Search results for "Methylnitrosourea"

showing 6 items of 6 documents

DNA repair protein MGMT protects against N-methyl-N-nitrosourea-induced conversion of benign into malignant tumors

2003

Tumor formation is a multi-step process that can be divided into the stages of tumor initiation, promotion and progression. Previously, we showed that overexpression in skin of mice of the DNA repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) protects against N-methyl-N-nitrosourea (MNU)-induced tumor initiation without affecting tumor promotion. This indicated that O(6)-methylguanine, which is specifically repaired by MGMT, is a major tumor-initiating lesion. Here we extended this transgenic approach to the study of tumor progression. Benign papillomas that arose on the skin of CkMGMT transgenic mice upon initiation with 7,12-dimethylbenz[a]anthracene (DMBA) and promotion by 1…

Cancer ResearchPathologymedicine.medical_specialtySkin NeoplasmsMethyltransferaseDNA RepairDNA repairDMBAMice TransgenicTumor initiationBiologymedicine.disease_causeMiceO(6)-Methylguanine-DNA MethyltransferaseDNA Repair ProteinmedicineAnimalsneoplasmsPapillomaMethylnitrosoureaGeneral MedicineTumor progressionCarcinogensCancer researchTumor promotionCarcinogenesisCarcinogenesis
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Nuclear Translocation of Mismatch Repair Proteins MSH2 and MSH6 as a Response of Cells to Alkylating Agents

2000

Mammalian mismatch repair has been implicated in mismatch correction, the prevention of mutagenesis and cancer, and the induction of genotoxicity and apoptosis. Here, we show that treatment of cells specifically with agents inducing O(6)-methylguanine in DNA, such as N-methyl-N'-nitro-N-nitrosoguanidine and N-methyl-N-nitrosourea, elevates the level of MSH2 and MSH6 and increases GT mismatch binding activity in the nucleus. This inducible response occurs immediately after alkylation, is long-lasting and dose-dependent, and results from translocation of the preformed MutSalpha complex (composed of MSH2 and MSH6) from the cytoplasm into the nucleus. It is not caused by an increase in MSH2 gen…

CytoplasmDNA RepairBase Pair MismatchRNA StabilityChromosomal translocationmedicine.disease_causeBiochemistrychemistry.chemical_compoundMismatch Repair Endonuclease PMS2Adenosine TriphosphatasesNuclear ProteinsMethylnitrosoureaNeoplasm ProteinsDNA-Binding ProteinsMutS Homolog 2 ProteinDNA mismatch repairMutL Protein Homolog 1Protein BindingAlkylating AgentsMethylnitronitrosoguanidinecongenital hereditary and neonatal diseases and abnormalitiesGuanineActive Transport Cell NucleusBiologyCell LineO(6)-Methylguanine-DNA MethyltransferaseProto-Oncogene ProteinsDNA Repair ProteinmedicineHumansRNA MessengerneoplasmsMolecular BiologyAdaptor Proteins Signal TransducingCell NucleusMutagenesisnutritional and metabolic diseasesDNACell BiologyDNA MethylationMolecular biologydigestive system diseasesMSH6DNA Repair EnzymesGene Expression RegulationchemistryMSH2Carrier ProteinsGenotoxicityDNADNA DamageHeLa CellsJournal of Biological Chemistry
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Nickel(II) inhibits the repair of O 6 -methylguanine in mammalian cells

1999

Nickel compounds are widespread carcinogens, and although only weakly mutagenic, interfere with nucleotide excision repair and with the repair of oxidative DNA base modifications. In the present study we investigated the effect of nickel(II) on the induction and repair of O6-methylguanine and N7-methylguanine after treatment with N-methyl-N-nitrosourea (MNU). We applied Chinese hamster ovary cells stably transfected with human O6-methylguanine-DNA methyltransferase (MGMT) cDNA (CHO-AT), and compared the results with the MGMT-deficient parental cell line. As determined by high-performance liquid chromatography/electrochemical detection (HPLC/ECD), there was a slight but mostly not significan…

GuanineMethyltransferaseDNA RepairHealth Toxicology and MutagenesisBlotting WesternHamsterMutagenCHO CellsBiologyTransfectionToxicologymedicine.disease_causeO(6)-Methylguanine-DNA MethyltransferaseNickelCricetinaemedicineAnimalsHumansCytotoxicityChromatography High Pressure LiquidCarcinogenChinese hamster ovary cellMethylnitrosoureaGeneral MedicineTransfectionMolecular biologyFemaleNucleotide excision repairArchives of Toxicology
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Retinas of the Diurnal RodentArvicanthis ansorgeiAre Highly Resistant to Experimentally Induced Stress and Degeneration

2011

International audience; PURPOSE. Environmentally induced stress plays a significant role in retinal degeneration and blindness both in animals and in humans. Among such sources of stress, phototoxicity is well studied and has been shown to lead to photoreceptor-specific loss in a number of species. However, the vast majority of studies have been conducted in nocturnal, albino rod-dominant rat and mouse strains, and the pertinence of such findings to human pathology and cone loss is debatable. The authors examined retinal vulnerability to damage in the diurnal murid rodent Arvicanthis ansorgei, a pigmented species with a large number of cones. METHODS. The authors used established protocols …

MaleRetinal degenerationLightRodentsprague dawlayFatty Acids Nonesterifiedbright cyclic lightMicechemistry.chemical_compound0302 clinical medicine[SDV.IDA]Life Sciences [q-bio]/Food engineeringoxidative stressmethyl-N-nitrosoufrea0303 health sciencesbiologymedicine.diagnostic_testmouse retinaRetinal DegenerationMethylnitrosoureaAnatomydocosahexaenoic acidCircadian Rhythmmedicine.anatomical_structureDocosahexaenoic acidRetinal Cone Photoreceptor CellsN-3 fatty acidsPhototoxicityAlkylating Agentsmedicine.medical_specialtylight-induced degeneration03 medical and health sciencesSpecies SpecificityStress Physiologicalbiology.animalInternal medicineElectroretinographymedicineAnimals[SPI.GPROC]Engineering Sciences [physics]/Chemical and Process Engineering030304 developmental biologyRetinaRetinalmedicine.diseaseMice Inbred C57BLMuridaeratsTissue DegenerationDisease Models AnimalEndocrinologyrhodopsinchemistryregenerationinduced photoreceptor apoptosis030221 ophthalmology & optometrysense organsElectroretinographyInvestigative Opthalmology & Visual Science
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In vivo antigenotoxic effects of dietary allyl sulfides in the rat

1997

The effects of dietary administration of diallyl sulfide (DAS), diallyl disulfide (DADS) and allyl mercaptan (AM) on the genotoxicity of different chemicals were studied in two experimental systems: (i) measurement of hepatic DNA single-strand breaks induced in rats by aflatoxin B1 (AFB1), N-nitrosodimethylamine (NDMA) or methylnitrosourea (MNU); (ii) mutagenicity of AFB1 or NDMA on Salmonella typhimurium TA100 using hepatic S9 from rats fed allyl sulfides as the activation system. All compounds strongly reduced hepatic DNA breaks induced by AFB1 and NDMA but did not modify the genotoxicity of MNU. In the Ames test, the mutagenicity of NDMA was strongly inhibited by hepatic S9 from rats fed…

MaleSalmonella typhimuriumCancer ResearchAflatoxin B1[SDV]Life Sciences [q-bio]Allyl compoundMutagenSulfidesmedicine.disease_cause030226 pharmacology & pharmacyDimethylnitrosamineAmes test03 medical and health scienceschemistry.chemical_compound0302 clinical medicineN-NitrosodimethylaminemedicineAnimalsAnticarcinogenic AgentsDisulfidesComputingMilieux_MISCELLANEOUSMutagenicity TestsDiallyl disulfidefood and beveragesAntimutagenic AgentsMethylnitrosoureaRats3. Good healthAllyl Compounds[SDV] Life Sciences [q-bio]LiverOncologychemistryBiochemistry030220 oncology & carcinogenesisRATAllyl MercaptanCARCINOGENESEAllyl SulfideGenotoxicityDNA DamageMutagensCancer Letters
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Uridine uptake inhibition as a cytotoxicity test for a human hepatoma cell line (HepG2 cells): comparison with the neutral red assay

2001

International audience; This study describes a sensitive microassay for measuring cytotoxicity based on the degree of inhibition of RNA synthesis in HepG2 cells. RNA synthesis is measured by the kinetic uptake of radiolabeled uridine. A large number of compounds were tested in a wide range of concentrations. The concentration required to induce 50% inhibition of HepG2 uridine uptake rates (IC50) was determined for each compound and used to rank its potency. These IC50s were compared with IC50s measured with the neutral red assay. 2-acetylaminofluorene, benzo[a]pyrene and methylnitrosourea were not cytotoxic in the neutral red assay. Uridine uptake was always inhibited at lower concentrations…

Neutral redCarcinoma Hepatocellular[SDV.TOX.TCA]Life Sciences [q-bio]/Toxicology/Toxicology and food chainToxicologyXenobiotics03 medical and health scienceschemistry.chemical_compoundInhibitory Concentration 500302 clinical medicineNeutral redToxicity TestsTumor Cells CulturedPotencyCytotoxic T cellHumansBenzopyrenesCytotoxicityColoring AgentsUridine030304 developmental biology0303 health sciencesReproducibility of ResultsMethylnitrosourea2-AcetylaminofluoreneUridine uptakeIn vitroUridineKineticschemistryBiochemistryCytotoxicity-helpG2 cell line[SDV.TOX.TCA] Life Sciences [q-bio]/Toxicology/Toxicology and food chain030220 oncology & carcinogenesisToxicityCarcinogensHepatocytesPyreneRNARegression AnalysisWater Pollutants Chemical
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