A genetically controlled luminescent bacterial reporter assay, the SOS lux test, was developed for rapid detection of environmental genotoxins. The bioassay is based on the recombinant plasmid pPLS-1, which was constructed as a derivative of pBR322, carrying the promoterless luxCDABFE genes of Photobacterium leiognathi downstream of a truncated cda gene from ColD with a strong SOS promoter. E. coli recA ؉ strains containing this construction are inducible to high levels of light production in the presence of substances or agents that cause damage to the DNA of the cells. The light signal, reflecting the SOS-inducing potency, is recorded from the growing culture within 1 s, and the test results are available within 1 to 2 h. Induction of bioluminescence was demonstrated by treatment of E. coli C600(pPLS-1) with 6 genotoxic chemicals (mitomycin C, N-methyl-N-nitro-N-nitrosoguanidine, nalidixic acid, dimethylsulfate, hydrogen peroxide, and formaldehyde) and with UV and ␥ radiation. A clear dose-response relationship was established for all eight genotoxins. The sensitivity of the SOS lux test is similar to that of other bioassays for genotoxicity or mutagenicity, such as the SOS chromotest, umu test, and Ames mutatest. These results indicate that the SOS lux test is potentially useful for the in situ and continuous detection of genotoxins.

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Lambda-prophage induction in repair-deficient and wild-type E. coli strains by heavy ions and gamma-rays has been investigated. The dose dependence of the fraction of induced cells has been measured and its initial slope (lambda-induction potency) determined. The induction by gamma-rays was found to be more efficient in a polA-repair-deficient strain; the value of lambda-induction potency is zero in lexA- and recA- strains. The lambda-induction potency increased with LET for wild-type cells but remained constant in the case of polA- mutant cells. It is suggested that the DNA damage triggering the lambda-prophage induction in the case of ionizing radiation could be a type of DNA single-strand break with complex structure which cannot be repaired by fast repair processes, and which requires a substantial level of energy deposition for induction in a DNA molecule.