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Sister chromatid exchange

About: Sister chromatid exchange is a research topic. Over the lifetime, 3187 publications have been published within this topic receiving 90029 citations. The topic is also known as: replication-born DSB repair by SCE & GO:1990414.


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Journal ArticleDOI
TL;DR: The induction of chromosomal aberrations and sister-chromatid exchanges (SCE) was studied in human lymphocyte cultures treated with camptothecin (CM), an inhibitor of mammalian topoisomerase I.
Abstract: The induction of chrosomal aberrations and sister-chromatid exchanges (SCE) was studied in human lymphocyte cultures treated with camptothecin (CM), an inhibitor of mammalian topoisomerase I. While no chromosome-type aberrations were found in G 1 -treated cells, instead there was a dose-dependent induction of chromatid-type aberrations. These types of chromosomal alteration were not induced during the treatment itself during the S phase, as CM is not efficiently removed with the normal washing procedure after treatment.

79 citations

Journal ArticleDOI
TL;DR: It is premature to conclude that O6mG is not a lesion lethal to certain cultured cells, but data linking O 6mG to causation are inconclusive, and a model invoking a mismatch and excision response to O6MG proposed by Sklar & Strauss (1980).
Abstract: SUMMARY O 6 -methylguanine ( O 6 mG) produced in DNA by such SN1 methylating agents as N -methyl- N -nitrososurea and N -methyl- N ′-nitro- N -nitrosoguanidine (MNNG) has been suggested by some to be the lesion that leads to certain biological endpoints in mammalian cells: cell killing, sister chromatid exchange (SCE) production, mutagenesis and cellular transformation. Other evidence is interpreted as inconsistent with this point of view. The finding of Karran & Williams (1985) that O 6 mG delivered to cells in culture resulted in the depletion of the activity of the protein responsible for repair of O 6 mG in DNA ( O 6 mG-DNA methyltransferase, O 6 MT) provided a tool for the assessment of the role of O 6 mG in producing biological endpoints. In this paper we review much of the literature on human cells pertinent to this question. In addition we present our survival data obtained using the depletion technique of Karran & Williams as well as data supporting a model invoking a mismatch and excision response to O 6 mG proposed by Sklar & Strauss (1980). Although data linking O 6 mG to causation are inconclusive, it is premature to conclude that O 6 mG is not a lesion lethal to certain cultured cells.

78 citations

Journal ArticleDOI
TL;DR: The data indicate that catechol and hydroquinone can be optimally metabolized to produce reactive species, presumably benzo(semi)quinones, under conditions of lower metabolic activity than those necessary for phenol and benzene.

78 citations

Journal ArticleDOI
TL;DR: It is confirmed that cyclophosphamide induced chromosome breakage and SCE only in the presence of a metabolic activating system (liver S9) and after metabolism, cycloph phosphamde was more active than the other agents in inducing SCE.
Abstract: The effects of cyclophosphamide and three of its known metabolites (nitrogen mustard, acrolein, and nor-nitrogen mustard on chromosome breakage and sister chromatid exchange (SCE) were analyzed in vitro with and without the presence of a metabolic activating system (liver S9). We confirmed that cyclophosphamide induced chromosome breakage and SCE only in the presence of S9. After metabolism, cyclophosphamde was more active than the other agents in inducing SCE. Thus, the agent(s) directly responsible for this induction of a high SCE rate was not analyzed in this study. On the other hand, acrolein was most toxic to cell proliferation and most active in inducing chromosome breakage. The cytogenetic toxicity of these agents in comparison with their mutagenic and therapeutic activities is discussed.

78 citations

Journal ArticleDOI
TL;DR: The results show that waterpipe smoking and cigarette smoking significantly increase the frequencies of SCEs compared with those of nonsmokers, indicating the genotoxic effect of tobacco smoking.
Abstract: Tobacco smoking is a major world health problem. Recently, waterpipe smoking has become more popular in many countries. Although the genotoxicity associated with cigarette smoking has been extensively investigated, studies evaluating such toxicity in waterpipe users are still lacking. In this study, we examined the genotoxicity of waterpipe smoking in lymphocytes compared with the genotoxicity of cigarette smoking. Genotoxicity was evaluated using the sister chromatid exchanges (SCEs) assay. Fifty waterpipe smokers and 18 healthy nonsmokers participated in this study. Additionally, 18 heavy cigarette smokers (CS) were recruited for comparison. The results show that waterpipe smoking and cigarette smoking significantly increase the frequencies of SCEs (P < 0.01) compared with those of nonsmokers, indicating the genotoxic effect of tobacco smoking. In addition, frequencies of SCEs were significantly higher among waterpipe smokers compared with CS (P < 0.01), indicating that waterpipe smoking is more genotoxic than cigarette smoking. Moreover, the frequency of SCEs increased with the extent of waterpipe use. In conclusion, waterpipe smoking is genotoxic to lymphocytes and the magnitude of its genotoxicity is higher than that induced by regular cigarette smoking.

78 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20238
202222
20215
202011
201914
201811