The exchange hypothesis and chromosome-type aberrations

Abstract

Regression analyses of the dose-response curves of radiation-induced chromosome aberrations in blood cells of Wallabia bicolor (2 n = 11) show that the kinetics of yield of terminal deletions, as well as classical two-lesion aberrations (rings, dicentrics, and intercalary deletions), best fit the model, Y = a + cD 2 . In addition, all aberrations, including terminal deletions, respond to a fractionated dose in the way expected of two-hit aberrations. These observations suggest that terminal deletions originate from two-hit events. It is proposed that they result from incomplete exchanges, in accord with Revell's 18–21 explanation of the origin of chromatid deletions, rather than from single breaks as proposed on the “breakage first” 28 model.