and oxidative damage to DNA in the patie…

MaleMethylnitronitrosoguanidineProgrammed cell deathAtaxiaDNA RepairApraxiasDNA damageMitomycinBlotting WesternPoly (ADP-Ribose) Polymerase-1Apoptosismedicine.disease_causeAntioxidantschemistry.chemical_compoundRadiation IonizingmedicineHumansDNA Breaks Single-StrandedOculomotor apraxiaMolecular BiologyCells CulturedEtoposideMembrane Potential MitochondrialbiologyCytochrome cHydrogen PeroxideCell BiologyFlow Cytometrymedicine.diseaseAntineoplastic Agents PhytogenicReactive Nitrogen SpeciesMolecular biologyOxidative StresschemistryApoptosisbiology.proteinAtaxiaCamptothecinFemalePoly(ADP-ribose) Polymerasesmedicine.symptomDNAOxidative stressDNA DamageCell Death & Differentiation
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The basal levels of 8-oxoG and other oxidative modifications in intact mitochondrial DNA are low even in repair-deficient (Ogg1(-/-)/Csb(-/-)) mice.

2007

Abstract Mitochondrial DNA (mtDNA) is assumed to be highly prone to damage by reactive oxygen species (ROS) because of its location in close proximity to the mitochondrial electron transport chain. Accordingly, mitochondrial oxidative DNA damage has been hypothesized to be responsible for various neurological diseases, ageing and cancer. Since 7,8-dihydro-8-oxoguanine (8-oxoG), one of the most frequent oxidative base modifications, is removed from the mitochondrial genome by the glycosylase OGG1, the basal levels of this lesion are expected to be highly elevated in Ogg1−/− mice. To investigate this hypothesis, we have used a mtDNA relaxation assay in combination with various repair enzymes …

MaleMitochondrial DNADNA RepairDNA repairHealth Toxicology and MutagenesisOxidative phosphorylationBiologyMitochondrionDNA MitochondrialDNA Glycosylaseschemistry.chemical_compoundMiceGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyMice KnockoutGuanosinePlant ExtractsCorticoviridaeMolecular biologyNuclear DNAMice Inbred C57BLDNA Repair EnzymeschemistryDNA glycosylaseDNA ViralFemaleDNANucleotide excision repairDNA DamageMutation research
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Inhibitors of poly (ADP-ribose) synthetase reduce renal ischemia-reperfusion injury in the anesthetized rat in vivo.

2000

The activation of poly (ADP-ribose) synthetase (PARS) subsequent to DNA damage caused by reactive oxygen or nitrogen species has been implicated in several pathophysiological conditions, including ischemia-reperfusion injury and shock. The aim of this study was to investigate whether PARS inhibitors could provide protection against renal ischemia-reperfusion injury in the rat in vivo. Male Wistar rats were subjected to 45 min bilateral clamping of the renal pedicles, followed by 6 h reperfusion (control animals). Animals were administered the PARS inhibitors 3-aminobenzamide, 1, 5-dihydroxyisoquinoline, or nicotinamide during the reperfusion period. Ischemia, followed by reperfusion, produc…

MaleNiacinamideIschemiaRenal functionNatriuresisKidney; Poly (ADP-ribose) synthetase inhibitors; Proximal tubule; Reactive oxygen species; Reperfusion injuryPharmacologyPoly(ADP-ribose) Polymerase InhibitorsKidneyBiochemistryExcretionchemistry.chemical_compoundIn vivoGeneticsmedicineAnimalsUreaAnesthesiaEnzyme InhibitorsRats WistarMolecular BiologyKidneyCreatinineNicotinamidemedicine.diseaseIsoquinolinesRatsOxidative Stressmedicine.anatomical_structurechemistryCreatinineReperfusion InjuryBenzamidesReactive Oxygen SpeciesReperfusion injuryBiotechnologyGlomerular Filtration RateFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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Dynamics of complement activation in aHUS and how to monitor eculizumab therapy.

2014

Atypical hemolytic-uremic syndrome (aHUS) is associated with genetic complement abnormalities/anti–complement factor H antibodies, which paved the way to treatment with eculizumab. We studied 44 aHUS patients and their relatives to (1) test new assays of complement activation, (2) verify whether such abnormality occurs also in unaffected mutation carriers, and (3) search for a tool for eculizumab titration. An abnormal circulating complement profile (low C3, high C5a, or SC5b-9) was found in 47% to 64% of patients, irrespective of disease phase. Acute aHUS serum, but not serum from remission, caused wider C3 and C5b-9 deposits than control serum on unstimulated human microvascular endotheli…

MaleTime FactorsClinical Trials and ObservationsComplement Membrane Attack Complexurologic and male genital diseasesBiochemistryGlomerulonephritisInside BLOOD Commentaryhemic and lymphatic diseasesMembranoproliferative glomerulonephritisMonoclonalHumanizedComplement ActivationAtypical Hemolytic Uremic SyndromeEndothelial CellHematologyRemission Inductionfood and beveragesHematologyComplement C3Eculizumabmedicine.anatomical_structureFactor HFemalecomplementaHUS eculizumabmedicine.drugMembranoproliferativeHumanmedicine.medical_specialtyEndotheliumMonitoringTime FactorGlomerulonephritis MembranoproliferativeImmunologyBiologyAntibodies Monoclonal HumanizedAntibodiesInternal medicineAtypical hemolytic uremic syndromemedicineHumansPhysiologicMonitoring PhysiologicAdenosine Diphosphate RiboseEndothelial CellsCell Biologymedicine.diseaseComplement systemImmunologyAdenosine Diphosphate Ribose; Antibodies Monoclonal Humanized; Atypical Hemolytic Uremic Syndrome; Complement Activation; Complement C3; Complement Membrane Attack Complex; Endothelial Cells; Female; Glomerulonephritis Membranoproliferative; Hemolytic-Uremic Syndrome; Humans; Male; Remission Induction; Time Factors; Monitoring Physiologic; Hematology; Biochemistry; Cell Biology; ImmunologyHemolytic-Uremic SyndromeComplement membrane attack complexBlood
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Antioxidant activity of anti-inflammatory plant extracts

2002

The antioxidant properties of twenty medical herbs used in the traditional Mediterranean and Chinese medicine were studied. Extracts from Forsythia suspensa, Helichrysum italicum, Scrophularia auriculata, Inula viscosa, Coptis chinensis, Poria cocos and Scutellaria baicalensis had previously shown anti-inflammatory activity in different experimental models. Using free radical-generating systems H. italicum. I. viscosa and F. suspensa protected against enzymatic and non-enzymatic lipid peroxidation in model membranes and also showed scavenging property on the superoxide radical. All extracts were assayed at a concentration of 100 microg/ml. Most of the extracts were weak scavengers of the hy…

MaleXanthine OxidaseErythrocytesAntioxidantmedicine.drug_classmedicine.medical_treatmentHelichrysum italicumAntioxidantsGeneral Biochemistry Genetics and Molecular BiologyAnti-inflammatoryRats Sprague-DawleyLipid peroxidationchemistry.chemical_compoundmedicineAnimalsGeneral Pharmacology Toxicology and PharmaceuticsXanthine oxidaseForsythia suspensaPlants MedicinalbiologyTraditional medicineDeoxyribosePlant ExtractsAnti-Inflammatory Agents Non-SteroidalFree Radical ScavengersGeneral MedicineCoptis chinensisbiology.organism_classificationRatsBiochemistrychemistryMicrosomes LiverScutellaria baicalensisLipid PeroxidationMedicine TraditionalAminopyrine N-DemethylaseLife Sciences
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Acute ammonia intoxication induces an NMDA receptor-mediated increase in poly(ADP-ribose) polymerase level and NAD+ metabolism in nuclei of rat brain…

2004

Acute ammonia toxicity is mediated by excessive activation of NMDA receptors. Activation of NMDA receptors leads to activation of poly(ADP-ribose) polymerase (PARP) which mediates NMDA excitotoxicity. PARP is activated following DNA damage and may lead to cell death via NAD+ and ATP depletion. The aim of the present work was to assess whether acute ammonia intoxication in vivo leads to increased PARP in brain cells nuclei and to altered NAD+ and superoxide metabolism and the contribution of NMDA receptors to these alterations. Acute ammonia intoxication increases PARP content twofold in brain cells nuclei.NAD+ content decreased by 55% in rats injected with ammonia. This was not due to decre…

Malemedicine.medical_specialtyPoly ADP ribose polymeraseExcitotoxicityBiologymedicine.disease_causeReceptors N-Methyl-D-AspartateBiochemistryCellular and Molecular Neurosciencechemistry.chemical_compoundNAD+ NucleosidaseAmide SynthasesAmmoniaSuperoxidesInternal medicinemedicineAnimalsNeurotoxinRats WistarReceptorBrain ChemistryCell NucleusProtein Synthesis InhibitorsSuperoxideNAD+ ADP-RibosyltransferaseBrainProteinsNADMolecular biologyRatsEndocrinologychemistryTyrosineNMDA receptorNAD+ kinasePoly(ADP-ribose) PolymerasesJournal of Neurochemistry
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