Sister chromosome exchange

Hexavalent chromium has been shown to be a strong clastogen in experimental animals producing chromosome aberrations, sister chromosome exchanges, DNA strand breaks, oxidized base damage, DNA -DNA and DNA - protein cross-links. Human genetic studies have shown mixed results and have been limited by insufficient numbers of subjects. 

Ethanol is negative in mutagenicity assays in bacteria, mouse sperm, cell transformation in hamster and rat embryo cells, and chromosome aberrations in vitro. It produces dominant lethal effects in rats and increases sister chromosome exchange in vitro in human and nonhuman lymphocytes. 

The nerve agents are generally considered to be acute toxicants and their delayed effects have been relatively little investigated. Li et al. (1998) reported an increase in sister chromosome exchange (SCE) in the lymphocytes of victims of the Tokyo sarin disaster. Because of the probability that the victims were exposed to by-products of sarin synthesis, diisopropyl methylphospho-nate, diethyl methylphosphonate and isopropyl ethyl methylphosphonate, these were also studied. The frequency of SCE was determined in human lymphocytes exposed to these by-products all three compounds increased the frequency of SCE compared with controls. Sarin and soman... 

Wu Y, Wang X, Chen C, et al. 1998. [Serum ras P21 level and peripheral blood lymphocyte sister chromosome exchange frequency in workers exposed to coal tar pitch], Henan Yike Daxue Xuebao 33(5) 59-61. (Chinese). 

Ethylene oxide has been shown to produce mutagenic and cytogenic effects in a variety of test systems (226). An increased frequency of chromosomal aberrations in peripheral lymphocytes of monkey exposed to ethylene oxide for 104 weeks has been reported (240). In mice, it is an effective inducer of chromosome breaks leading to dominant-lethal mutations. In addition, ethylene oxide has been shown to induce heritable effects in the heritable translocation test conducted in mice exposed to ethylene oxide by inhalation (241,242). In this study, male mice were exposed to ethylene oxide ranging from 165 to 300 ppm for 6 h per day 5 or 7 days/week for 8.5 weeks. Ethylene oxide has also been shown to bind to proteins (243) as well as to DNA (244). Several studies on ethylene oxide-exposed workers have demonstrated an increased incidence of chromosomal aberrations and sister chromatid exchanges the relevance of such effects to human health evaluation is currendy uncertain. 

Mitomycin C was found to have broad activity against a range of tumors and has been used clinically since the early 1960s [14, 15]. It causes many specific cellular effects, including inhibition of DNA synthesis, recombination, chromosome breakage, sister chromatid exchange, induction of DNA repair, and induction of... 

Results of methyl parathion assays involving effects on chromosomes have also been contradictory. For sister chromatid exchange, Waters et al. (1982) reported a positive response in Chinese hamster ovary cells only in the presence of metabolic activation system, while methyl parathion tested positive without a metabolic activation system in Chinese hamster V79 cells (Chen et al. 1981), cultured normal human lymphoid cells (Chen et al. 1981 Gomez-Arroyo et al. 1987 Sobti et al. 1982), and Burkitt s l5miphoma cells (Chen et al. 1981). Chen et al. (1981) found a significant dose-related increase in sister chromatid exchange in both hamster and human cultured cells, but dose-related cell cycle delays were less pronounced in human cell lines than in V79 cells. Negative results were obtained for chromosomal aberrations in human lymphocytes without a metabolic activation system (Kumar et al. 1993). 

Since in vivo tests in exposed human populations would involve concomitant exposure to other toxicants, it would be difficult to assess the genotoxic potential of methyl parathion alone. Therefore, additional well-designed in vitro studies using human cell lines are needed to determine the effects of methyl parathion on various genotoxic parameters (e.g., sister chromatid exchange, chromosomal aberrations, unscheduled DNA synthesis). 

Das P, John G. 1999. Induction of sister chromatid exchanges and chromosome aberrations in vivo in Etroplus suratensis (Bloch) following exposure to organophosphorus pesticides. Toxicol Lett 104 111-116. 

De Ferrari M, Artuso M, Bonassi S, et al. 1991. Cytogenic biomonitoring of an Italian population exposed to pesticides Chromosome aberration and sister-chromatid exchange analysis in peripheral blood lymphocytes. Mutat Res 260 105-113. 

Dulout FN, Pastori MC, Olivero OA, et al. 1985. Sister-chromatid exchanges and chromosomal aberrations in a population exposed to pesticides. Mutat Res 143 237-244. 

Figure 36-12. Sister chromatid exchanges between human chromosomes. These are detectabie by Giemsa staining of the chromosomes of ceiis repiicated for two cycies in the presence of bromodeoxyuridine. The arrows indicate some regions of exchange. (Courtesy of S Wolff and J Bodycote.)...

Chromosomal aberrations Gene mutation Dominant lethal mutation Micronucleus formation Micronucleus formation Micronucleus formation Chromosomal aberrations Sister chromatid exchange Micronucleus formation Chromosomal aberrations Sister chromatid exchange DNA-protein cross-links Nondisjunction of Y chromosome in sperm DNA damage (single-strand breaks)... 

Genotoxic Effects. Evaluation of the genotoxicity of lead in humans has focused on evaluations of lymphocytes from occupationally or environmentally exposed persons (Table 2-10) and in vitro studies of structural chromosomal aberrations and sister chromatid exchange in cultures of lymphocytes taken from healthy individuals (Table 2-11). Results of studies with human lymphocyte cultures exposed in vitro to lead acetate were nearly equally divided between positive (Beek and Obe 1974 Niebuhr and Wulf 1984) and negative (Beek and Obe 1975 Deknudt and Deminatti 1978 Gasiorek and Bauchinger 1981 Schmid etal. 1972). 

Huang XP, Feng ZY, Zhai WL, et al. 1998b. Chromosomal aberrations and sister chromatid exchanges in workers exposed to lead. Biomed Environ Sci 1 382-387. 

Kowalska-Wochna E, Moniuszko-Jakoniuk J, Kulikowska E, et al. 1988. The effect of orally applied aqueous solutions of lead and zinc on chromosome aberrations and induction of sister chromatid exchanges in the rat (Rattus sp). Genetica Polonice 29 181-189. 

Maki-Paakkanen J, Sorsa M, Vainio H. 1981. Chromosome aberrations and sister chromatid exchanges in lead-exposed workers. Hereditas 94 269-275. 

The nucleus of all eucariotic cells contains the carrier of the genetic information in the chromosomes. It is possible to visualize the chromosomes and analyze their number and pattern during a special period of cell division (the metaphase). Alterations from their normal shapes are observed as structural chromosome aberrations. These are chromosome type aberrations (terminal and interstitial deletions, dicentrics and rings), chromatid aberrations (gaps, breaks and exchanges) and sister chromatid exchanges. Spontanous frequencies of such chromosome... 

Priston RA J, Dean BJ. 1985. Tests for the induction of chromosome aberrations, polyploidy and sister chromatid exchanges in rat liver (RL4) cells. In Ashby J, de Serres FJ, et al., eds. Progress in mutation research. Vol. 5. Evaluation of short-term tests for carcinogens. Amsterdam, The Netherlands Elsevier Science Publishers, 387-395. 

Sharief Y, Brown AM, Backer LC, et al. 1986. Sister chromatid exchange and chromosome aberration analyses in mice after iruvivo exposure to acrylonitrile, styrene, or butadiene monoxide. Environ Mutagen 8 439-448. 

Nitro PAHs have been shown to exhibit a large variety of biological activities. Included in these are the induction of mutations in bacterial (Table I) and eukaryotic cells (9,17,54-57), the neoplastic transformation of cultured mammalian cells (58-59), and the induction of DNA strand breaks (60), DNA repair (61-62), sister chromatid exchanges (63-64), and chromosomal aberrations (65-66). Nitro PAHs have also been demonstrated to bind cellular DNA in bacteria (67-73) and mammalian cells (74-77), to inhibit preferentially the growth of repair-deficient bacteria (78), to have recombinogenic activity in yeast (66,79-80) and to induce tumors in experimental animals (Table II). 

An increased frequency of sister chromatid exchanges was obtained in vivo in bone-marrow cells of male Swiss mice at intraperitoneal doses of 210 and 420 mg/kg (Parodi et al. 1982, 1983) and in vitro Chinese hamster cells (Abe and Sasaki 1977), although in the latter study, no chromosomal aberrations were observed. 

Abe, S., and M. Sasaki. 1977. Chromosome aberrations and sister chromatid exchanges in Chinese hamster cells exposed to various chemicals. J. Natl. Cancer Inst. 58 1635-1641. 

Human cells exposed to various nickel compounds have an increased frequency of chromosomal aberrations, although sister chromatid exchange frequency is unaffected. Cells from nickel refinery workers exposed to nickel monosulfide (0.2 mg Ni/m3) or nickel subsulfide (0.5 mg Ni/m3) showed a significant increase in the incidence of chromosomal aberrations (Boysen et al. 1980 WHO 1991 USPHS 1993). No correlation was evident between nickel exposure level and the frequency of aberrations (USPHS 1993). 

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