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.

Mitotic toxicity, sister chromatid exchange, and rec assay of pesticides.

Abstract: Genotoxicity of 10 pesticides (chlornitrofen, chlomethoxyfen, molinate, thiobencarb, simazine, simetryn, diazinon, iprofenfos, piperofos and oxadiazone) was studied by mitotic toxicity, sister chromatid exchange, and rec assay. The pesticides are detected frequently at high levels in the Yodo River water in Osaka, Japan, which is used for drinking water by thirteen million people. Mitotic toxicity was evaluated by mitotic index (MI) and second mitosis index (SI), using a Chinese hamster cell line V79. SI is the rate of twice divided metaphases in chromosome preparation for sister chromatid exchange. All the pesticides decreased the two indices dose-dependently. MI50 and SI50, the concentrations of pesticides which lowered the indices to 50% of the solvent control, was determined. The MI50 and SI50 of each pesticide were very similar, and the pesticides did not hinder cell division specifically. None of the pesticides induced more sister chromatid exchanges than 1.5 times the solvent control. Chlomethoxyfen and simazine induced sister chromatid exchanges significantly in V79 cells, but the dose dependencies were poor. Simetryn had rec effect and was concluded to have DNA damaging activity.

Characterization of a rat lymphocyte culture system for assessing sister chromatid exchange after in vivo exposure to genotoxic agents

Abstract: Lymphocyte culture systems have the major advantage of permitting the analysis of in vivo cytogenetic damage with minimal injury to the animal under study. This paper describes a rat lymphocyte culture system designed for the study of sister chromatid exchange (SCE) induced by in vivo exposure to genotoxic agents. A standard protocol was established in which 1 to 2 ml of blood are removed from rats by cardiac puncture, washed three times with phosphate-buffered saline (pH 7.4), and grown in RPMI 1640. 5-Bromodeoxyuridine (BrdU) (1.0 microM) is added after 24 hr, and cells are harvested after 56 hr of culture. Critical steps for successful blast transformation include washing the blood in buffered saline and the adding of 2.0 to 4.0 microgram phytohemagglutinin/ml to the culture medium. The use of low concentrations of BrdU (less than or equal to 5.0 microM) is recommended to maintain low baseline SCE levels and to avoid cytotoxicity. The mutagenic carcinogen, ethyl methanesulfonate (EMS), was used as a positive control agent and at a dose of 300 mg/kg caused a fourfold increase in SCE frequency. Twenty-eight days after EMS administration (30, 100, 300 mg/kg), lymphocytes from treated animals still displayed SCE levels at least 50% above baseline. This system provides a reliable means of investigating chemically induced SCE in the rat.

Relationship of carcinogen-induced sister chromatid exchange and neoplastic cell transformation.

Abstract: Sister chromatid exchange (SCE) and morphological transformation induced by five chemical carcinogens, N-acetoxy-2-fluorenyl-acetamide (AcAAF), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), methyl methanesulfonate (MMS), benzo[a]-pyrene (BP), and cisplatinum(II) diamine dichloride (PT) as well as by X-irradiation were quantified in parallel experiments with cultures of Syrian hamster embryo cells (HEC). Incubation of HEC with 5-bromodeoxyuridine (10(-5)M) for two rounds of replication (24 h) required for SCE visualization neither caused morphological transformation nor altered the transformation frequency induced by carcinogen alone. All chemical carcinogens, but not X-irradiation, produced a dose-dependent increase in SCE and transformation frequency, demonstrating the sensitivity of both assays to carcinogens. The ratios of induced SCE relative to transformation frequency, however, varied with the carcinogen. BP, MMNG, and AcAAF were similarly efficient in inducing SCE compared to transformation but were considerably less effective than MMS and PT. X-irradiation at doses of 200, 300, and 500 R did not cause transformation and induced a low frequency of SCE. On a molar basis, MMS and PT were the most effective in SCE induction relative to transformation, MNNG and AcAAF were less effective, and BP was the least effective carcinogen. The positive linear correlation between chemical carcinogen-induced SCE and transformation suggests a relationship between the two cellular responses.

Spontaneous and induced sister chromatid exchanges and delayed cell proliferation in peripheral lymphocytes of Bowen's disease patients and matched controls of arseniasis-hyperendemic villages in Taiwan.

Abstract: A total of 15 newly-developed Bowen's disease patients and 34 age-sex-residence-matched controls were recruited from three arseniasis-hyperendemic villages in Taiwan to compare spontaneous and arsenic-induced sister chromatid exchanges (SCEs), proportion of cells with high frequencies of SCEs (HFCs), and replication index (RI) in their peripheral lymphocytes. Arsenic-induced Bowen's disease patients were found to have significantly higher spontaneous SCEs and HFCs and a lower spontaneous RI than in matched controls without or with adjustment for age, gender, cigarette smoking, alcohol drinking, tea drinking, status of major diseases, HBsAg carrier status and arsenic exposure indices through multivariate analysis. Sodium arsenite was found to increase SCEs and HFCs and to decrease RI in a dose-response pattern for both cases and controls. The arsenic-induced decrease in RI was significantly greater in arsenic-induced Bowen's disease patients than in matched controls. The arsenic-induced increases in SCEs and HFCs were also consistently, but not statistically significantly, higher in arsenic-induced Bowen's disease patients than in matched controls at all arsenite treatment levels of 0.5, 1.0 and 2.0 μM. The arsenic-induced increase in cytogenetic damages and decrease in cell proliferation among arsenic-induced Bowen's disease patients compared with matched controls may result from their long-term exposure to inorganic arsenic through consumption of high-arsenic artesian well water, elevated individual genetic and acquired susceptibility to arsenic-induced damage, or both.