The additive effect of X-rays and maleic hydrazide in inducing chromosomal aberrations at different stages of the mitotic cycle in Vicia faba

Abstract When mitotically proliferating cells are X-irradiated, chromosome structural changes are found, at the first (T 1 ) mitotic division after irradiation, in cells which were in all stages of the mitotic cycle at the time of treatment. On the other hand, after treatment of cells with certain radiomimetic chemicals such as maleic hydrazide (MH) or alkylating agents, chromosomal aberrations at T 1 mitosis are only found in those cells which were synthesising DNA (S cells) and those in the pre-synthetic (G 1 ) phase of the time when these agents were applied; cells in the post-synthetic (G 2 ) phase at the time of treatment contain no aberrations at their T 1 mitosis but do so at T 2 mitosis 11, 12, 45 . These results indicate that, in contrast to the lesions induced by X-rays, those induced by certain radiomimetic chemicals require the intervention of chromosome replication (or DNA synthesis) before they can be converted to chromosomal aberrations observable at mitosis. In view of the difference between the lesions induced by these agents, an experiment was performed in order to determine whether or not such lesions are able to interact with one another in the formation of aberrations. In the experiment reported here Vicia faba roots were treated with X-rays, MH, or X-rays+ MH, and [ 3 H]thymidine autoradiography was used as a “marker” for the mitotic cycle. The results indicate that, after the combined X-ray/MH treatment, the frequency of all types of chromosomal aberration, at all stages of the mitotic cycle, is merely the sum of the frequencies induced by X-rays and MH when given separately. No evidence was obtained of any interaction between lesions induced by these two agents. This result is completely at variance with the conclusions of others and this is thought to be due to the fact that other workers have made observations at only a limited number of times after treatment and have not adequately taken into account the differential mitotic delay induced by these agents. It is suggested that the lack of interaction is due to the fact that, whereas the lesions induced by X-rays are available for interaction for a short period of time immediately after irradiation, those induced by MH cannot interact until the chromosomes, in which they have been induced, undergo replication. Thus there is a temporal barrier to interaction, since the times, after treatment, when the lesions induced by these two agents are available for interaction, do not coincide.