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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 male contraceptive agent gossypol was found to induce a dose related increase of DNA strand breaks in human fibroblasts in vitro at concentrations of 5 to 40 micrograms/ml.
Abstract: The male contraceptive agent gossypol was found to induce a dose related increase of DNA strand breaks in human fibroblasts in vitro at concentrations of 5 to 40 micrograms/ml. The effect was reduced in the presence of 2% fetal calf serum. A weak but reproducible increase in the SCE frequency was found in human lymphocytes treated for 1 hour in serum-free medium with 0.04 to 4 micrograms/ml of gossypol.

26 citations

Journal ArticleDOI
TL;DR: It is suggested that tannic acid modifies DNA-excision repair and that the decrease in the amount of unrepaired DNA damage might cause the reduction of induced SCEs.
Abstract: The effects of tannic acid (m-galloyl gallic acid) and 7 of its analogues on the frequencies of sister-chromatid exchanges (SCEs) were investigated in cultured Chinese hamster cells. SCEs induced by UV-light or mitomycin C (MMC) were suppressed by post-treatment with tannic acid and 5 of its analogues. These effects were independent of the extension of the cell cycle. The compounds which showed an SCE-suppressing effect have a common structure of 3 neighboring hydroxy or methoxy groups substituted on the phenyl group in benzoic acid or ester. These decreasing effects of tannic acid were observed in the G1 phase but not in the S or G2 phase of the cell cycle and a greater decline of the frequencies of UV-induced SCEs during liquid holding was seen in the presence of tannic acid. However, cells irradiated with X-rays were not influenced by tannic acid. In cells from a xeroderma pigmentosum (XP) patient, a Fanconi's anemia (FA) patient, and a normal human embryo, MMC-induced SCEs were also decreased by post-treatment with tannic acid. Tannic acid reduced the SCE frequencies in UV-irradiated FA and normal human cells but not in UV-irradiated XP cells. Our results suggest that tannic acid modifies DNA-excision repair and that the decrease in the amount of unrepaired DNA damage might cause the reduction of induced SCEs.

26 citations

Book ChapterDOI
TL;DR: Cell cycle kinetics by the sister chromatid differential staining method revealed that MMC treatments of FA and normal cells led to a clearly dose-related delay in cell turnover times, the duration of delay being much longer in FA than in normal cells.
Abstract: Many investigators have described strong correlations between the frequency of sister chromatid exchanges (SCEs) in blood lympho cytes and health situations of the blood donor. Recent studies have further shown that cigarette smoking as well as certain genetic factors, can potentiate the cellular response to chemical treatment. The chemical stress method might thus be a sensitive test for quan-titating the cellular damage or defects that have been induced environmentally and genetically.

26 citations

Journal ArticleDOI
TL;DR: The study adds more proof that Cd exposure has a genotoxic effect and highlighted the importance of using cytogenetic studies as a sensitive and effective means for early detection of Cd-induced mutagenicity.
Abstract: Many studies proved the genotoxic effect of cadmium (Cd) exposure and highlighted the importance of the cytogenetic studies as a sensitive and effective means for early detection of Cd-induced mutagenicity. The relationship between occupational exposure to Cd and increased risk of cancer, particularly lung cancer, has been explored in number of epidemiological studies. The aim of this study is to assess the role of chromosomal abnormalities and sister chromatid exchange as sensitive indicators for the genotoxicity of occupational exposure to Cd. Cytogenetic studies was done for 40 workers (27 smokers and 13 non-smokers) exposed to Cd dust and fumes with 40 control subjects (28 smokers and 12 non-smokers) not exposed to Cd before. Both exposed and control groups were similar in age and other sociodemographic factors. Clinical examination, laboratory investigation including urinary and blood Cd, cytogenic analysis for detection of chromosomal aberrations and sister chromatid exchange and environmental study of the work places were done. Statistical analysis of cytogenetic studies revealed the presence of significant elevation of chromosomal aberrations and sister chromatid exchanges of the exposed group. Urinary and blood Cd of the exposed group were significantly higher than that of the control group. These abnormalities were not significantly affected with age, duration of exposure, smoking habits, blood and urinary Cd. In conclusion, the study adds more proof that Cd exposure has a genotoxic effect and highlighted the importance of using cytogenetic studies as a sensitive and effective means for early detection of Cd-induced mutagenicity.

26 citations

Journal ArticleDOI
TL;DR: The present study suggests that replication fork arrest, which is similar to the early phases of HR, leads to a high frequency of recombination, resulting in SCEs, and shows that SCE may be mediated by HR.
Abstract: We conducted the recombination and sister chromatid exchange (SCE) assays with five chemicals (hydroxyurea (HU), resveratrol, 4-hydroxy-trans-stilbene, 3-hydroxy-trans-stilbene, and mitomycin C) in Chinese hamster cell line SPD8/V79 to confirm directly that SCE is a result of homologous recombination (HR) SPD8 has a partial duplication in exon 7 of the endogenous hprt gene and can revert to wild type by homologous recombination All chemicals were positive in both assays except for 3-hydroxy-trans-stilbene, which was negative in both HU, resveratrol, and 4-hydroxy-trans-stilbene were scavengers of the tyrosyl free radical of the R2 subunit of mammalian ribonucleotide reductase Tyrosyl free radical scavengers disturb normal DNA replication, causing replication fork arrest Mitomycin C is a DNA cross-linking agent that also causes replication fork arrest The present study suggests that replication fork arrest, which is similar to the early phases of HR, leads to a high frequency of recombination, resulting in SCEs The findings show that SCE may be mediated by HR

25 citations


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