[Induction of the SOS response in Escherichia coli cells under osmotic stress and in the presence of N-methyl-N'-nitro-N-nitrosoguanidine].

We investigated the dynamics of the SOS response induction and the frequency of reversions induced by the monofunctional alkylating compound N-methyl-N'-nitro-N-nitrosoguanidine in Escherichia coli cells exposed to osmotic stress for 1 h. During the stress treatment of the wild-type cultures adapted and not adapted to the alkylating agent, the maximum SOS response values and induced reversion frequencies were recorded twice. The SOS response values and induced reversion frequencies remained unchanged during the whole period after attaining the maximum values in adapted and nonadapted cells carrying a mutation in the excision repair gene. Presumably, the SOS mutagenesis mechanisms are turned on in the cells with an inactivated excision repair system earlier than in wild-type cells.

[Microbioluminescent study of the general toxicity and mutagenicity of pollutants].

Bacterial bioluminescence was applied to detection of general toxicity (MIT test) and genotoxicity (SOS-lux test) of some chemicals, seawater, and fresh water. The SOS-induced luminescence of E. coli WP2s (cda::luxCDABE) cells was higher than in E. coli C 600 (cda::luxCDABE) at 37 degrees C and pH 6.5. The mutagenic effect of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), mitomycin C, and hydrogen peroxide determined from the induction of E. coli WP2s cell luminescence was detected at lower concentrations than in the assessment of reversion frequencies. General toxicity was demonstrated by using luminescence inhibition for hydrogen peroxide, Zn2+, and Cd2+ at low concentrations. Regions of the Krasnodar Krai where sea and fresh waters exerted toxic action on luminescence were determined by the microbioluminescent method.

[Mismatch repair].

Specific repair systems are activated in response to the DNA damage. Mismatch repair protects the genome of prokaryotic and eukaryotic cells from lesions that appear during process of DNA replication or are induced by mutagenic factors. The methyl directed mismatch repair distinguishes the new strand from the old strand by the hemi-methylated state of the DNA and controls the fidelity of genetic information after homologous recombination. The very short patch repair restores the mismatches at the sites with nucleotide sequence CC(W/T)GG. The "8-oxoG" pathway is independent of the hemi-methylated state of the DNA, and removes the oxidated nucleotides from the genome of prokaryotes and eukaryotes. Mutations in genes of mismatch repair enhance the process of mutagenesis in prokaryotic cell, and are the reason for the development of the colon cancer in humans. The mechanisms of mismatch repair and the role of defective repair proteins in mutagenesis and carcinogenesis are discussed in this review.

[Growth of Escherichia coli cell culture and frequency of mutation, induced by N-methyl-N'-nitro-N-nitrosoguanidine]. / Vozrast kul'tury kletok Escherichia coli i chastota mutatsii, indutsirovannykh N-metil-N'-nitro-N-nitrozoguanidinom.

The rate of Escherichia coli mutation with N-methyl-N'-nitro-N-nitrosoguanidine was found to depend on the age of the culture and the pH value of the incubation medium. The mutability of late-logarithmic cells was higher than that of mid-logarithmic cells. Rifampicin, a transcription inhibitor, enhanced the mutagenic action of MNNG on cells from the late logarithmic and early stationary phases suspended in a medium with a pH of 7.4, and on cells from the mid-logarithmic phase suspended in a medium with a pH of 6.5. Conversely, streptomycin decreased the frequency of induced mutations in cells from the late logarithmic and early stationary phases suspended in the medium with a pH of 7.4, and in cells from the mid-logarithmic and early stationary phases suspended in the medium with a pH of 6.5. These data were interpreted as showing that the repair of premutational DNA lesions induced by MNNG depends on the level of DNA transcription and translation.