Search results for "DNA Repair"

showing 10 items of 295 documents

Human Monocytes, but not Dendritic Cells Derived from Them, Are Defective in Base Excision Repair and Hypersensitive to Methylating Agents

2007

Abstract Monocytes and dendritic cells are key players in the immune response. Because dendritic cells drive the tumor host defense, it is important that monocytes and dendritic cells survive cytotoxic tumor therapy. Although most of the anticancer drugs target DNA, the DNA repair capacity of monocytes and dendritic cells has not yet been investigated. We studied the sensitivity of monocytes and monocyte-derived dendritic cells against various genotoxic agents and found monocytes to be more sensitive to overall cell kill and apoptosis upon exposure to methylating agents (e.g., N-methyl-N′-nitro-N-nitrosoguanidine, methyl methanesulfonate, and the anticancer drug temozolomide). On the other …

Alkylating AgentsMethylnitronitrosoguanidineCancer ResearchDNA RepairCell SurvivalDNA repairBiologyMonocytesDrug HypersensitivityXRCC1Immune systemTemozolomidemedicineHumansCytotoxic T cellAntigen-presenting cellCells CulturedMonocyteDendritic CellsBase excision repairDendritic cellDNA MethylationMethyl MethanesulfonateDacarbazinemedicine.anatomical_structureOncologyImmunologyCancer researchMutagensCancer Research
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Kinetics of gamma-H2AX focus formation upon treatment of cells with UV light and alkylating agents.

2008

Histone H2AX is rapidly phosphorylated in response to DNA double-strand breaks (DSBs) induced by ionizing radiation (IR). Here we show that DNA damage induced by alkylating agents [methyl methanesulfonate (MMS) and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)] and ultraviolet light (UV-C) leads to a dose and time dependent accumulation of phosphorylated H2AX (gamma-H2AX). Time course experiments revealed that the number of gamma-H2AX foci reached peak levels 8 hr after MMS or MNNG treatment and declined to almost control values within 24 hr after exposure. Upon UV-C treatment, a biphasic response was observed with a maximum 12 hr after treatment. In 43-3B cells deficient in nucleotide excisi…

Alkylating AgentsMethylnitronitrosoguanidineTime FactorsDNA RepairEpidemiologyDNA damageMethylnitronitrosoguanidineDNA repairUltraviolet RayscellsHealth Toxicology and MutagenesisFluorescent Antibody TechniqueCHO CellsBiologyenvironment and public healthHistoneschemistry.chemical_compoundCricetulusCricetinaeUltraviolet lightAnimalsPhosphorylationGenetics (clinical)DNA replicationMethyl MethanesulfonateMolecular biologyMethyl methanesulfonateenzymes and coenzymes (carbohydrates)KineticschemistryBiochemistrybiological phenomena cell phenomena and immunityDNANucleotide excision repairDNA DamageEnvironmental and molecular mutagenesis
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MGMT: Key node in the battle against genotoxicity, carcinogenicity and apoptosis induced by alkylating agents

2007

O(6)-methylguanine-DNA methyltransferase (MGMT) plays a crucial role in the defense against alkylating agents that generate, among other lesions, O(6)-alkylguanine in DNA (collectively termed O(6)-alkylating agents [O(6)AA]). The defense is highly important, since O(6)AA are common environmental carcinogens, are formed endogenously during normal cellular metabolism and possibly inflammation, and are being used in cancer therapy. O(6)AA induced DNA damage is subject to repair, which is executed by MGMT, AlkB homologous proteins (ABH) and base excision repair (BER). Although this review focuses on MGMT, the mechanism of repair by ABH and BER will also be discussed. Experimental systems, in wh…

Alkylating AgentsMethyltransferaseAlkylationDNA RepairDNA repairDNA damageGene ExpressionApoptosisIn Vitro TechniquesBiologyDNA Mismatch RepairModels BiologicalBiochemistryNecrosisO(6)-Methylguanine-DNA MethyltransferaseNeoplasmsAnimalsHumansDNA Modification MethylasesneoplasmsMolecular BiologyCarcinogenChromosome AberrationsGeneticsTumor Suppressor ProteinsO-6-methylguanine-DNA methyltransferaseDNACell BiologyBase excision repairdigestive system diseasesDNA Repair EnzymesMutationCancer researchDNA mismatch repairSister Chromatid ExchangeDNA DamageAlkyltransferaseDNA Repair
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Primary mouse fibroblasts deficient for c-Fos, p53 or for both proteins are hypersensitive to UV light and alkylating agent-induced chromosomal break…

2000

The important regulatory proteins, c-Fos and p53 are induced by exposure of cells to a variety of DNA damaging agents. To investigate their role in cellular defense against genotoxic compounds, we comparatively analysed chromosomal aberrations and apoptosis induced by ultraviolet (UV-C) light and the potent alkylating agent methyl methanesulfonate (MMS) in primary diploid mouse fibroblasts knockout for either c-Fos or p53, or double knockout for both genes. We show that c-Fos and p53 deficient fibroblasts are more sensitive than the corresponding wild-type cells as to the induction of chromosomal aberrations and apoptosis. Double knockout fibroblasts lacking both c-Fos and p53 are viable an…

Alkylating AgentsUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisDrug ResistanceMutagenesis (molecular biology technique)ApoptosisBiologyRadiation ToleranceCell LineMicechemistry.chemical_compoundGeneticsAnimalsMolecular BiologyGene knockoutChromosome AberrationsMice KnockoutGenes fosFibroblastsCell cycleGenes p53Molecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Mismatch G-T binding activity and MSH2 expression is quantitatively related to sensitivity of cells to methylating agents

1998

To elucidate mechanisms involved in alkylating drug resistance, Chinese hamster cells resistant to methylating agents have been generated upon transfection with human DNA. Here it is shown that these Chinese hamster ovary (CHO) variants exhibit the tolerance phenotype: they are alkyltransferase deficient (Mex-), cross-resistant to 6-thioguanine, exhibit reduced G-T binding (MutS alpha) activity and express the mismatch repair protein MSH2 at a significantly lower level than the corresponding control. By comparing wild-type cells with different tolerant strains that show gradual differences in resistance to methylating agents, it was shown that both the G-T binding activity and the amount of…

Alkylating Agentscongenital hereditary and neonatal diseases and abnormalitiesCancer ResearchDNA RepairHamsterCHO CellsBiologyMethylationChinese hamsterCricetinaeProto-Oncogene ProteinsAnimalsHumansRNA MessengerChinese hamster ovary cellCell CycleGeneral MedicineMismatch Repair ProteinTransfectionbiology.organism_classificationMolecular biologyDNA-Binding ProteinsMutS Homolog 2 ProteinMSH2DNA mismatch repairAlkyltransferaseCarcinogenesis
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Theoretical Study on the Photo-Oxidation and Photoreduction of an Azetidine Derivative as a Model of DNA Repair

2021

Photocycloreversion plays a central role in the study of the repair of DNA lesions, reverting them into the original pyrimidine nucleobases. Particularly, among the proposed mechanisms for the repair of DNA (6-4) photoproducts by photolyases, it has been suggested that it takes place through an intermediate characterized by a four-membered heterocyclic oxetane or azetidine ring, whose opening requires the reduction of the fused nucleobases. The specific role of this electron transfer step and its impact on the ring opening energetics remain to be understood. These processes are studied herein by means of quantum-chemical calculations on the two azetidine stereoisomers obtained from photocyc…

AnionsAcetonitrilesPyrimidineLightPhotochemistryAzetidinePharmaceutical ScienceOrganic chemistryDNA repair010402 general chemistryRing (chemistry)PhotochemistryOxetane01 natural sciencesArticleAnalytical ChemistryNucleobaseElectron transferchemistry.chemical_compoundElectron transferQUIMICA ORGANICAQD241-441AzetidineCationsredox propertiesDrug DiscoveryPhotosensitizerPhysical and Theoretical ChemistryPhotolyasering openingdensity functional theoryphotochemistry010405 organic chemistryRing openingModels Theoreticalelectron transfer0104 chemical scienceschemistryChemistry (miscellaneous)Density functional theoryMolecular MedicineAzetidinesThermodynamicsGasesazetidineOxidation-ReductionRedox propertiesMolecules
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Influence of DNA damage and repair upon the risk of treatment related leukemia

2008

Therapy-related myelodysplasia and acute myeloid leukemia (t-MDS/AML) are malignancies occurring after exposure to chemotherapy and/or radiotherapy. Several studies have addressed cumulative dose, dose intensity and exposure to specific agents of preceding cytotoxic therapy in relation to the risk of developing such leukemia. Since only a small percentage of patients exposed to cytotoxic therapy develop t-MDS/AML, it has been suggested that some genetic predisposition may be involved, specifically associated to polymorphisms in certain genes involved in chemotherapy/radiotherapy response - fundamentally genes intervening in drug detoxification and DNA synthesis and repair. A review is made …

Antimetabolites AntineoplasticCancer ResearchDNA RepairDNA repairDNA damagemedicine.medical_treatmentAntineoplastic AgentsBiologyhemic and lymphatic diseasesmedicineGenetic predispositionHumansTopoisomerase II InhibitorsGenetic Predisposition to DiseaseAntineoplastic Agents AlkylatingChemotherapyPolymorphism GeneticDrug detoxificationMyeloid leukemiaNeoplasms Second PrimaryHematologymedicine.diseaseRadiation therapyLeukemiaOncologyImmunologyCancer researchDNA DamageLeukemia & Lymphoma
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Oxidative stress and DNA damage in agricultural workers after exposure to pesticides

2021

Abstract Background Recent epidemiological studies on workers describe that exposure to pesticides can induce oxidative stress by increased production of free radicals that can accumulate in the cell and damage biological macromolecules, for example, RNA, DNA, DNA repair proteins and other proteins and/or modify antioxidant defense mechanisms, as well as detoxification and scavenger enzymes. This study aimed to assess oxidative stress and DNA damage among workers exposed to pesticides. Methods For this purpose, 52 pesticide exposed workers and 52 organic farmers were enrolled. They were assessed: the pesticide exposure, thiobarbituric acid reactive substances (TBARS), total glutathione (TG)…

AntioxidantDNA repairThiobarbituric acidDNA damagemedicine.medical_treatmentOxidative phosphorylation010501 environmental sciencesPharmacologyToxicologymedicine.disease_cause01 natural sciencesAgricultural workerlcsh:RC963-96903 medical and health scienceschemistry.chemical_compoundAgricultural workersTBARSMedicineDiseasePesticides030304 developmental biology0105 earth and related environmental sciencesCancer0303 health sciencesbusiness.industryResearchPublic Health Environmental and Occupational HealthROSPesticidePesticidechemistryBiomonitoringlcsh:Industrial medicine. Industrial hygienebusinessSafety ResearchOxidative stress
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Senataxin defective in ataxia oculomotor apraxia type 2 is involved in the defence against oxidative DNA damage

2007

Adefective response to DNA damage is observed in several human autosomal recessive ataxias with oculomotor apraxia, including ataxia-telangiectasia. We report that senataxin, defective in ataxia oculomotor apraxia (AOA) type 2, is a nuclear protein involved in the DNA damage response. AOA2 cells are sensitive to H2O2, camptothecin, and mitomycin C, but not to ionizing radiation, and sensitivity was rescued with full-length SETX cDNA. AOA2 cells exhibited constitutive oxidative DNA damage and enhanced chromosomal instability in response to H2O2. Rejoining of H2O2-induced DNA double-strand breaks (DSBs) was significantly reduced in AOA2 cells compared to controls, and there was no evidence fo…

Ataxiagenetic structuresDNA RepairDNA damageApraxiasBiologyArticlechemistry.chemical_compoundComplementary DNAChromosome instabilitymedicineHumansDNA Breaks Double-StrandedOculomotor apraxiaCells CulturedResearch ArticlesNeurodegenerationMitomycin CDNA HelicasesCell BiologyHydrogen Peroxidemedicine.diseaseMolecular biologyMultifunctional EnzymesOxidative StresschemistryAtaxiamedicine.symptomDNARNA HelicasesDNA Damage
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Synthesis of 131I-labeled glucose-conjugated inhibitors of O6-methylguanine-DNA methyltransferase (MGMT) and comparison with nonconjugated inhibitors…

2006

O 6 -Substituted guanine derivatives are powerful agents used for tumor cell sensitization by inhibition of the DNA repair enzyme O 6 -methylguanine-DNA methyltransferase (MGMT). To provide targeted accumulation of MGMT inhibitors in tumor tissue as well as tools for in vivo imaging, we synthesized iodinated C 8 -alkyl-linked glucose conjugates of 2-amino-6-(5-iodothenyl)-9H-purine (O 6 -(5-iodothenyl) guanine, ITG) and 2-amino-6-(3-iodobenzyloxy)-9H-purine (O 6 -(5-iodobenzyl) guanine, IBG). These compounds have MGMT inhibitor constants (IC 5 0 values) of 0.8 and 0.45 μM for ITGG and IBGG, respectively, as determined in HeLa S3 cells after 2-h incubation with inhibitor. To substantiate tha…

BiodistributionMethyltransferaseGuanineTime FactorsDNA repairGuanineTransplantation HeterologousMice NudeAntineoplastic AgentsIn Vitro Techniqueschemistry.chemical_compoundMiceO(6)-Methylguanine-DNA MethyltransferaseStructure-Activity RelationshipIn vivoIodine IsotopesDrug DiscoveryAnimalsHumansEnzyme Inhibitorschemistry.chemical_classificationbiologyMolecular StructureXenograft Model Antitumor AssaysEnzymeGlucosechemistryBiochemistryEnzyme inhibitorbiology.proteinMolecular MedicineEx vivoHeLa CellsJournal of medicinal chemistry
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