ArticleCarcinogenesis2009
Aromatic DNA adducts and polymorphisms in metabolic genes in healthy adults: findings from the EPIC-Spain cohort.
Article in Carcinogenesis, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 35 citations in OpenAlex.
- Mini-review: Human N-acetyltransferase genetic polymorphisms in susceptibility to aromatic amine and alkylaniline genotoxicity.The Journal of pharmacology and experimental therapeutics · 2025Review
- Contribution of Genetic Polymorphisms in Human Health.International journal of environmental research and public health · 2023Review
- CYP1A1 I462V polymorphism is associated with reduced genotoxicity in yeast despite positive association with increased cancer risk.Mutation research. Genetic toxicology and environmental mutagenesis · 2017Article
- Microsomal epoxide hydrolase 1 (EPHX1): Gene, structure, function, and role in human disease.Gene · 2015Review
- Variants in phospholipid metabolism and upstream regulators and non-small cell lung cancer susceptibility.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2014Article
- Variation in PAH-related DNA adduct levels among non-smokers: the role of multiple genetic polymorphisms and nucleotide excision repair phenotype.International journal of cancer · 2013Article
- Glutathione-S-transferase (GST) polymorphisms are associated with relapse after radical prostatectomy.Prostate cancer and prostatic diseases · 2013Article
- Seasonal variations in the levels of PAH-DNA adducts in young adults living in Mexico City.Mutagenesis · 2011Article
- Bulky DNA adducts in white blood cells: a pooled analysis of 3,600 subjects.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2010Article
- Pooled analysis of studies on DNA adducts and dietary vitamins.Mutation research · 2010Review
- Synergistic effects of NAT2 slow and GSTM1 null genotypes on carcinogen DNA damage in the lung.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2010Article
- Simultaneous genotyping of GSTT1 and GSTM1 null polymorphisms by melting curve analysis in presence of SYBR Green I.The Journal of molecular diagnostics : JMD · 2010Article
- Relationship between N-acetyltransferase 2 single-nucleotide polymorphisms and phenotype.Carcinogenesis · 2010Article
- Differences between human slow N-acetyltransferase 2 alleles in levels of 4-aminobiphenyl-induced DNA adducts and mutations.Mutation research · 2009Article
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Authors and funding
20 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Aromatic compounds such as polycyclic aromatic hydrocarbons, arylamines and heterocyclic amines require metabolic activation to form metabolites able to bind to DNA, a process mediated by polymorphic enzymes. We measured aromatic DNA adducts in white blood cells by the (32)P-post-labelling assay in a sample of 296 healthy adults (147 men and 149 women) from five regions of Spain. We also analyzed functional polymorphisms in the metabolic genes CYP1A1, CYP1A2, EPHX1, GSTM1, GSTT1, NAT2 and SULT1A1. A significant increased level of DNA aromatic adducts was found related to the fast oxidation-hydrolysis phenotype defined by the polymorphism I462V in CYP1A1, the allele A in IVS1-154C>A of CYP1A2 and the combination Tyrosine-Arginine for Y113H and H139R of EPHX1. Geometric means (adducts per 10(-9) normal nucleotides) were 2.17, 4.04 and 6.30 for slow, normal and fast phenotypes, respectively (P-trend = 0.01). Slow acetylation by NAT2 was associated with a significant decrease in adduct level; subjects with slow alleles *5A and *7A/B had in average 1.56 x 10(-9)adducts, as compared with 5.60 for those with normal NAT2 activity (P-value = 0.01). No association was seen with polymorphisms of other metabolic genes such as GSTM1, GSTT1 or SULT1A1. We concluded that the metabolic pathways of oxidation, hydrolysis and acetylation are relevant to the formation of bulky DNA adducts. This could suggest a potential involvement of aromatic compounds in the formation of such adducts; however, given lack of specificity of the post-labeling assay, a firm conclusion cannot be drawn.
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