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The Phenomenon of the Uvr+ Dependent Mutagenesis in Salmonella typhimurium

The Salmonella typhimurium phenotype is comparable to the Escherichia coli ada mutant in having a low but significant constitutively expressed cellular activity of enzyme O6-methylguanine DNA-methyltransferase II (MT II) for repair of promutagen lesions O6-methylguanine and O4-methylthymine in DNA. The role of nucleotide excision repair in the mutagenicity of the monofunctional alkylating agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), methyl methanesulfonate (MMS), N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG), N-ethyl-N-nitrosouren (ENU), N-propyl-N'-nitro-N-nitrosoguanidine (PNNG) and N-butyl-N'-nitro-N-nitrosoguanidine (BNNG) in S. typhimurium was examined. Comparing the S. typhimurium uvrB mutant with the nucleotide excision repair proficient strain it has been noticed that the latter is mutagenized more efficiently at low doses and less efficiently at high doses of methylating (MMS, MNNG) or ethylating (ENU, ENNG) agents. No uvr+ dependent mutagenesis has been noticed in S. typhiumurium after treatment by propylating (PNNG) and butylating (VNNG) agents. Our results suggest that the uvr+ dependent mutagenesis is probably a consequence of the specific competition between enzyme activity involved in nucleotide excision repair enzymes and MT II which are responsible for the overall mutagenic effects of low doses of methylating and ethylating agent in S. typhimurium.

Salmonella typhimurium; Escherichia coli; mutagenesis

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