Mutagenicity of 3-azido-1,2-propanediol and 9-(3-azido-2-hydroxypropyl)-adenine in repair deficient strains of Escherichia coli
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu časopisecké články
PubMed
7690900
DOI
10.1016/0165-7992(93)90002-d
PII: 0165-7992(93)90002-D
Knihovny.cz E-zdroje
- MeSH
- adenin analogy a deriváty toxicita MeSH
- azidy toxicita MeSH
- Escherichia coli účinky léků genetika MeSH
- exprese genu účinky léků MeSH
- molekulární struktura MeSH
- mutageny toxicita MeSH
- oprava DNA * MeSH
- propylenglykoly toxicita MeSH
- SOS odpověď (genetika) MeSH
- testy genotoxicity MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- 9-(3-azido-2-hydroxypropyl)adenine MeSH Prohlížeč
- adenin MeSH
- azidoglycerol MeSH Prohlížeč
- azidy MeSH
- mutageny MeSH
- propylenglykoly MeSH
The mutagenicity of two non-aromatic organic azido compounds, 3-azido-1,2-propanediol (AG) and 9-(3-azido-2-hydroxypropyl)-adenine (AHPA), was studied in E. coli repair deficient strains uvrA6, uvrA6 + umuC36, uvrA6+ umuC122::Tn5, polA1, tagA1+ alkA1, ada and dam3. The mutagenicity of both agents was markedly enhanced by defects of UvrABC excinuclease (uvrA6) and was independent of umuC function of the SOS error-prone pathway. Neither azido compound promoted umuDC operon expression. The mutagenicity of AG in tag A1, alkA1 and ada mutants does not differ from that found in the wild-type strain. The expression of both ada and alkA genes was not elevated by AG. Experiments on polA1 and dam3 mutants suggest that DNA polymerase I as well as the mutHLS mismatch repair pathway does not contribute to the removal of putative DNA lesions induced by AG.
Citace poskytuje Crossref.org
