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.

Chromosome aberration analysis in Concorde pilots.

Abstract: Chromosomal aberrations, micronuclei, and sister chromatid exchanges have been analysed in human peripheral lymphocytes of 18 Concorde pilots and 10 controls. There was an eightfold significant increase of dicentric chromosomes in the Concorde group. The yield of micronuclei was also significantly elevated. Sister chromatid exchanges in the Concorde group did not differ from the control. Comparing the results to flight personnel from subsonic routes, the dicentric yield was higher in personnel from supersonic crews but the difference was not statistically significant. The overdispersion of dicentric chromosomes showed the influence of high LET cosmic radiation. The estimated mean dose per year ranged from 11 to 37 mSv depending on the radiation weighting factor for neutrons. It is recommended that actual and future high-speed transport should consider not only physical measurements, but also biological data like the frequencies of chromosomal aberrations because the latter reflect sensitively the high biological effectiveness of cosmic radiation.

Factors influencing the induction of sister chromatid exchanges in mammalian cells by 12-O-tetradecanoyl-phorbol-13-acetate

Abstract: The induction of sister chromatid exchanges (SCE) by 12-O-tetradecanoyl-phorbol-13-acetate (TPA) was measured in mouse 10T1/2 and 3T3 cells released from density; inhibition, and Chinese hamster CHO cells synchronized by mitotic selection. The induced frequency of SCE was similar in each cell type, but depended upon the concentration of TPA employed, its source, and the particular lot from the same source. Most SCE occurred in the first two rounds of cell replication after addition of TPA. The induction of SCE by TPA was markedly suppressed if the fetal calf serum in the incubation medium was not heat-inactivated. The addition of superoxide dismutase to medium with heat-inactivated serum also suppressed the induction of SCE. These results suggest that free radicals, particularly the superoxide anion, may be important intermediates in some of the biologic effects of TPA.

Significant differences in the structural basis of the induction of sister chromatid exchanges and chromosomal aberrations in chinese hamster ovary cells

Abstract: The structural basis of the induction of sister chromatid exchanges (SCE) and chromosomal aberrations (Cvt) in Chinese hamster ovary cells was investigated by the CASE (Computer Automated Structure Evaluation) method, on artificial-intelligence-based system. Using the relevant National Toxicology Program data bases CASE identified a set of structural determinants responsible for the induction of SCE and another one for Cvt. A comparison between the structural determinants associated with SCE and Cvt revealed an overlap of only 22.6%, while the overlap between SCE and the determinants of mufagenicity in Salmonella is 54.5%. This indicates a) that the structural bases of the two phenomena differ and b) that it is likely that SCE, but not Cvt, involves a significant electrophilic/DNA-damaging component.

Cell Cycle Dependence of Sister Chromatid Exchange Induction by DNA Topoisomerase II Inhibitors in Chinese Hamster V79 Cells

Abstract: The cell cycle dependence of sister chromatid exchange (SCE) induced by topoisomerase II inhibitors was studied in Chinese hamster V79 cells. 4′-(9-Acridinylamino)methansulfon- m -anisidide, which increases the concentration of covalently linked DNA-topoisomerase II complexes (cleavable complexes), induces SCE strongly in only a short period of the cell cycle. The sensitive period was identified as occurring in early to mid-S phase through the use of labeled thymidine incorporation and flow cytometry. Novobiocin, an inhibitor which prevents formation of the cleavable complex, did not induce SCEs in any part of the cell cycle. However, novobiocin did decrease the level of 4′-(9-acridinylamino)methansulfon- m -anisidide-induced SCEs. These results indicate that the cleavable complex may be important in 4′-(9-acridinylamino)methansulfon- m -anisidide-induced SCE.