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The survival of UV irradiated phage lambda was increased on X-irradiated E. coli K-12 host cells over that on unirradiated cells. The frequency of c mutants among the surviving phages was to a similar extent increased by the X-ray exposure of the host cells as by UV light. This W-reactivation of phage lambda occurred in uvrA, polA, and recB mutants besides the wild type at about equal X-ray doses, however, at a reduced reactivation efficiency compared with the wild type. W-reactivation was undetectable in recA mutants. While maximal UV induced W-reactivation occurred 30 min after irradiation, the maximal X-ray induced reactivation was found immediately after irradiation. Chloramphenicol (100 micrograms/ml) and nitrofurantoin (50 micrograms/ml) inhibited W-reactivation of phage lambda if added before irradiation of the host cells, indicating the necessity of protein synthesis for W-reactivation.

Extracellular phage lambda has been successively exposed to X-rays and U.V. light. The plaque-forming ability of the irradiated phages was determined on host cells with different repair capacities. No change in sensitivity was found with a pre-treatment of one type of radiation to lethal damage inflicted by the other. This indicates that a prerequisite for an interaction of different types of radiation is either an active metabolism or repair process occurring during the two radiation exposures.

Wild-type cells of E. coli K-12 showed increasing U.V. resistance if they were X-irradiated and incubated at 37 degrees C in growth medium before the U.V. exposure. Development of higher U.V. resistance could be inhibited by incubating the X-irradiated cells either at temperatures below 15 degrees C, or in the presence of 0.01 M KCN. Nitrofurantoin (NF), which was recently found specifically to inhibit inducible enzyme synthesis, had only a transient inhibitory effect on X-ray-induced U.V. resistance. Cells grown in glucose medium showed less inhibition by NF of X-radiation-induced resistance to U.V.-radiation than did cells grown in glycerol, or in glucose medium with added cyclic AMP. It is suggested that X-ray-induced U.V. resistance requires active cellular metabolism, but it is not subject to catabolite repression. The following hypothesis is offered to explain the action of NF: Under de-repressed conditions (without catabolite repression by glucose) nitrofurantoin could counteract the radiation-induced inhibition of a repair inhibitor (such as post-irradiation DNA degradation).