Abstract
If cells exposed to X-rays or chemical agents are incubated with inhibitors of DNA repair (cytosine arabinoside or aphidicolin), it is possible to accumulate single-strand gaps in the DNA at repairing regions. Upon reversal of the inhibition, these gaps can interact to form chromosome aberrations. It appears that the aberration frequency observed following treatment with radiation or chemical agents is greatly influenced by the rate of repair of damage that is converted into aberrations. This argument also extends to considerations of the different cell-cycle-stage sensitivities, the relative sensitivities of different species, and the probability of observing interactive effects between two agents. These aspects are discussed in terms of their contribution to the interpretation of the mechanisms of induction of chromosome aberrations.

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