Search results for "Sister Chromatid Exchange"

showing 10 items of 30 documents

Sister-chromatid exchange in cultured lymphocytes of ewes and their newborn lambs

1984

The incidence of sister-chromatid exchange (SCE) in cultured lymphocytes of ewes and their newborn lambs was determined using the BrdU-Giemsa technique. In all ewe-lamb pairs, the SCE rate in the lambs was less than that of the ewes. The mean SCE frequencies per chromosome of the ewes after lambing and of the newborn lambs were 0.1909 and 0.1581, respectively. The statistical analysis shows that a significant difference exists between SCE in the adult female sheep and their lambs. At the same time, a negative correlation was observed between SCE rate and cell proliferation. The results of this study are compared with those of previous reports on age-dependency of SCE.

AdultAgingAdolescentanimal diseasesSister chromatid exchangeBiologyAndrologyPregnancyparasitic diseasesAnimalsHumansStatistical analysisCrossing Over GeneticLymphocytesChildCells CulturedAgedGeneticsSheepAdult femaleIncidence (epidemiology)Domestic sheep reproductionSignificant differenceInfant NewbornInfantChromosomeGeneral MedicineMiddle Agedrespiratory systemAnimals NewbornChild PreschoolFemaleNegative correlationSister Chromatid ExchangeCell DivisionMutation Research Letters
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Sister chromatid exchange, (SCE), High-Frequency Cells (HFCs) and SCE distribution patterns in peripheral blood lymphocytes of Spanish adult smokers …

2014

According to the International Agency for Research on Cancer, smoking tobacco is a major cause of cancer in humans. It causes about half of all male cancer deaths and an ever increasing number of cancer deaths in females. The aim of this study was to establish whether cigarette smoking increases sister chromatid exchanges (SCEs) in peripheral blood lymphocytes in two Spanish population groups; light and heavy smokers. The mean number of High-Frequency Cells (HFCs) was determined and, the SCE distribution pattern among the chromosomes was analysed represented by a ratio described below. A local sample of 101 adult smokers (n = 48) and non-smokers (n = 53), aged from 18 to 49 years, was studi…

AdultMaleAdolescent[SDV]Life Sciences [q-bio]PhysiologySister chromatid exchangeBiologyToxicologyINGENIERIA NUCLEARToxicology03 medical and health sciencesYoung Adult0302 clinical medicineTobaccomedicineDistribution (pharmacology)Sister chromatidsHumansLymphocytes030304 developmental biologySCEs0303 health sciencesHeavy smokingSmoking TobaccoSmokingCytogenetic assessmentCancerGeneral MedicineBiomarkerMiddle Agedmedicine.diseasePeripheral blood3. Good healthSpanish populationSpain030220 oncology & carcinogenesisCase-Control StudiesFemaleSister Chromatid ExchangeFood Science
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Sister chromatid exchange in Waldenström's macroglobulinemia

1993

Results on sister chromatid exchange (SCE) frequency and interchromosomal distribution in bone marrow and peripheral blood cultures from patients with Waldenström's macroglobulinemia are reported. PHA-stimulated bone marrow cultures showed increased SCE frequencies in all 12 patients examined. The increase was particularly high in two cases (17.07 and 16.77 SCE/cell, respectively) and, in one of them, a very high SCE level was found in PHA-stimulated peripheral blood culture (40.81 SCE/cell). In LPS-stimulated cultures, increased SCE levels were observed in some patients. Comparison between SCE frequency in bone marrow cell cultures with either mitogen showed a significant increase in PHA-s…

AdultMaleCancer ResearchG chromosomeCellSister chromatid exchangeBiologyGeneticsmedicineHumansPooled dataMolecular BiologyAgedCell CycleMacroglobulinemiaWaldenstrom macroglobulinemiaMiddle AgedCell cyclemedicine.diseaseMolecular biologySettore BIO/18 - Geneticamedicine.anatomical_structureImmunologySister chromatid exchanges Waldenstrom's macroglobulinemiaFemaleBone marrowWaldenstrom MacroglobulinemiaSister Chromatid ExchangeCancer Genetics and Cytogenetics
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Genotoxicity of selected pesticides in the mouse bone-marrow micronucleus test and in the sister-chromatid exchange test with human lymphocytes in vi…

1996

Selected pesticides (aldicarb, 1,3-dichloropropene, methidathion, parathion, triadimefon, vinclozolin) were tested for their clastogenic and aneugenic activities in the mouse bone-marrow micronucleus (MN) test in vivo and for their sister-chromatid exchange-inducing activities in human lymphocytes in vitro in the presence and absence of an exogenous metabolizing system from rat-liver S9. 1,3-Dichloropropene significantly increased the frequencies of micronucleated polychromatic erythrocytes (PCE) in bone-marrow cells of female mice from 3.3 MN/1000 PCE to 15.3 MN/1000 PCE (187 mg per kg body weight). 1,3-Dichloropropene (100 microM) induced 16.0 SCE/metaphase after 24 h of incubation as com…

AdultMaleSister chromatid exchangeMethidathion010501 environmental sciencesBiologyToxicologymedicine.disease_cause01 natural sciencesMice03 medical and health scienceschemistry.chemical_compoundClastogenBone MarrowHydrocarbons ChlorinatedmedicineAnimalsHumansLymphocytesVinclozolinPesticidesOxazolesMetaphaseCells CulturedMicronuclei Chromosome-Defective030304 developmental biology0105 earth and related environmental sciences0303 health sciencesMicronucleus TestsParathionOrganothiophosphorus CompoundsGeneral MedicineTriazolesMolecular biology3. Good healthAllyl CompoundschemistryImmunologyMicronucleus testFemaleMicronucleusSister Chromatid ExchangeAldicarbGenotoxicityToxicology Letters
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Chromosomal aberrations in patients with primary biliary cirrhosis.

1990

Chromosomal aberrations in untreated lymphocyte cultures, bleomycin (BLM)-induced aberrations and sister chromatid exchanges (SCE) in the peripheral blood lymphocytes of 11 patients suffering from primary biliary cirrhosis (PBC) and 14 matched control individuals were analysed. The lymphocytes of the PBC patients had on average a lower mitotic index (2.3) compared with controls (3.5) in the untreated cultures. The mean baseline rate of aberrations of the cultured lymphocytes of the patients was 5.3 aberrations per 100 metaphases (%); this was significantly different (P = 0.0291) from that of the controls with a mean of 2.3%. In lymphocytes of the patients and controls, most of the aberratio…

Adultmedicine.medical_specialtyMitotic indexLymphocyteBiliary cirrhosisBiologyBleomycinGastroenterologychemistry.chemical_compoundBleomycinPrimary biliary cirrhosisInternal medicineGeneticsmedicineMitotic IndexSister chromatidsHumansLymphocytesGenetics (clinical)Cells CulturedAgedChromosome AberrationsLiver Cirrhosis BiliaryKaryotypeMiddle Agedmedicine.diseaseMolecular medicinemedicine.anatomical_structurechemistryKaryotypingImmunologyFemaleSister Chromatid ExchangeHuman genetics
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Cytogenetic effects of promutagens in genetically engineered V79 Chinese hamster cells expressing cytochromes P450.

1993

Abstract V79 Chinese hamster cell lines genetically engineered to express rat CYP2B1, CYP1A1, CYP1A2, and their parental cell lines V79-MZ, without acetyltransferase, and V79-NH, with acetyltransferase, were studied for chromosome aberrations and sister chromatid exchange induced by aflatoxin B 1 , cyclophosphamide, benzo[a]pyrene, 7,12-dimethylbenz[a]anthracene and dimethylnitrosamine. The parental V79 cell lines did not show clastogenic effects. Significant clastogenic effects were observed after an 18 h exposure to aflatoxin B 1 and cyclophosphamide in CYP2B1 expressing cells, to benzo[a]pyrene in CYP1A1 and CYP1A2 expressing cells, to 7,12-dimethylbenz[a]anthracene and dimethylnitrosami…

Aflatoxin B1910-Dimethyl-12-benzanthraceneHamsterSister chromatid exchangeMutagenToxicologymedicine.disease_causeChinese hamsterCell LineDimethylnitrosamineClastogenCricetulusCytochrome P-450 Enzyme SystemCricetinaepolycyclic compoundsmedicineBenzo(a)pyreneAnimalsCyclophosphamideBiotransformationPharmacologyChromosome Aberrationsbiologyrespiratory systembiology.organism_classificationPollutionMolecular biologyIn vitroRatsCell cultureAcetyltransferaseGenetic EngineeringSister Chromatid ExchangeMutagensEuropean journal of pharmacology
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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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The DNA methylation inhibitor 5-azacytidine modulates 6-thioguanine toxicity in mammalian cells

2003

In order to assess the effects of combining two antimetabolites used separately to treat human leukemias, we carried out an experimental study by exposing V79 Chinese hamster cells, a 6-thioguanine (6-tG)-sensitive cell line, to sequential and concurrent treatments with 5-azacytidine (5-azaC) and 6-tG. In this paper, we demonstrate that there is a clear dependency for the way in which this combination was tested. Pre-treatment with 5-azaC made V79 cells more resistant to 6-tG by a substantial reduction in 6-tG incorporation into DNA; this effect could still be detected for several cell divisions after the removal of 5-azaC, and was achieved neither by reduced cell growth nor by the inductio…

Antimetabolites AntineoplasticHypoxanthine Phosphoribosyltransferasemedicine.drug_classCell SurvivalCellHamsterToxicologyAntimetaboliteChinese hamster6-thioguanineCricetulus5-azacytidineCricetinaeAntineoplastic Combined Chemotherapy ProtocolsmedicineAnimalsThioguanineCells CulturedbiologyCell growthtoxicityDrug SynergismGeneral MedicineDNAProdrugDNA Methylationbiology.organism_classificationMolecular biologySettore BIO/18 - Geneticamedicine.anatomical_structureBiochemistryCell cultureToxicityAzacitidineSister Chromatid ExchangeCell Division
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In vitro cytogenetic and genotoxic effects of curcumin on human peripheral blood lymphocytes

2012

International audience; Curcumin has shown a wide range of properties such as anti-inflammatory and anti-carcinogenic properties. Many of these effects, mainly the anti-carcinogenic effect, could be linked to its anti-oxidant effects. Nevertheless, some studies suggest that this natural compound possesses both pro- and anti-oxidative effects and that curcumin could be a genotoxic agent for some cell lines. We evaluated the genetic damage induced by curcumin to human lymphocytes exposed to increasing concentrations (0-50 μg/ml) of curcumin. Biomarkers such as chromosome aberrations (CAs) and sister chromatid exchange (SCE) were analyzed. In addition to the cytogenetic analysis, the effect of…

CurcuminProliferation indexCarcinogenicity Tests[SDV]Life Sciences [q-bio]Sister chromatid exchangeIn Vitro TechniquesPharmacologyBiologyToxicologymedicine.disease_cause03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineHumansLymphocytesCytotoxicityCell Proliferation030304 developmental biologyChromosome AberrationsGenetics0303 health sciencesMutagenicity TestsCell growthGeneral MedicineIn vitro3. Good healthchemistryCell culture030220 oncology & carcinogenesisCurcuminSister Chromatid ExchangeGenotoxicityFood ScienceFood and Chemical Toxicology
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Mechanisms and consequences of methylating agent-induced SCEs and chromosomal aberrations: a long road traveled and still a far way to go.

2003

Since the milestone work of Evans and Scott, demonstrating the replication dependence of alkylation-induced aberrations, and Obe and Natarajan, pointing to the critical role of DNA double-strand breaks (DSBs) as the ultimate trigger of aberrations, the field has grown extensively. A notable example is the identification of DNA methylation lesions provoking chromosome breakage (clastogenic) effects, which made it possible to model clastogenic pathways evoked by genotoxins. Experiments with repair-deficient mutants and transgenic cell lines revealed both O<sup>6</sup>-methylguanine (O<sup>6</sup>MeG) and N- methylpurines as critical lesions. For S<sub>N</sub&g…

DNA ReplicationAlkylating AgentsGuanineDNA RepairDNA damageDNA repairBase Pair MismatchApoptosisBiologyMethylationLesionAnimals Genetically ModifiedMiceO(6)-Methylguanine-DNA MethyltransferaseCricetulusCricetinaeGeneticsmedicineAnimalsHumansPoint MutationAP siteMolecular BiologyGenetics (clinical)Chromosome AberrationsRecombination GeneticGuanosineModels GeneticCell CycleDNA replicationDNAFibroblastsMolecular biologyCell killingCell Transformation NeoplasticCancer researchDNA mismatch repairChromosome breakagemedicine.symptomSister Chromatid ExchangeDNA DamageMutagensCytogenetic and genome research
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