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

Summary

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.