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Biomedical subjects

N V Goliasnaia

Publications and source records attributed to N V Goliasnaia.

2 recordsLinked to original sources

[Growth of Escherichia coli cell culture and frequency of mutation, induced by N-methyl-N'-nitro-N-nitrosoguanidine].

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.

Culture Media↗

[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.

Animals↗