The theory of dual radiation action (A. M. Kellerer and H. H. Rossi, Curr. Top. Radiat. Res. Q. 8, 85-158, 1972) has attributed the effects of ionizing radiation on eukaryotes to the production of molecular changes (sublesions) that combine pairwise to produce injury (lesions) responsible for radiation effects. If the yield of sublesions is independent of radiation quality (as is currently assumed), dual radiation action results in the well-known proportionality between the average yield of lesions and <tex-math>$\alpha D+\beta D^{2}$</tex-math>, where β is a radiation-independent quantity. It has, however, been observed that β changes with radiation type. In this paper we propose an explanation of this discrepancy. Specifically, we suggest that dual radiation action-type processes where β is variable are the result of a mechanism-termed compound dual radiation action-which consists of a sequence of simple dual radiation action processes, each process being the causative agent for the next one. The sequence, single-strand DNA breaks, double-strand DNA breaks (chromosome breaks), and exchange-type chromosomal aberrations, is one such example examined in the paper.

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