Chemical Steps Involved in the Production of Mutations and Chromosome Aberrations by X-irradiation in Drosophila

Abstract
Post-treatment with hydrocyanic acid results in a significant increase of the mutation frequency in spermatids, if x-radiation is delivered at a high dose-rate, but not after irradiation at a low dose-rate. A greater overall genetic effect of intensity per se has not been observed. Following radiation at both low and high intensities, post-treatment with cyanide increases the frequency of translocations in spermatids. Consequently, it has been inferred that cyanide causes a prolonged opening of chromosome breaks in spermatids and thus favours the formation of translocations. Both this finding and the fact that cyanide post-treatment also raises the mutation rate in a ring-shaped chromosome suggest that the increase in lethal frequency due to post-treatment refers not only to position-effect lethals but also to gene mutations and possibly small deletions. Data relating differential sensitivity in successive broods to oxygen tension are presented. Post-treatment with cyanide is equally effective in raising the mutation rate if high-intensity radiation is given in pure N2, as in O2. It is assumed that cyanide inhibits a mechanism responsible for repair of the initial radiation damage. Recovery from changes leading to lethal gene mutations then seems a metabolic process, possibly connected with respiratory energy. Injury to this repair system is independent of oxygen tension, and the reparable fraction of the initial damage after radiation in N2 is equal to that after radiation in O2.