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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.


Papers
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Journal ArticleDOI
TL;DR: Sister chromatid exchange frequencies were studied in differentially stained chromosomes from lymphocytes of 17 patients with viral disease and Elevated SCE elevations were also present in long term cultured Epstein Barr virus positive human B lymphocytes.

40 citations

Journal ArticleDOI
TL;DR: Determined DNA sequences of the germ-line regions in which the duplication of the IgG2a heavy chain constant region gene (C gamma 2a) in the murine myeloma cell line MPC-11 occurred via unequal sister chromatid exchange suggest a novel mechanism for the recombination and strongly implicates the simple sequence in the process.
Abstract: Previous studies from this laboratory have provided evidence that the duplication of the IgG2a heavy chain constant region gene (C gamma 2a) in the murine myeloma cell line MPC-11 occurred via unequal sister chromatid exchange. We now report the determination of the DNA sequences of the germ-line regions in which this exchange has occurred. The two donor sequences have long regions of virtual identity. Furthermore, both chromatids contain stretches of T-C and T-G dinucleotides; the latter has the potential to form Z-DNA. Localization of the actual breakpoints via genomic Southern blot analysis suggests a novel mechanism for the recombination and strongly implicates the simple sequence in the process.

40 citations

Journal Article
TL;DR: Results showed that EtO exposure was significantly associated with the levels of HEV adducts and SCE after adjusting for cigarette smoking and other potential confounders, and suggested that individuals with homozygous deletion of the GSTT1 gene may be more susceptible to the genotoxic effects of ETO.
Abstract: Ethylene oxide (EtO) is a genotoxic carcinogen with widespread uses as an industrial chemical intermediate and sterilant. We examined the effects of glutathione S-transferase T1 ( GSTT1 ) and M1 ( GSTM1 ) genotypes on the levels of N -(2-hydroxyethyl)valine (HEV) adducts in the erythrocytes and sister chromatid exchange (SCE) in lymphocytes from a group of 58 operators of sterilizers that used EtO and nonexposed workers from nine hospitals in the United States and one hospital in Mexico City. Cumulative exposure to EtO was estimated during the 4-month period before the collection of blood samples. Results showed that EtO exposure was significantly associated with the levels of HEV adducts and SCE after adjusting for cigarette smoking and other potential confounders. A significantly higher HEV adduct level (0.17 ± 0.03 versus 0.08 ± 0.01, mean ± SE; P = 0.02) but lower SCE frequency (5.31 ± 0.39 versus 6.21 ± 0.17; P = 0.04) was observed in subjects with homozygous deletion of the GSTT1 gene (null genotype) as compared with those with at least one copy of the gene (positive genotype). In multiple regression analysis, the GSTT1 -null genotype was associated with an increase in HEV adduct level (β = 1.62; P = 0.02) and a decrease in SCE frequency (β = −1.25; P = 0.003) after adjusting for age, gender, race, education, cigarette smoking, and EtO exposure status. The inverse SCE- GSTT1 relationship remained unchanged when SCE was further examined in relation to HEV adducts as an indicator of the internal EtO dose. The GSTM1 genotype was not associated with the level of either HEV adduct or SCE. These data indicate that the GSTT1 -null genotype is associated with increased formation of EtO-hemoglobin adducts in relation to occupational EtO exposure, suggesting that individuals with homozygous deletion of the GSTT1 gene may be more susceptible to the genotoxic effects of EtO. The unexpected finding of decreased SCEs, which is less clear, may be attributed to the nonchemical specificity of this end point and the lack of expression of the GSTT1 enzyme in lymphocytes.

40 citations

Journal ArticleDOI
TL;DR: It is found that neither baseline sister chromatid exchanges (SCEs) nor mitomycin-C-induced increments in SCEs showed any significant differences among family members or between AT heterozygotes or homozygotes.

40 citations

Journal ArticleDOI
TL;DR: Permethrin could be characterized as a S-phase independent agent with greater potential for inducing chromosomal damage than sister chromatid exchanges and micronuclei when it was evaluated in the absence of a metabolic activation system.
Abstract: The pyrethroid insecticide permethrin was tested for its ability to induce sister chromatid exchanges (SCE), micronuclei (MN) and structural chromosome aberrations (CA) in cultured human peripheral blood lymphocytes. Permethrin was tested in the range of 5-500 micrograms/ml in the absence and in the presence of a rat liver activation system (S9 mix). Small elevations in the SCE frequencies were found and even though statistically significant may have no biological meaning, the more so since there was no dose-effect relationship. Permethrin induced both MN and CA when it was evaluated in the absence of a metabolic activation system. Nevertheless, it cannot be said that S9 mix suppressed the activity in itself. The effect of permethrin seemed to be time of exposure dependent. Permethrin could be characterized as a S-phase independent agent with greater potential for inducing chromosomal damage than sister chromatid exchanges.

40 citations


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