Effect of Bis (haloalkyl) piperidines, a New Antitumor Agent, on Various Repair-deficient Mutants of Escherichia coli B

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Abstract
To clarify the mechanism of action of new antitumor agents like bis(haloalkyl)piperidine derivatives, sensitivity of various DNA repair-deficient mutants of E. coli B to these derivatives was examined. When bacteria were treated with 1-(.beta.-chloroethyl)-2-chloromethylpiperidine hydrobromide (CAP-1), UV-sensitive (uvrA-) mutant and recombination-deficient (recA-)mutant were killed, and DNA polymerase I-minus (pol I-) mutant was moderately killed. The killing kinetics of CAP-1 on bacteria were very similar to those of UV ray. Repair-deficient mutants were remarkably sensitive to 1-(.gamma.-chloropropyl)-2-chloromethylpiperidine hydrobromide (CAP-2), and its killing kinetics were similar to those of mitomycin-C. In the case of 2,6-bis(iodomethyl)piperidine hydrochloride (CAP-12), pol I- mutant was very rapidly killed and recA- and uvrA- mutants were moderately killed, though the viability of wild type strain was hardly affected. These results indicate that the higher sensitivity of repair-deficient E. coli mutants to bis(haloalkyl)piperidine derivatives is due mainly to their impaired repair ability for DNA damage caused by these derivatives. Therefore, these derivatives act on bacterial DNA and produce DNA lesions repairable by the repair systems of the wild type strain.

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