ArticleChemical research in toxicology2011
Tobacco-specific nitrosamine-derived O2-alkylthymidines are potent mutagenic lesions in SOS-induced Escherichia coli.
Article in Chemical research in toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 33 citations in OpenAlex.
- DNA adduct and mutational profiles reveal a threshold of cellular defenses againstNAR molecular medicine · 2026Article
- 5-(Pyridin-3-yl)-3,4-dihydro-2Royal Society open science · 2024Article
- Article
- Establishing Linkages Among DNA Damage, Mutagenesis, and Genetic Diseases.Chemical research in toxicology · 2022Review
- Metabolism and DNA Adduct Formation of Tobacco-SpecificInternational journal of molecular sciences · 2022Review
- Physico-chemical properties of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) diazonium ion: a theoretical investigation.RSC advances · 2021Article
- Mitochondrial Transcription Factor A Binds to and Promotes Mutagenic Transcriptional Bypass ofAnalytical chemistry · 2021Article
- Replication of Pyridyloxobutyl Phosphotriester Lesions in Cells.Chemical research in toxicology · 2020Article
- Biological Evaluation of DNA Biomarkers in a Chemically Defined and Site-Specific Manner.Toxics · 2019Review
- Uncovering a unique approach for damaged DNA replication: A computational investigation of a mutagenic tobacco-derived thymine lesion.Nucleic acids research · 2019Article
- Impact of tobacco-specific nitrosamine-derived DNA adducts on the efficiency and fidelity of DNA replication in human cells.The Journal of biological chemistry · 2018Article
- Article
- Methyl DNA Phosphate Adduct Formation in Rats Treated Chronically with 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanone and Enantiomers of Its Metabolite 4-(Methylnitrosamino)-1-(3-pyridyl)-1-butanol.Chemical research in toxicology · 2018Article
- Chemical Analysis of DNA Damage.Analytical chemistry · 2018Review
- Liquid Chromatography-Tandem Mass Spectrometry for the Quantification of Tobacco-Specific Nitrosamine-Induced DNA Adducts in Mammalian Cells.Analytical chemistry · 2017Article
- Context Matters: Contribution of Specific DNA Adducts to the Genotoxic Properties of the Tobacco-Specific Nitrosamine NNK.Chemical research in toxicology · 2017Review
- DNA Polymerase ν Rapidly Bypasses OChemical research in toxicology · 2016Article
- DNA Polymerases η and ζ Combine to Bypass O(2)-[4-(3-Pyridyl)-4-oxobutyl]thymine, a DNA Adduct Formed from Tobacco Carcinogens.Chemical research in toxicology · 2016Article
- Roles of translesion synthesis DNA polymerases in the potent mutagenicity of tobacco-specific nitrosamine-derived O2-alkylthymidines in human cells.DNA repair · 2015Article
- Carcinogenicity and DNA adduct formation of 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone and enantiomers of its metabolite 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanol in F-344 rats.Carcinogenesis · 2014Article
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3 authors at 2 institutions in 1 country.
Funding
Abstract
To investigate the biological effects of the O(2)-alkylthymidines induced by the tobacco-specific nitrosamine 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK), we have replicated a plasmid containing O(2)-methylthymidine (O(2)-Me-dT) or O(2)-[4-(3-pyridyl-4-oxobut-1-yl]thymidine (O(2)-POB-dT) in Escherichia coli with specific DNA polymerase knockouts. High genotoxicity of the adducts was manifested in the low yield of transformants from the constructs, which was 2-5% in most strains but increased 2-4-fold with SOS. In the SOS-induced wild type E. coli, O(2)-Me-dT and O(2)-POB-dT induced 21% and 56% mutations, respectively. For O(2)-POB-dT, the major type of mutation was T → G followed by T → A, whereas for O(2)-Me-dT, T → G and T → A occurred in equal frequency. For both lesions, T → C also was detected in low frequency. The T → G mutation was reduced in strains with deficiency in any of the three SOS polymerases. By contrast, T → A was abolished in the pol V(-) strain, while its frequency in other strains remained unaltered. This suggests that pol V was responsible for the T → A mutations. The potent mutagenicity of these lesions may be related to NNK mutagenesis and carcinogenesis.
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