Inhibition of X-ray-induced Protection ofEscherichia ColiK-12 Cells against the Lethal Effects of Ultra-violet Light by Nitrofurantoin

Abstract

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).

Homologous Recombination—Experimental Systems, Analysis, and Significance

“…It is well known that treatment of cells with one DNA damaging agent, followed by incubation in growth conditions, makes them better prepared to repair DNA lesions from subsequent exposures to different DNA damaging treatments (216, 255). This inducible response to DNA damage, called the SOS response by Miroslav Radman (262), is best demonstrated by the effect of split-dose DNA damaging treatments, during which repair-proficient cells show better survival after a particular dose of DNA damaging treatment if the treatment is delivered in several sub-doses separated by short time intervals (77, 277).…”