Abstract
THE nature of the involvement of DNA repair in the formation of sister chromatid exchanges (SCEs) and their connection with chromosome aberrations is unknown. Some mutagens that damage DNA, including ultraviolet light and mitomycin C, considerably increase the incidence of SCEs1–6, whereas other agents, such as X rays6–8, nitrosoguanidine2 and 8-ethoxycaffeine5 cause only a slight increase, although they are potent inducers of lesions at the DNA and chromosome levels. Hamster cells infected with adenovirus 12 show no increased SCEs in spite of extensive fragmentation of the entire chromosome complement (our unpublished results). These findings suggest that the mechanism of formation of SCEs is not unitary. Whereas the mechanism of induction of SCEs could be studied by analysing their frequency after application of agents with known action on DNA, spontaneously occurring SCEs can be studied in cells with defects in the DNA repair system. This report deals chiefly with the frequency of spontaneous SCEs in several strains of xeroderma pigmenosum (XP) fibroblasts which show various levels of repair capacities, in Fanconi's anaemia (FA) cells and in control human cells at different stages of ageing.
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