scispace - formally typeset
Search or ask a question
Topic

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
More filters
Journal Article
TL;DR: Although sample sizes were small, a genetic contribution to the SCE frequency was suggested by the observed pattern of familial correlations, and familial factors affecting mean SCE frequencies were indicated by detection of significant differences among, but not within, families.
Abstract: The frequency of spontaneous sister chromatid exchanges (SCEs) was determined in PHA-stimulated peripheral lymphocytes of 52 individuals, comprising 12 complete 2-generation pedigrees. Neither intraindividual variation between replicate cultures established from the same blood sample nor variation among samples from the same individual initiated at different times was significant. However, familial factors affecting mean SCE frequencies were indicated by detection of significant differences among, but not within, families. Although sample sizes were small, a genetic contribution to the SCE frequency was suggested by the observed pattern of familial correlations.

29 citations

Journal ArticleDOI
TL;DR: The experiments have shown that the suitability of hepatocytes as an activation system is not restricted to microbial or eukaryotic point mutation assays, but that hepatocyte metabolism can also be successfully included in cytogenetic tests with short- and long-term cultures of mammalian target cells.
Abstract: Two external metabolizing systems, S9 mix from Aroclor-induced rat livers and freshly isolated hepatocytes, were used for activation in cultures of human lymphocytes and V79 cells. 7, 12-dimethylbenzanthracene (DMBA) and aflatoxin B1 (AFB1) were employed as indirectly acting reference mutagens. Mutagenic effects were measured by induction of sister chromatid exchange (SCE). With DMBA, SCE-inducing effects were found to be quite similar after activation by S9 mix and activation by hepatocytes. In human lymphocytes nearly the same dose-effect relationships were found with both metabolizing systems; in V79 cells the hepatocyte-mediated induction of SCE was detectable at slightly lower concentrations than the S9-mediated SCE induction. In contrast with AFB1, S9 activation led to a stronger SCE induction than hepatocyte activation in both target cells. The induction of chromosomal aberrations by AFB1 after activation by the two metabolizing systems was also analysed in V79 cells. This experiment again revealed that AFB1 was more efficiently activated by S9 mix than by hepatocytes, and it appeared that AFB1 is a more potent inducer of chromosomal aberrations than of SCE. The different activation capacities of the two metabolizing systems for AFB1 may be due to the maintenance of inactivation mechanisms in hepatocytes or to the Aroclor induction of the S9 fraction. Our experiments have shown that the suitability of hepatocytes as an activation system is not restricted to microbial or eukaryotic point mutation assays, but that hepatocyte metabolism can also be successfully included in cytogenetic tests with short- and long-term cultures of mammalian target cells.

29 citations

Journal ArticleDOI
TL;DR: ECH exposure may be associated with genetic toxicity and that DMF does not appear to be genotoxic, in plant workers exposed to these two agents.
Abstract: Workers in epoxy resin, synthetic leather, and printed circuit board manufacturing plants are exposed to epichlorohydrin (ECH), or dimethylformamide (DMF), or both. ECH, an alkylating agent, has been shown to cause malignancy in animals, but its genotoxicity in humans is unclear. DMF is a well-known hepatotoxic chemical, although evidence of its genotoxicity in humans is also limited. In this study, we examined the effects of exposure to ECH and DMF on sister chromatid exchange (SCE) in plant workers, in order to examine the genotoxicity of these two agents. Because the genotoxicity of certain agents can be modulated by metabolic traits, we also investigated influence of the glutathione S-transferase (GST) μ (GST M1) and GST θ (GST T1) genes on the genotoxicity of ECH and DMF. A total of 85 male plant workers were included in this study. The subjects were divided into five exposure groups, based on their job titles and the airborne ECH and DMF concentrations in their areas of work. A questionnaire was administered to obtain detailed occupational, smoking, alcohol consumption, and medication histories. Standardized cytogenetic methods were used to determine the frequency of sister chromatid exchange (SCE) in peripheral blood lymphocytes. GST M1 and GST T1 genotypes were identified using polymerase chain reaction (PCR). In analysis, smoking was significantly associated with increased SCE frequency (P < 0.01). Workers with high ECH exposure also had significantly higher SCE frequencies than those with low or no ECH exposure (P < 0.05). However, DMF exposure was not associated with SCE frequency. The GST M1 null genotype was also found to be associated with an increased SCE frequency (P = 0.06). We conclude that ECH exposure may be associated with genetic toxicity and that DMF does not appear to be genotoxic.

29 citations

Journal ArticleDOI
TL;DR: It is concluded that EBD is an efficient inducer of SEC in cultured human lymphocytes, although not quite as effective as MEB and clearly less effective than DEB.
Abstract: The induction of sister chromatid exchanges (SCEs) by a 48-h treatment with 3,4-epoxybutane-1,2-diol (EBD), a metabolite of 1,3-butadiene, was studied in whole-blood lymphocyte cultures of 22 human donors with known genotypes of two polymorphic glutathione S-transferases (GSTs), GSTT1 and GSTM1 For both genes, donors representing a homozygous ‘null’ genotype lacking the respective GST gene and isozyme and a ‘positive’ genotype with at least one intact gene and GST activity were included The mean frequencies of SCE/cell were similar in all genotype groups: GSTT1 null (n = 10) (mean 220 for 250 μM and 329 for 250 500 μM of EBD), GSTT1 positive (n = 14) (213 and 346, respectively), GSTM1 null (n = 10) (203 and 335) and GSTM1 positive donors (n = 15) (206 and 348) At 500 μM concentration of EBD, the lymphocyte cultures of all donors showed a significantly decreased replication index No differences in EDB-induced SCEs or in replication index could be associated with the GSTM1 and GSTT1 genotypes either separately or in combination When SCEs induction by EBD was compared to that of two other known epoxide metabolites of butadiene, 1,2:3,4-diepoxybutane (DEB) was effective at concentrations over two orders of magnitude lower than EBD or 1,2-epoxy-3-butene (MEB) It is concluded that EBD is an efficient inducer of SCE in cultured human lymphocytes, although not quite as effective as MEB and clearly less effective than DEB Contrary to previous findings with DEB and MEB, the polymorphic GSTM1 and GSTT1 do not appear to be involved in the detoxification of EBD in human lymphocytes

29 citations

Journal ArticleDOI
TL;DR: Cyclophosphamide-induced SCE frequencies remained constant in maternal cells but declined dramatically in the fetus throughout the latter half of development, while mutagen- induced SCE levels were compared in different fetal organs and the direct-acting drugs were found to induce similar levels in all tissues.
Abstract: Frequencies of baseline and cyclophosphamide-induced sister chromatid exchanges (SCE) were measured in mouse maternal and fetal cells between days 11 and 19 of gestation. Baseline levels of SCE did not vary as a function of gestational age in either the mother or fetus. Cyclophosphamide-induced SCE frequencies remained constant in maternal cells but declined dramatically in the fetus throughout the latter half of development. Because cyclophosphamide is a metabolically activated mutagen, a direct-acting drug, mitomycin C, was given on days 11 and 15 to determine if the decline in induced SCE levels seen with gestational results from alterations in activating enzymes. A similar decline in mitomycin C-induced SCE levels was noted in fetal tissues as a function of gestational age. Dose-response curves to cyclophosphamide performed on day 13 of gestation showed increases in SCE as a function of cyclophosphamide concentration in both the mother and the fetus. When mutagen-induced SCE levels were compared in different fetal organs, the direct-acting drugs (mitomycin C and daunomycin) were found to induce similar levels in all tissues. Cyclophosphamide, which is metabolically activated, induced higher SCE levels in fetal liver than in lung or gut. Whereas cyclophosphamide induced similar SCE levels in fetal and maternal cells on day 13 of gestation, daunomycin produced fetal SCE levels that were approximately 50% of maternal levels. Simultaneous measurement of the distribution of [14C]cyclophosphamide and [3H]daunomycin in maternal and fetal cells revealed that the lower SCE induction by daunomycin was probably due to decreased ability to cross the placental barrier.

29 citations


Network Information
Related Topics (5)
DNA damage
47K papers, 2.4M citations
84% related
DNA repair
41.5K papers, 2.4M citations
83% related
DNA
107.1K papers, 4.7M citations
77% related
Mutation
45.2K papers, 2.6M citations
76% related
Carcinogenesis
60.3K papers, 3.1M citations
75% related
Performance
Metrics
No. of papers in the topic in previous years
YearPapers
20238
202222
20215
202011
201914
201811