Search results for "Methyl Methanesulfonate"

showing 10 items of 18 documents

Genotoxicity testing: Comparison of the γH2AX focus assay with the alkaline and neutral comet assays

2017

Genotoxicity testing relies on the quantitative measurement of adverse effects, such as chromosome aberrations, micronuclei, and mutations, resulting from primary DNA damage. Ideally, assays will detect DNA damage and cellular responses with high sensitivity, reliability, and throughput. Several novel genotoxicity assays may fulfill these requirements, including the comet assay and the more recently developed γH2AX assay. Although they are thought to be specific for genotoxicants, a systematic comparison of the assays has not yet been undertaken. In the present study, we compare the γH2AX focus assay with the alkaline and neutral versions of the comet assay, as to their sensitivities and li…

0301 basic medicineDNA damageHealth Toxicology and MutagenesisCometCHO CellsBiologymedicine.disease_causeSensitivity and SpecificityHistones03 medical and health scienceschemistry.chemical_compoundCricetulus0302 clinical medicineGeneticsmedicineAnimalsDose-Response Relationship DrugMutagenicity TestsComet tailMitomycin CMolecular biologyMethyl methanesulfonateComet assay030104 developmental biologychemistry030220 oncology & carcinogenesisMicronucleus testComet AssayGenotoxicityDNA DamageMutagensMutation Research/Genetic Toxicology and Environmental Mutagenesis
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Karyotype Abnormalities in a Variant Chinese Hamster Cell Line Resistant to Methyl Methanesulphonate

2004

A variant cell population, isolated from V79-CI 3 Chinese hamster cells after two consecutive treatments with methyl methanesulphonate (MMS), was found to be highly resistant to killing by this alkylating agent. The resistant cell line was cytogenetically characterized both by the presence of a stable translocation involving metacentric chromosome 2 and acrocentric chromosome 6 and by a supernumerary chromosome originated by the duplication of a small telocentric chromosome. This cell population also showed a transient transformed phenotype, seen as formation of transformed foci containing cells with high chromosomes counts and multiple chromosomal aberrations. As MMS-resistance and karyoty…

Alkylating AgentsCellPopulationDrug ResistanceChromosome DisordersChromosomal translocationChinese hamsterCell LineCricetulusCricetinaeGene duplicationGeneticsmedicineAnimalseducationChromosome AberrationsGeneticseducation.field_of_studybiologyChromosome MappingChromosomeKaryotypeGeneral MedicineMethyl Methanesulfonatebiology.organism_classificationMolecular biologyChromosome Bandingmedicine.anatomical_structureCell cultureKaryotypingHereditas
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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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Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression.

1999

Activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases is an early response of cells upon exposure to DNA-damaging agents. JNK-mediated phosphorylation of c-Jun is currently understood to stimulate the transactivating potency of AP-1 (e.g., c-Jun/c-Fos; c-Jun/ATF-2), thereby increasing the expression of AP-1 target genes. Here we show that stimulation of JNK1 activity is not a general early response of cells exposed to genotoxic agents. Treatment of NIH 3T3 cells with UV light (UV-C) as well as with methyl methanesulfonate (MMS) caused activation of JNK1 and an increase in c-Jun protein and AP-1 binding activity, whereas antineoplastic drugs such as mafosfamide, mito…

Alkylating AgentsProto-Oncogene Proteins c-junUltraviolet RaysStimulationBiologyenvironment and public healthWortmanninTransactivationchemistry.chemical_compoundMiceAnimalsPhosphatidylinositolCollagenasesProtein kinase AMolecular BiologyCell Growth and DevelopmentMitogen-Activated Protein Kinase 1Kinasec-junJNK Mitogen-Activated Protein KinasesCell Biology3T3 CellsMethyl MethanesulfonateMolecular biologyAndrostadienesEnzyme ActivationGene Expression Regulation NeoplasticTranscription Factor AP-1chemistryCalcium-Calmodulin-Dependent Protein KinasesPhosphorylationMitogen-Activated Protein KinasesWortmanninMolecular and cellular biology
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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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Phosphorylation of the DNA repair protein APE/REF-1 by CKII affects redox regulation of AP-1

1999

The DNA repair protein apurinic endonuclease (APE/Ref-1) exerts several physiological functions such as cleavage of apurinic/apyrimidinic sites and redox regulation of the transcription factor AP-1, whose activation is part of the cellular response to DNA damaging treatments. Here we demonstrate that APE/Ref-1 is phosphorylated by casein kinase II (CKII). This was shown for both the recombinant APE/Ref-1 protein (Km=0.55 mM) and for APE/Ref-1 expressed in COS cells. Phosphorylation of APE/Ref-1 did not alter the repair activity of the enzyme, whereas it stimulated its redox capability towards AP-1, thus promoting DNA binding activity of AP-1. Inhibition of CKII mediated phosphorylation of A…

Cancer ResearchDNA RepairProto-Oncogene Proteins c-junDNA repairDNA damageCarbon-Oxygen LyasesCHO CellsProtein Serine-Threonine KinasesBiologyTransfectionSubstrate SpecificityCricetinaeDNA Repair ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseGeneticsAnimalsHumansAP sitePhosphorylationCasein Kinase IIProtein kinase AMolecular BiologyMethyl MethanesulfonateCyclic AMP-Dependent Protein KinasesMolecular biologyDNA-(apurinic or apyrimidinic site) lyaseTranscription Factor AP-1COS CellsPhosphorylationCasein kinase 2Oxidation-ReductionDNA DamageHeLa CellsMutagensOncogene
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Use of HepG2 cell line for direct or indirect mutagens screening: comparative investigation between comet and micronucleus assays.

2003

International audience; In the present study, DNA-damage and clastogenic or aneugenic effects of genotoxic compounds were examined in a metabolically competent human cell line (HepG2 cells) using the micronucleus and the comet assays. Compounds with various action mechanisms were tested: direct mutagens such as 4-nitroquinoline-N-oxide (4-NQO) and methyl methanesulfonate (MMS) and indirect mutagens requiring biotransformation to be active such as N-nitrosodimethylamine (NDMA), benzo[a]pyrene (B[a]P) and 2-acetylaminofluorene (2-AAF). The compounds were first tested for cytotoxicity by measuring their effects on RNA synthesis inhibition in HepG2 cells. 4-NQO, B[a]P and 2-AAF were the most po…

Carcinoma HepatocellularNitrosaminesHealth Toxicology and Mutagenesis[SDV]Life Sciences [q-bio]Mutagen[SDV.TOX.TCA]Life Sciences [q-bio]/Toxicology/Toxicology and food chain010501 environmental sciencesQuinolonesmedicine.disease_cause01 natural sciencesSensitivity and SpecificityDimethylnitrosamine03 medical and health sciencesClastogenchemistry.chemical_compoundInhibitory Concentration 50GeneticsmedicineBenzo(a)pyreneTumor Cells CulturedHumansCytotoxicityComputingMilieux_MISCELLANEOUS030304 developmental biology0105 earth and related environmental sciencesGenetics0303 health sciencesMicronucleus TestsChemistryLiver Neoplasms2-AcetylaminofluoreneMethyl MethanesulfonateMolecular biology4-Nitroquinoline-1-oxideMethyl methanesulfonateComet assay[SDV] Life Sciences [q-bio]Micronucleus testComet AssayMicronucleusGenotoxicityMutagensMutation research
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Late activation of stress kinases (SAPK/JNK) by genotoxins requires the DNA repair proteins DNA-PKcs and CSB.

2005

Although genotoxic agents are powerful inducers of stress kinases (SAPK/JNK), the contribution of DNA damage itself to this response is unknown. Therefore, SAPK/JNK activation of cells harboring specific defects in DNA damage-recognition mechanisms was studied. Dual phosphorylation of SAPK/JNK by the genotoxin methyl methanesulfonate (MMS) occurred in two waves. The early response (≤2 h after exposure) was similar in cells knockout for ATM, PARP, p53, and CSB or defective in DNA-PKcscompared with wild-type cells. The late response however (≥4 h), was drastically reduced in DNA-PKcsand Cockayne's syndrome B (CSB)-deficient cells. Similar results were obtained with human cells lacking DNA-PKc…

DNA ReplicationAlkylationDNA RepairDNA damageDNA repairPoly ADP ribose polymeraseDNA-Activated Protein KinaseBiologyModels Biologicalchemistry.chemical_compoundMiceAnimalsHumansPhosphorylationPoly-ADP-Ribose Binding ProteinsMolecular BiologyDNA-PKcsCells CulturedKinaseDNA HelicasesJNK Mitogen-Activated Protein KinasesNuclear ProteinsCell BiologyBase excision repairDNAArticlesMethyl MethanesulfonateMolecular biologyMethyl methanesulfonateDNA-Binding ProteinsEnzyme Activationenzymes and coenzymes (carbohydrates)DNA Repair EnzymeschemistryPhosphorylationProtein Processing Post-TranslationalDNA DamageMutagensSignal TransductionMolecular biology of the cell
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The autoradiographic test for unscheduled DNA synthesis: a sensitive assay for the detection of DNA repair in the HepG2 cell line

2004

International audience; We assessed the DNA-repair capacity of HepG2 cells, which were derived from a human hepatoma, by the unscheduled DNA synthesis assay, using the autoradiography protocol (UDS-AR). We evaluated DNA repair following exposure to direct mutagens (4-nitroquinoline-N-oxide (4-NQO), methyl methanesulfonate (MMS)), to mutagens requiring metabolic activation (benzo[a]pyrene (B[a]P), 2-acetylaminofluorene (2-AAF), N-dimethylnitrosoamine (NDMA)) or to structurally related non-mutagens such as pyrene and 4-acetylaminofluorene (4-AAF). All positive compounds tested induced UDS in HepG2 cells. With 4-NQO and MMS, a concentration-dependent increase in net nuclear grains per cell was…

DNA ReplicationDNA RepairEndpoint DeterminationDNA damageDNA repairHealth Toxicology and Mutagenesis[SDV]Life Sciences [q-bio]Mutagen[SDV.TOX.TCA]Life Sciences [q-bio]/Toxicology/Toxicology and food chainBiologymedicine.disease_causeHEPG203 medical and health scienceschemistry.chemical_compound0302 clinical medicineTumor Cells CulturedGeneticsmedicineHumansComputingMilieux_MISCELLANEOUS030304 developmental biologyGeneticsAnalysis of Variance0303 health sciencesfungiMolecular biologyMethyl methanesulfonate[SDV] Life Sciences [q-bio]chemistryCell culture030220 oncology & carcinogenesisAutoradiographyRegression AnalysisPyreneGenotoxicityDNAMutagens
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