Production by Radiation of DNA Double Strand Breaks in Three Mammalian Cell Lines and their Repair in Foetal Human Fibroblasts

Abstract

When first techniques became available to measure radiation induced DNA double strand breaks (DSB) (1), it was postulated that such lesions could not be repaired by living cells and were, therefore, responsible for cell death (2, 3). It was later realized that DSB were instead extensively repaired both in bacterial (4) and mammalian cells (5). Nevertheless, the assumption the DSB could be involved in the mechanism of radiation induced cell death, was not dismissed but transferred to unrepaired DSB (6). Unfortunately, the possibility of directly checking this hypothesis is severely hampered by technical reasons. Even with the more recent methodologies, radiation doses necessary to obtain significant measurement of DSB are far beyond the range of cell survival, particularly when sedimentation techniques are used. A second drawback is due to the difficulties of handling large DNA molecules attached to nuclear proteins and to isolate DNA without degrading it too much. On the other hand, it should be taken into account that, even if we were able to isolate intact chromosomal DNA of mammalian cells, no analytical techniques are actually available to deal with it.