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.

MUTATION AND SISTER CHROMATID EXCHANGE INDUCTION IN CHINESE HAMSTER OVARY (CHO) CELLS BY PULSED EXCIMER LASER RADIATION AT 93 nm AND 308 nm AND CONTINUOUS UV RADIATION AT 254 nm

Abstract: — We compared mutagenesis and sister chromatid exchange (SCE) induction by 193 nm and 308 nm pulsed excimer laser radiation with 254 nm low intensity continuous wave UV light in Chinese hamster ovary (CHO) cells in culture. The 254 nm radiation was most mutagenic of the radiations, in accordance with expectation, and also was most effective in increasing the level of SCEs. The 193 nm radiation was mutagenic at the ouabain resistance locus, but not at the HGPRT locus. However, 193 nm radiation was also strongly cytotoxic at energies producing measurable mutations. This radiation also caused a dose-related increase in SCEs. Pulsed excimer radiation at 308 nm was mutagenic at both loci, and also increased the incidence of SCEs. Comparison of the ratio of mutants/surviving cells at the D37 after radiation showed similar values for 254 nm and 308 nm at the HGPRT locus, but at the ouabain resistance locus, the ratio for the 308 nm radiation was about 5 times that for 254 nm radiation. These results indicate that some risk for mutagenesis may accompany the use of excimer radiation in the UVA region in therapeutic applications.

Normalisation of sister chromatid exchange frequencies in Bloom's syndrome by euploid cell hybridisation.

Abstract: BLOOM'S syndrome (BS) is a rare autosomal recessive genetic disorder characterised by stunted growth, Sun-sensitive telangiectatic erythema of the face and an abnormally high risk of cancer1. Cultured lymphocytes and fibroblasts from BS patients have a high frequency of spontaneous structural chromosome aberrations and characteristically high levels of sister chromatid exchanges (SCE)2. The primary defect at the molecular level is unknown, but the cytological findings are compatible with a deficiency in a DNA repair function3. The presence of a defect of DNA replication is also suggested by the demonstration that the rate of fork motion during replication in BS is slower than normal4. German et al.5 have reported the coexistence of cells with both high and normal levels of SCE, suggesting that the defect in BS is regulatory. Tice et al.6 concluded from co-cultivation experiments that SCE frequency is mediated by a diffusable agent(s) present in the medium of BS fibroblasts. Other investigators, however have shown suppression of SCE in conditions of co-cultivation7,8. We have clarified the conflict between these results by examining euploid somatic cell hybrids between BS and normal human fibroblasts.

Cryopreservation of mouse oocytes: mutagenic effects in the embryo?

Abstract: We have shown in previous studies that the complete cycle of cryopreservation and prefreezing manipulations increases the degeneration and decreases the fecundability of mouse oocytes. The present study confirms these results. Moreover, we show that the increase of polyploidy previously observed in one-cell zygotes derived from frozen-thawed oocytes persists during the early stages of embryonic development. Furthermore, embryos obtained from frozen oocytes or oocytes exposed to prefreezing manipulations show an increase in the frequency of sister chromatid exchanges. Since the estimation of sister chromatid exchange is a sensitive test of mutagenicity, this suggests that the complete cycle of cryopreservation might alter the oocyte and, more particularly, induce DNA damage.

Determination of the baseline sister chromatid exchange frequency in human and mouse peripheral lymphocytes using monoclonal antibodies and very low doses of bromodeoxyuridine.

Abstract: We measured the frequency of sister chromatid exchanges (SCEs) in human and mouse peripheral lymphocytes using doses of bromodeoxyuridine (BrdU) ranging from 30 ΠM to 100 µ M (human)

Genotoxic effects of styrene-7,8-oxide in human white blood cells: comet assay in relation to the induction of sister-chromatid exchanges and micronuclei.

Abstract: Styrene is used in the production of plastics, resins and rubber. The highest human exposures to styrene take place by inhalation during the production of fiberglass reinforced plastics. Styrene is metabolized mainly in the liver to styrene-7,8-oxide (SO), its principal in vivo mutagenic metabolite. In this study, human peripheral white blood cells were exposed to several SO concentrations (10–200 μM) in order to evaluate its genotoxic properties by means of comet assay, sister-chromatid exchanges (SCE) and cytokinesis-blocked micronucleus (MN) test, in addition to determine its clastogenic or aneugenic properties by combining MN with fluorescence in situ hybridization (FISH) procedures. Our results show that SO induces DNA damage, SCE and MN in human leukocytes in vitro at concentrations above 50 μM, and that there is a strong relationship between DNA damage, as measured by the comet assay, and cytogenetic damage induced by SO at the doses employed. SO shows preferently a clastogenic activity and produces a cytostatic effect at high doses, reflected by the significant decrease of the calculated proliferation indices. A good dose-effect relationship is obtained in the three tests performed at the concentration range assayed.