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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 results suggest that DEB and MEB cause chromosome-specific aneuploidy in human cells and may produce chromosome damage of the type found in leukemia following exposure to butadiene.
Abstract: 1,3-Butadiene is a carcinogen in rodents, but its potential carcinogenicity to humans remains controversial. Numerous studies have shown that butadiene and its metabolites cause sister chromatid exchanges in vitro and in vivo. To test for other types of genotoxicity, the micronucleus assay and fluorescence in situ hybridization (FISH) have been used to detect chromosome damage in human lymphocytes caused by two reactive metabolites of butadiene, diepoxybutane (DEB) and monoepoxybutene (MEB). DEB (0.5-5.0 microM) significantly increased micronucleus formation 4- to 6-fold (P <0.01) and MEB (1-500 microM) by 2- to 4-fold (P <0.01) over control levels. The ability of DEB and MEB to induce aneuploidy of chromosomes 7, 8, 12, and X was examined using dual-color FISH in both interphase and metaphase cells. These chromosomes were chosen because of their involvement in leukemogenesis. Both DEB and MEB caused dose-dependent increases in hyperdiploidy of chromosomes 12 and X, but had no discernible effect on chromosomes 7 and 8. These results suggest that DEB and MEB cause chromosome-specific aneuploidy in human cells. If formed in sufficient amounts, DEB and MEB may produce chromosome damage of the type found in leukemia following exposure to butadiene.

48 citations

Journal ArticleDOI
TL;DR: The weight of the evidence leads to the conclusion that F- exposure results in increased chromosome aberrations in cultured human and rodent cells, and the question of whether F- produces chromosome damage in vivo should be considered unresolved.
Abstract: F- is not mutagenic in standard bacterial systems, but produces chromosome aberrations and gene mutations in cultured mammalian cells. Although there is disagreement in the literature concerning the ability of F- to induce chromosome aberrations in cultured human and rodent cells, the weight of the evidence leads to the conclusion that F- exposure results in increased chromosome aberrations in these test systems. NaF induced primarily chromatid gaps and chromatid breaks, indicating that the rodent cells are responsive in the G2 stage of the cell cycle. In contrast, studies with synchronized human cells indicated that the S phase was the most sensitive. If F- does have a cell cycle-specific effect, it could be expected that differences in the cell treatment and harvest protocols could lead to conflicting results for the induction of chromosome aberrations. Gene mutations were produced in cultured rodent and human cells in the majority of the studies. Unfortunately, a number of the in vitro and in vivo cytogenetic studies are of questionable utility because of the protocols used, the quality of the responses reported, or the interpretations of the data. The conflicting results in the in vivo cytogenetic studies are difficult to reconcile. There are reports of increased chromosome aberrations in rat bone marrow and testes, but other studies, using similar protocols and dose ranges, have reported no induced chromosome damage. Although some of the studies were performed at toxic levels of F-, other studies, including those that showed positive results, were at F- concentrations (1-5 ppm) equivalent to human exposure levels. In the majority of studies that were reported to be positive, there were high background frequencies, or the investigators reported categories of nuclear or chromosome damage that are difficult to interpret. Interestingly, many of the positive results were obtained when anaphase cells were scored, whereas similar treatment protocols in other laboratories yielded negative results when metaphase cells were the only cell type examined. It is difficult, without additional data, to determine the reasons for finding chromosome breaks in anaphase, but not metaphase, cells. Other reports have presented insufficient information to allow adequate evaluations. Therefore, at this time, the question of whether F- produces chromosome damage in vivo should be considered unresolved.

48 citations

Journal ArticleDOI
TL;DR: The results suggest that VCM workers with ALDH2 1-2/2-2 genotypes, who also smoke, may have increased risk of DNA damage.
Abstract: Vinyl chloride monomer (VCM) is a human carcinogen. However, the exact mechanism of carcinogenesis remains unclear. VCM may be metabolized by cytochrome P450 2E1 (CYP2E1), aldehyde dehydrogenase 2 (ALDH2) and glutathione S-transferases (GSTs). Thus workers with inherited variant metabolic enzyme activities may have an altered risk of genotoxicity. This study was designed to investigate which risk factors might affect sister chromatid exchange (SCE) frequency in polyvinyl chloride (PVC) workers. Study subjects were 44 male workers from three PVC factories. Questionnaires were administered to obtain detailed histories of cigarette smoking, alcohol consumption, occupations, and medications. SCE frequency in peripheral lymphocytes was determined using a standardized method, and CYP2E1, GSTM1, GSTT1 and ALDH2 genotypes were identified by the polymerase chain reaction (PCR). Analysis revealed that smoking status and exposure to VCM were significantly associated with increased SCE frequency. The presence of ALDH2 1–2/2–2 genotypes was also significantly associated with an elevation of SCE frequency (9.5 vs. 8.1, p

48 citations

Journal Article
TL;DR: It is found that both commercial (already rather pure) and repurified aniline are clearly positive to a similar extent in inducing DNA damage in vivo in liver and kidney of rats.
Abstract: Aniline of unknown purity has been reported to induce spleen hemangiosarcoma in rats. Aniline has been found to be negative in terms of mutagenicity in both bacteria and yeasts. We have found that both commercial (already rather pure) and repurified aniline are clearly positive to a similar extent in inducing DNA damage in vivo in liver and kidney of rats. Both the commercial and repurified product are also clearly positive in induction of sister chromatid exchanges in vivo in male Swiss mice bone marrow cells. Liver, kidney, and bone marrow DNA damage was absent in male Swiss mice.

48 citations

Journal Article
TL;DR: Peripheral lymphocytes from cancer patients receiving mitomycin C treatment were examined for cytogenetic effects and the significance of the specific kinetics of change in the sister chromatid exchnage frequency after in vivo treatments is discussed in relation to cancer chemotherapy.
Abstract: Peripheral lymphocytes from cancer patients receiving mitomycin C treatment were examined for cytogenetic effects The treatment consisted of iv injections of mitomycin C at a dose of 4 mg given twice a week for 2 weeks The lymphocytes were cultured in vitro for 72 hr with phytohemagglutinin and 5-bromodeoxyuridine, and then sister chromatid exchanges were scored Before treatment with mitomycin C, the frequencies of sister chromatid exchanges in lymphocytes of cancer patients were similar to those of healthy controls After the first and second treatments in vivo with mitomycin C, the frequencies of sister chromatid exchanges increased with time, reached a peak in about 24 hr, and then returned to the pretreatment level in about 48 hr, in contrast to the case of in vitro exposure to mitomycin C After the third and fourth injections, however, the frequency increased further and did not return to the original level The significance of the specific kinetics of change in the sister chromatid exchange frequency after in vivo treatments is discussed in relation to cancer chemotherapy

47 citations


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