When Chinese hamster cells are lysed on top of an alkaline sucrose gradient, in time a fairly discrete DNA-containing molecular species is released from an apparently more complex material. Small doses of X-radiation speed the resolution of this complex while large doses degrade the material released from it. Incubation after irradiation reverses both effects.

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A comparative study was made of the toxic properties of actinomycin D and X‐rays using synchronized populations of Chinese hamster cells cultured in vitro. X‐irradiated cells are most resistant in the latter half of the DNA synthetic period (late S). While cells treated with actinomycin D appear to go through a survival maximum at the same age, they are most resistant after the completion of DNA synthesis; i.e. in G2 (or G2‐mitosis). In spite of these differences, we found that actinomycin D damage in late S cells interacts with X‐ray damage. Thus, a common locus for the site of actions of both agents is suggested which may be in or around the genome of a cell in view of the well‐known DNA binding properties of actinomycin D.