Prior UV irradiation increased the X-ray sensitivity of wild-type E. coli K-12. This synergistic effect of combined UV and X irradiation was also observed, but to a reduced extent, in uvrA, uvrB, uvrC. and pool mutants, but was absent in exrA, recA, recB, or recC mutants of E. coli K-12. Alkaline sucrose gradient studies demonstrated that the rec and exr gene-controlled, growth-mediumdependent (Type 111) repair of X-ray-induced DNA single-strand breaks was inhibited by prior UV irradiation. This inhibition probably explains the synergistic effect of these two radiations on survival.

Abstract— When log phase cells of wild‐type E. coli K‐12 were maintained in growth medium after X irradiation, they became progressively more resistant to a subsequent exposure to UV or X radiation. The time to achieve maximum resistance was about 60 min. The uvrB, uvrD, polA and certain exrA strains (W3110 background) also demonstrated this X ray‐induced resistance to subsequent UV or X irradiation but recA, recB, lex (AB1157 or W3110 backgrounds) and other exrA strains (AB1157 background) did not. The resistance induced in wild‐type, uvrB and uvrD cells was characterized by the production or enhancement of a shoulder on the survival curves obtained for the second irradiation, while the resistance induced in the W3110 exrA strains was expressed only as a change in slope. The induction of resistance in the W3110 exrA strain was not inhibited by the presence of chloramphenicol, but that in the wild‐type cells appeared to be. The production or enhancement of a shoulder on the survival curves of the rec+lex+exr+ cells is consistent with the concept of the radiation induction of repair enzymes. Alternative explanations, however, are discussed.

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).