Abstract

Quiescent human lymphocytes were X-irradiated and allowed to repair for various times at 37°C before the cells were challenged with the DNA-repair inhibitor ara-C. The observed yield of chromosome exchange aberrations (dicentrics) was about twice the yield induced by X-rays alone, if ara-C was added immediately after irradiation. The yield as a function of the repair time between X-irradiation and ara-C treatment decreased with a half-life of 15–30 min and was almost down to the baseline yield for X-rays alone after 1 h. This shows that an exchange aberration can be formed from a short-lived DNA break. In contrast, previously published results from dose-split experiments demonstrate that the half-life of the interacting DNA breaks is of the order of several hours. A model is proposed which can account for the different estimates of the time course of the interactions involved in the process which leads to an exchange aberration.

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