Search results for "Genotoxicity"

showing 10 items of 104 documents

Determination of haemoglobin adducts of acrylamide and glycidamide in smoking and non-smoking persons of the general population

2005

Acrylamide (AA) is a food-borne toxicant suspected to be carcinogenic to humans. It is formed in the heating process of starch-containing food. Currently, there is a great discussion about the possible human health risks connected with the dietary uptake of acrylamide. Haemoglobin adducts of acrylamide and its oxidative metabolite glycidamide are both markers of biochemical effect. However, because glycidamide has a higher carcinogenic potency than acrylamide itself, the glycidamide adduct might mirror the genotoxicity better than acrylamide adducts. In order to gain more information about the human metabolism of acrylamide, we investigated a small group of persons for the effective interna…

AdultMalemedicine.medical_specialtyAdolescentMetabolitePopulationmedicine.disease_causeGas Chromatography-Mass SpectrometryHemoglobinschemistry.chemical_compoundGermanyInternal medicinemedicineHumansGlobineducationCarcinogenAgedAcrylamideAcrylamideseducation.field_of_studySmokingPublic Health Environmental and Occupational HealthValineMetabolismMiddle AgedEndocrinologychemistryBiochemistryAcrylamideEpoxy CompoundsFemaleBiomarkersGenotoxicityProtein BindingToxicantInternational Journal of Hygiene and Environmental Health
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Transgenic systems in studies on genotoxicity of alkylating agents: critical lesions, thresholds and defense mechanisms

1998

Abstract Transgenic systems, both cell lines and mice with gain or loss of function, are being used in order to modulate the expression of DNA repair proteins, thus allowing to assess their contribution to the defense against genotoxic mutagens and carcinogens. In this review, questions have been addressed concerning the use of transgenic systems in elucidating critical primary DNA lesions, their conversion into genotoxic endpoints, low-dose effects, and the relative contribution of individual cellular functions in defense. It has been shown that the repair protein alkyltransferase (MGMT) is decisive for protection against methylating and chloroethylating compounds. Protection pertains also…

Alkylating AgentsDNA repairDNA polymeraseHealth Toxicology and MutagenesisTransgeneMice Transgenicmedicine.disease_causeCell LineMiceGeneticsmedicineAnimalsHumansMolecular BiologyGeneticsbiologyMutagenicity TestsNeoplasms ExperimentalBase excision repairDNA glycosylaseCancer researchbiology.proteinDNA mismatch repairGenotoxicityMutagensAlkyltransferaseMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Assessment of mechanisms driving non-linear dose-response relationships in genotoxicity testing.

2014

In genetic toxicology, risk assessment has traditionally adopted linear dose-responses for any compound that causes genotoxic effects. Increasing evidence of non-linear dose-responses, however, suggests potential cellular tolerance to low levels of many genotoxicants with diverse modes of action. Such putative non-linear dose-responses need to be substantiated by strong mechanistic data that identifies the mechanisms responsible for the tolerance to low doses. This can be achieved by experimental demonstration of cytoprotective mechanisms and by providing experimental support for the existence of tolerance mechanisms against low dose effects. By highlighting key experiments into low dose me…

Alkylating AgentsDNA repairmedicine.drug_classTopoisomerase InhibitorsHealth Toxicology and MutagenesisTransgeneComputational biologyBiologyRisk AssessmentGenotoxicity testingToxicologyGeneticsmedicineAnimalsHumansGene knockoutDose-Response Relationship DrugMutagenicity TestsLow doseNucleosidesAneugensOxidantsModels ChemicalParticulate MatterTopoisomerase inhibitorGenetic ToxicologyDNA DamageMutagensMutation research. Reviews in mutation research
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Biological effects of inorganic arsenic on primary cultures of rat astrocytes

2010

It is well established that inorganic arsenic induces neurotoxic effects and neurological defects in humans and laboratory animals. The cellular and molecular mechanisms of its actions, however, remain elusive. Herein we report the effects of arsenite (NaAsO2) on primary cultures of rat astrocytes. Cells underwent induction of heat shock protein 70 only at the highest doses of inorganic arsenic (30 and 60 microM), suggesting a high threshold to respond to stress. We also investigated arsenic genotoxicity with the comet assay. Interestingly, although cells treated with 10 microM arsenite for 24 h maintained >70% viability, with respect to untreated cells, high DNA damage was already observed…

ArsenitesCell SurvivalDNA damagechemistry.chemical_elementBiologymedicine.disease_causeRats Sprague-Dawleychemistry.chemical_compoundSuperoxide Dismutase-1Settore BIO/10 - BiochimicaGeneticsmedicineAnimalsCell damageCells CulturedArsenicArseniteSuperoxide DismutaseGeneral Medicinemedicine.diseaseMolecular biologyCarcinogens EnvironmentalRatsHsp70Comet assaySettore BIO/18 - GeneticachemistryBiochemistryApoptosisAstrocytesComet Assayinorganic arsenic astrocytes cell damage DNA damage PIPPin.Reactive Oxygen SpeciesGenotoxicityDNA DamageInternational Journal of Molecular Medicine
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Influence of nitric oxide on the generation and repair of oxidative DNA damage in mammalian cells

2002

We have analysed the effects of endogenously and exogenously generated nitric oxide (NO) in cultured mammalian fibroblasts on: (i) the steady-state (background) levels of oxidative DNA base modifications; (ii) the susceptibility of the cells to the induction of additional DNA damage and micronuclei by H(2)O(2); and (iii) the repair kinetics of various types of DNA modifications. Steady-state levels of oxidative DNA base modifications, measured by means of an alkaline elution assay in combination with the repair endonuclease Fpg protein, were similar in NO-overproducing B6 mouse fibroblasts stably transfected with an inducible NO synthase (iNOS) and in control cells. Increased oxidative dama…

Cancer ResearchDNA RepairDNA damageDNA repairNitric Oxide Synthase Type IIMutagenAlkenesBiologyNitric OxideTransfectionmedicine.disease_causeMicechemistry.chemical_compoundmedicineAnimalsNitric Oxide DonorsDose-Response Relationship DrugHydrogen PeroxideGeneral MedicineTransfectionFibroblastsCell biologyBiochemistrychemistryNitric Oxide SynthaseDNAGenotoxicityPeroxynitriteOxidative stressDNA DamageCarcinogenesis
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Tumor-initiating activity of the (+)-(S,S)- and (−)-(R,R)-enantiomers of trans-11,12-dihydroxy-11,12-dihydrodibenzo[a,l]pyrene in mouse skin

1999

Abstract A single administration of enantiomerically pure 11,12-dihydrodiols of dibenzo[ a,l ]pyrene (DB[ a,l ]P) on the back of NMRI mice and subsequent chronic treatment with 12- O -tetradecanoylphorbol 13-acetate (TPA) (initiation/promotion assay) revealed strikingly different carcinogenic activities of both enantiomers. Tumor-initiating activity of (−)-(11 R ,12 R )-DB[ a,l ]P-dihydrodiol, which is the metabolic precursor of the (−)- anti -(11 R ,12 S )-dihydrodiol (13 S ,14 R )-epoxide, was exceptionally higher than the corresponding effect of (+)-(11 S ,12 S )-DB[ a,l ]P-dihydrodiol, the metabolic precursor of (+)- syn -(11 S ,12 R )-dihydrodiol (13 S ,14 R )-epoxide. After topical ap…

Cancer ResearchSkin NeoplasmsTime FactorsCarcinogenicity TestsStereochemistryEpoxideTumor initiationmedicine.disease_causeMicechemistry.chemical_compoundpolycyclic compoundsmedicineAnimalsBenzopyransCarcinogenCarcinogenic Polycyclic Aromatic HydrocarbonDose-Response Relationship DrugChemistryStereoisomerismSurvival RateOncologyBiochemistryCarcinogensPyreneFemaleStereoselectivityEnantiomerGenotoxicityCancer Letters
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Development and application of test methods for the detection of dietary constituents which protect against heterocyclic aromatic amines

2003

This article describes the development and use of assay models in vitro (genotoxicity assay with genetically engineered cells and human hepatoma (HepG2) cells) and in vivo (genotoxicity and short-term carcinogenicity assays with rodents) for the identification of dietary constituents which protect against the genotoxic and carcinogenic effects of heterocyclic aromatic amines (HAs). The use of genetically engineered cells expressing enzymes responsible for the bioactivation of HAs enables the detection of dietary factors that inhibit the metabolic activation of HAs. Human derived hepatoma (HepG2) cells are sensitive towards HAs and express several enzymes [glutathione S-transferase (GST), N-…

Carcinoma HepatocellularDNA damage[SDV]Life Sciences [q-bio]Health Toxicology and Mutagenesismedicine.disease_causeIsozyme03 medical and health sciences0302 clinical medicineANTICARCINOGENEHeterocyclic CompoundsIn vivoTumor Cells CulturedGeneticsmedicineAnticarcinogenic AgentsHumansMolecular BiologyAnticarcinogenComputingMilieux_MISCELLANEOUSCarcinogen030304 developmental biologychemistry.chemical_classification0303 health sciencesChemistryLiver NeoplasmsCANCERIn vitroDietEFFET PROTECTEUREnzymeBiochemistry030220 oncology & carcinogenesisColonic NeoplasmsFood AnalysisGenotoxicityMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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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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Modulating effects of humic acids on genotoxicity induced by water disinfectants in Cyprinus carpio

2005

The use of chlorinated disinfectants during drinking-water production has been shown to generate halogenated compounds as a result of interactions of humic acids with chlorine. Such chlorinated by-products have been shown to induce genotoxic effects and consumption of chlorinated drinking-water has been correlated with increased risk for cancer induction in human populations. The aim of this work was to test the potential genotoxic effects on circulating erythrocytes of the fish Cyprinus carpio exposed in vivo to well-waters disinfected with sodium hypochlorite (NaClO), chlorine dioxide (ClO2) or peracetic acid (CH3COO2H, PAA), in the absence or presence of standard humic acids (HA). The ef…

CarpsErythrocytesDrinking-water disinfectantsSodium HypochloriteHealth Toxicology and MutagenesisHumic acidschemistry.chemical_elementmedicine.disease_causeWater PurificationFish erythrocytesToxicologychemistry.chemical_compoundMicronucleus testPeracetic acidpolycyclic compoundsGeneticsChlorinemedicineAnimalsHumic acidPeracetic AcidFood scienceComet assayHumic Substanceschemistry.chemical_classificationChlorine dioxideMicronucleus TestsComet assay; Drinking-water disinfectants; Fish erythrocytes; Humic acids; Micronucleus testOxidesComet assaySettore BIO/18 - GeneticachemistrySodium hypochloriteMicronucleus testChlorine CompoundsGenotoxicityDNA DamageDisinfectantsMutation Research/Genetic Toxicology and Environmental Mutagenesis
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Genotoxicity of 1,4-benzoquinone and 1,4-naphthoquinone in relation to effects on glutathione and NAD(P)H levels in V79 cells.

1989

1,4-Benzoquinone is cytotoxic in V79 Chinese hamster cells and induces gene mutations and micronuclei. The cell-damaging effects of quinones are usually attributed to thiol depletion, oxidation of NAD(P)H, and redox-cycling involving the formation of semiquinone radicals and reactive oxygen species. To elucidate the role of these mechanisms in the genotoxicity of 1,4-benzoquinone, we measured various genotoxic effects, cytotoxicity, and the levels of glutathione, NADPH, NADH, and their oxidized forms all in the same experiment. 1,4-Naphthoquinone, which does not induce gene mutations in V79 cells, was investigated for comparative reasons. The quinones had a similar effect on the levels of c…

Cell SurvivalHealth Toxicology and MutagenesisGlutathione reductaseGene mutationBiologymedicine.disease_causeCell Linechemistry.chemical_compoundBenzoquinonesmedicineAnimalschemistry.chemical_classificationReactive oxygen speciesMutagenicity TestsQuinonesPublic Health Environmental and Occupational HealthGlutathioneNADGlutathioneBiochemistrychemistryMicronucleus testNAD+ kinaseOxidation-ReductionNADPGenotoxicityOxidative stressMutagensNaphthoquinonesResearch ArticleEnvironmental Health Perspectives
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