Is Sister Chromatid Exchange Formation an Inducible Process?
Sister chromatid exchange (SCE) formation is well correlated with the carcinogenic and mutagenic properties of DNA damaging agentsl. However, the mechanism of induction of SCE is still unknown and this correlation is not well understood. At the present time many hypotheses have been advanced to explain this correlation but none is fully satisfactory. In particular many efforts have been made to link SCE formation and DNA repair, since treatment of cells with DNA damaging agents such as X-rays, UV light, alkylating or DNA cross-linking agents, increases considerably SCE frequency2,3,4,5,6. However, it does not seem that SCE induction depends on excision repair mechanisms. Indeed it has been shown that cells with different excision repair capacities exhibit the same level of SCE after treatment with DNA damaging agents. After an UV-irradiation at 254 nm, Xeroderma nigmentosum cells from the different complementation groups which excise pyrimidine dimers at various rates, exhibit the same SCE frequency7. There is not an inverse correlation between excision repair measured by unschedule DNA synthesis (UDS) and SCE frequency. Moreover it is not clear what kind of lesion is responsible for SCE induction after an UV-irradiation. Indeed some cells are able to monomerize pyrimidine dimers by a process called photoreactivation, and it has been shown that photoreactivation in protorous and in chick embryo cells does not affect SCE production8. It is therefore possible that lesions responsible for SCE formation are some minor photoproducts which are not excised, and not pyrimidine dimers.
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