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.

Sister chromatid exchange induction and persistence in peripheral blood and spleen lymphocytes of mice treated with ethylnitrosourea

Abstract: The induction and persistence of sister chromatid exchanges (SCEs) were studied in peripheral blood and spleen lymphocytes of mice given a single i.p. injection of ethylnitrosourea (ENU) of 100, 350, or 600 muMoles ENU/kg. SCE frequencies were measured on days 1, 3, 5, and 7, and at seven additional times up to 172 days post-injection. SCEs were analyzed statistically by comparing the mean frequencies as well as the distribution of SCEs per cell at each time. The latter approach was based on a non-parametric method of identifying high frequency cells (HFCs). The SCE frequencies and proportion of HFCs in each dose and tissue remained elevated for up to 172 days following treatment, although the degree and statistical significance of the increase varied according to the tissue, dose, and statistical test employed. The SCE frequencies were found to oscillate during the first week. Following this, however, the return of the SCE frequencies to control levels was fit to a linear regression model with time as the only independent variable. The persistence of SCE-forming lesions was found to be dose-dependent for the spleen but not for blood. Within each dose the persistence of SCE-forming lesions was significantly greater for the blood relative to the spleen. The results emphasize that tissue, dose, and time since exposure are important factors to consider when quantifying SCEs in vivo; analysis of high frequency cells may be a more sensitive method of detecting exposure than the t-test; and a single determination of SCE frequencies may not be sufficient to quantitatively assess genotoxic damage in the first week following exposure.

A high yield of translocations parallels the high yield of sister chromatid exchanges in the CHO mutant EM9

Abstract: The fluorescence plus Giemsa (FPG) and fluorescence in situ hybridization (FISH) techniques have been used to determine, respectively, the frequencies of sister chromatid exchanges (SCEs) and stable chromosome aberrations (translocations) induced by different concentrations of BrdU in the Chinese hamster ovary cell mutant EM9 and its parental line AA8. The results indicate that BrdU induced a high frequency of SCEs and translocations in EM9 as compared with AA8, and that the translocation/dicentric ratio was also higher in the mutant cell line than in the parental cell line in both untreated and BrdU-treated cultures. These observations may indicate a possible relationship between the molecular mechanisms involved in the formation of SCEs and translocations.

XRCC1 down-regulation in human cells leads to DNA-damaging agent hypersensitivity, elevated sister chromatid exchange, and reduced survival of BRCA2 mutant cells.

Abstract: Previous studies using rodent cells indicate that a deficiency in XRCC1 results in reduced single-strand break repair, increased sensitivity to DNA-damaging agents, and elevated levels of sister chromatid exchange (SCE). Epidemiological studies have suggested an association of certain human XRCC1 polymorphisms with genetic instability and cancer susceptibility. However, investigations on the molecular functions of XRCC1 in human cells are limited. To determine the contributions of this nonenzymatic scaffold protein, we suppressed XRCC1 levels in several human cell lines using small interfering RNA (siRNA) technology. We report that XRCC1 down-regulation in HeLa cells leads to a concomitant decrease in the DNA ligase 3 protein level and an impaired nick ligation capacity. In addition, depletion of XRCC1 resulted in a significantly increased sensitivity to the alkylating agent methyl methanesulfonate and the thymidine base analog 5-hydroxymethyl-2'-deoxyuridine, a slightly increased sensitivity to ethyl methanesulfonate and 1,3-bis(2-chloroethyl)-1-nitrosourea, and no change in the response to camptothecin. We also discovered that a 70-80% reduction in XRCC1 protein leads to an elevated level of SCE in both HeLa cells and normal human fibroblasts, but does not affect chromosome aberrations in the diploid fibroblasts. Last, XRCC1 siRNA transfection led to an approximately 40% decrease in the survival of BRCA2-deficient cells, supporting a model whereby the accumulation of unrepaired SSBs leads to the accumulation of cytotoxic DNA double strand breaks following replication fork collapse in cells defective in homologous recombination.

Sister chromatid exchanges in Vicia faba induced by arsenic-contaminated drinking water from Zimapan, Hidalgo, Mexico.

Abstract: Sister chromatid exchanges (SCE) in Vicia faba root tips were used to examine well water containing high levels of arsenic. The increased amount of arsenic was contained in well water from different towns of Zimapan, Hidalgo, Mexico. Treatments of 3 h were applied followed by the differential staining technique of Tempelaar et al. (Mutation Res. 103 (1982) 321–326). Concentrations of arsenic from 0.267 up to 1.070 mg/l were determined by colorimetry in the polluted samples used for this study. These values were above the permissible limit of 0.05 mg/l in drinking water. In all cases, except one in which the As concentration was 0.021, the arsenic-contaminated water produced significant increases of SCE compared with the control ( p

Oncogenic Transformation and Cell Lysis in C3H/10T½ Cells and Increased Sister Chromatid Exchange in Human Lymphocytes by Nickel Subsulfide

Abstract: We have scored frequency of transformation and appearance of the oncogenic marker “long microvilli” in mouse embryo fibroblast C3H/10T½ cells in culture for the compound Ni 3 S 2 . Furthermore, we have scored for Ni 3 S 2 -induced sister chromatid exchange in cultured human lymphocytes. Nickel subsulfide in moderate doses caused morphological transformation to type I, II, and III foci and induced long microvilli on the cells in the transformed cultures, demonstrating oncogenic transforming ability. Higher doses led to cell lysis after a lag period. The carcinogenic potency of Ni 3 S 2 in this system was not as strong as that of methylcholanthrene. Ni 3 S 2 increased the sister chromatid exchange frequency in human lymphocytes in a marginal, not dose-dependent way. The increased sister chromatid exchange may indicate that the carcinogenic effect of Ni 3 S 2 is genetic rather than epigenetic.