Search results for "DNA glycosylase"

showing 10 items of 50 documents

Circulating leukocyte telomere length and oxidative stress: A new target for statin therapy

2011

International audience; Objectives: We investigated the relationship between prior statin therapy and leukocyte telomere length (LTL), as well as their interaction with potential new biomarkers of oxidative deoxyribonucleic acid (DNA) lesions and reactive oxygen species-induced inflammation.Methods and results: From patients admitted for an acute myocardial infarction, LTL was assessed by quantitative polymerase chain reaction (Q-PCR), and leukocyte Finkel-Biskis-Jinkins osteosarcoma (FOS) and 8-oxoguanine DNA glycosylase (OGG1) messenger ribonucleic acid (mRNA) levels were measured by retrotranscription Q-PCR. Patients under prior chronic statin therapy were compared with patients without …

OncologyMaleMyocardial Infarction030204 cardiovascular system & hematologymedicine.disease_causeDNA Glycosylases0302 clinical medicineRisk FactorsLeukocytesMyocardial infarctionComputingMilieux_MISCELLANEOUSAged 80 and over0303 health sciencesReverse Transcriptase Polymerase Chain ReactionConfoundingMiddle AgedTelomere3. Good health[SDV.MHEP.CSC] Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemReal-time polymerase chain reactionOsteosarcomaFemalemedicine.symptomCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-fosGenetic Markersmedicine.medical_specialtyStatinmedicine.drug_classInflammationReal-Time Polymerase Chain ReactionRisk Assessment03 medical and health sciences[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineHumansRNA MessengerPropensity Score030304 developmental biologyAgedDyslipidemiasChi-Square Distributionbusiness.industrystatinoxidative stress 2medicine.diseaseLeukocyte telomere lengthSurgeryOxidative StressLogistic ModelsinflammationLinear ModelsHydroxymethylglutaryl-CoA Reductase InhibitorsbusinessChi-squared distributionOxidative stress
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Photochemical and photobiological studies with acridine and phenanthridine hydroperoxides in cell-free DNA.

1997

The acridine and phenanthridine hydroperoxides 3 and 7 were synthesized as photochemical hydroxyl radical sources for oxidative DNA damage studies. The generation of hydroxyl radicals upon UVA irradiation (lambda = 350 nm) was verified by trapping experiments with 5,5-dimethyl-1-pyrroline N-oxide and benzene. The enzymatic assays of the damage in cell-free DNA from bacteriophage PM2 caused by the acridine and phenanthridine hydroperoxides 3 and 7 under near-UVA irradiation revealed a wide range of DNA modifications. Particularly, extensive single-strand break formation and DNA base modifications sensitive to formamidopyrimidine DNA glycosylase (Fpg protein) were observed. In the photooxidat…

PhenanthridineCell-Free SystemDNA damageDNA SuperhelicalHydroxyl RadicalPhotochemistryUltraviolet RaysRadicalGeneral MedicineFormamidopyrimidine DNA glycosylasePhotochemistryBiochemistryPhotoinduced electron transferPeroxidesCyclic N-Oxideschemistry.chemical_compoundchemistryAcridineHydroxyl radicalSpin LabelsPhysical and Theoretical ChemistryOxidation-ReductionDNADNA DamagePhotochemistry and photobiology
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Photochemical and Photobiological Studies of a Furonaphthopyranone as a Benzo-spaced Psoralen Analog in Cell-free and Cellular DNA

1997

Photobiological activities of the benzo-spaced psoralen analog furonaphthopyranone 3 have been investigated in cell-free and cellular DNA. The molecular geometry parameters of 3 suggest that it should not form interstrand crosslinks with DNA. With cell-free DNA no evidence for crosslinking but also not for monoadduct formation was obtained; rather, the unnatural furocoumarin 3 induces oxidative DNA modifications under near-UVA irradiation. The enzymatic assay of the photosensitized damage in cell-free PM2 DNA revealed the significant formation of lesions sensitive to formamidopyrimidine DNA glycosylase (Fpg protein). In the photooxidation of calf thymus DNA by the furonaphthopyranone 3, 0.2…

PhotochemistryUltraviolet RaysDNA damageMolecular ConformationCHO CellsPhotochemistryBiochemistryOxazolonechemistry.chemical_compoundCricetinaeFurocoumarinsAnimalsDeoxyguanosinePhysical and Theoretical ChemistryPsoralenPhotosensitizing AgentsCell-Free SystemMolecular StructureMutagenicity TestsFurocoumarinFicusinDeoxyguanosineDNAGeneral MedicineFormamidopyrimidine DNA glycosylaseComet assaychemistryDNA ViralMethoxsalenCattleDNADNA DamagePhotochemistry and Photobiology
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Interference by toxic metal ions with zinc-dependent proteins involved in maintaining genomic stability.

2002

Metal ions are essential components of biological systems; nevertheless, even essential elements may have toxic or carcinogenic properties. Thus, besides As(III) and Cd(II), also Ni(II) and Co(II) have been shown previously to disturb different types of DNA repair systems at low, non-cytotoxic concentrations. Since some metals exert high affinities for SH groups, we investigated whether zinc finger structures in DNA-binding motifs of DNA repair proteins are potential targets for toxic metal ions. The bacterial formamidopyrimidine-DNA glycosylase (Fpg protein) involved in base excision repair was inhibited by Cd(II), Cu(II) and Hg(II) with increasing efficiencies, whereas Co(II), As(III), Pb…

Protein FoldingDNA RepairDNA repairCations DivalentPoly ADP ribose polymeraseToxicologymedicine.disease_causechemistry.chemical_compoundMetals HeavymedicineMetallothioneinHumansN-Glycosyl HydrolasesChemistryRNA-Binding ProteinsZinc FingersGeneral MedicineBase excision repairXeroderma Pigmentosum Group A ProteinDNA-Binding ProteinsZincBiochemistryDNA glycosylaseZinc toxicityDNAFood ScienceNucleotide excision repairFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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Age-related and tissue-specific accumulation of oxidative DNA base damage in 7,8-dihydro-8-oxoguanine-DNA glycosylase (Ogg1) deficient mice.

2001

Mutations that influence the repair of oxidative DNA modifications are expected to increase the steady-state (background) levels of these modifications and thus create a mutator phenotype that predisposes to malignant transformation. We have analysed the steady-state levels and repair kinetics of oxidative DNA modifications in cells of homozygous ogg1(-/-) null mice, which are deficient in Ogg1 protein, a DNA repair glycosylase that removes the miscoding base 8-hydroxyguanine (8-oxoG) from the genome. Oxidative purine modifications including 8-oxoG were quantified by means of an alkaline elution assay in combination with Fpg protein, the bacterial functional analogue of Ogg1 protein. In pri…

PurineMaleCancer ResearchGuanineDNA RepairOxidative phosphorylationBiologymedicine.disease_causeMalignant transformationchemistry.chemical_compoundMiceTranscription (biology)medicineAnimalsN-Glycosyl HydrolasesMice KnockoutCell growthAge FactorsGeneral MedicineDNAFibroblastsMolecular biologyOxygenOxidative StresschemistryDNA-Formamidopyrimidine GlycosylaseDNA glycosylaseOrgan SpecificityImmunologyHepatocytesOxidative stressDNACell DivisionDNA DamageCarcinogenesis
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Familial risk-colorectal cancer: ESMO Clinical Practice Guidelines.

2013

J. Balmana1, F. Balaguer2, A. Cervantes3 & D. Arnold4, on behalf of the ESMO Guidelines Working Group* Department of Medical Oncology, Hospital Vall d’Hebron, Vall d’Hebron Institute of Oncology (VHIO), Universitat Autonoma de Barcelona, Barcelona; Department of Gastroenterology, Hospital Clinic, CIBERehd, IDIBAPS, University of Barcelona, Barcelona; Department of Hematology and Medical Oncology, INCLIVA, University of Valencia, Valencia, Spain; Department of Medical Oncology, Tumor Biology Clinic, Albert Ludwigs University, Freiburg, Germany;

Riskmedicine.medical_specialtyColorectal cancerChemopreventionDNA Mismatch RepairDNA GlycosylasesNeoplastic Syndromes Hereditaryhealth services administrationMedicineHumansGenetic Predisposition to DiseaseGenetic TestingMultiple PolypsSigmoidoscopyEarly Detection of CancerAgedTumor biologybusiness.industryBrain NeoplasmsGeneral surgeryHematologyColonoscopyFamilial riskMiddle Agedmedicine.diseaseColorectal Neoplasms Hereditary NonpolyposishumanitiesClinical PracticeEuropeOncologyAdenomatous Polyposis Colipopulation characteristicsFemaleMicrosatellite InstabilitybusinessColorectal NeoplasmsColorectal Surgerygeographic locationsAnnals of oncology : official journal of the European Society for Medical Oncology
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The repair of oxidized purines in the DNA of human lymphocytes requires an activation involving NF-YA-mediated upregulation of OGG1.

2014

8-Oxoguanine DNA glycosylase (OGG1), which initiates the repair of DNA purine modifications such as 8-oxo-7,8-dihydroguanine (8-oxoG), is often regarded as a house keeping protein ubiquitously active in mammalian cells. We have analysed the repair rates of oxidized purines generated by photosensitization in peripheral human lymphocytes and observed that the cells were virtually unable to remove these lesions (less than 10% removal within 24h). However, stimulation of the lymphocytes with phytohemagglutinin (PHA) strongly accelerated the repair so that ∼30% of the lesions were repaired within 4h. Within 24h following PHA stimulation and preceding the induction of cell proliferation, Western …

Transcriptional ActivationDNA RepairBiologyBiochemistryDNA Glycosylaseschemistry.chemical_compoundDownregulation and upregulationHumansLymphocytesPhytohemagglutininsMolecular BiologyGeneTranscription factorCell Line TransformedCell growthCell BiologyBase excision repairDNAMolecular biologyUp-RegulationchemistryCCAAT-Binding FactorDNA glycosylasePurinesChromatin immunoprecipitationOxidation-ReductionDNADNA DamageDNA repair
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BER, MGMT, and MMR in defense against alkylation-induced genotoxicity and apoptosis

2001

Methylating carcinogens and cytostatic drugs induce different methylation products in DNA. In cells not expressing the repair protein MGMT or expressing it at a low level, O6-methylguanine is the major genotoxic, recombinogenic, and apoptotic lesion. Genotoxicity and apoptosis triggered by O6-methylguanine require mismatch repair (MMR). In cells expressing O6-methylguanine-DNA methyl transferase (MGMT) at a high level or for agents producing low amounts of O6-methylguanine, N-alkylations become the major genotoxic lesions. N-Alkylations are repaired by base excision repair (BER). In mammalian cells, naturally occurring mutants of BER have not been detected, which points to the importance of…

biologyDNA polymeraseTransfectionBase excision repairmedicine.disease_causeMolecular biologyDNA glycosylaseCancer researchbiology.proteinmedicineTranscriptional regulationAP siteDNA mismatch repairGenotoxicity
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Characterization of hOGG1 Promoter Structure, Expression During Cell Cycle and Overexpression in Mammalian Cells

2001

Oxygen radicals are produced in all cells either by the normal cellular metabolism or by the exposure to external mutagens. The reactive oxygen species (ROS) generated can induce DNA damage. Among the principal lesions found in DNA due to ROS is an oxidized form of guanine, 8-oxo-7,8-dihydroguanine (8-oxoG). The biological relevance of this lesion has been unveiled by the study of Escherichia colt and Saccharomyces cerevisiae genes involved in the neutralization of the mutagenic effects of 8-oxoG (Cabrera et al., 1988; Nghiem et al., 1988; Radicella et al., 1988; van der Kemp et al., 1996). These genes fpg and mutY for E. colt and OGG1 for yeast, code for DNA glycosylases. Inactivation of a…

chemistry.chemical_compoundbiologychemistryDNA glycosylaseDNA damageGene expressionSaccharomyces cerevisiaeAlternative splicingbiology.organism_classificationGeneMolecular biologyDNADNA-formamidopyrimidine glycosylase
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A global DNA repair mechanism involving the Cockayne syndrome B (CSB) gene product can prevent the in vivo accumulation of endogenous oxidative DNA b…

2002

The Cockayne syndrome B (CSB) gene product is involved in the repair of various types of base modifications in actively transcribed DNA sequences. To investigate its significance for the repair of endogenous oxidative DNA damage, homozygous csb(-/-)/ogg1(-/-) double knockout mice were generated. These combine the deficiency of CSB with that of OGG1, a gene coding for the mammalian repair glycosylase that initiates the base excision repair of 7,8-dihydro-8-oxoguanine (8-oxoG). Compared to ogg1(-/-) mice, csb(-/-)/ogg1(-/-) mice were found to accumulate with age severalfold higher levels of oxidited purine modifications in hepatocytes, splenocytes and kidney cells. In contrast, the basal (ste…

musculoskeletal diseasescongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairTranscription GeneticDNA damageDNA repairBiologyGene productMicechemistry.chemical_compoundGeneticsAnimalsPoly-ADP-Ribose Binding ProteinsMolecular BiologyGeneDNA PrimersMice KnockoutBase SequenceHomozygoteDNA HelicasesDeoxyguanosinenutritional and metabolic diseasesBase excision repairMolecular biologyOxidative StressDNA Repair EnzymesBiochemistrychemistry8-Hydroxy-2'-DeoxyguanosineDNA glycosylaseDNADNA DamageNucleotide excision repairOncogene
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