Analysis of 4-aminobiphenyl-DNA adducts in human urinary bladder and lung by alkaline hydrolysis and negative ion gas chromatography-mass spectrometry.

Lin, Dong; Lay, Jackson O.; Bryant, Matthew; Malaveille, Christian; Friesen, Marlin D.; Bartsch, Helmut; Lang, Nicholas P.; Kadlubar, Fred F.

doi:10.1289/ehp.94102s611

Cited by 60 publications

(25 citation statements)

References 18 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…GC-MS analysis of 4-aminobiphenyl released from human lung DNA provides evidence in support of the presence of the C-8 adduct, as also indicated by 32 Ppostlabeling and immunoassay (Culp et al, 1997;Lin et al, 1994). Levels of this adduct were not related to smoking.…”

Section: Adduct Detectionsupporting

confidence: 55%

Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

et al. 2002

View full text Add to dashboard Cite

It is estimated that cigarette smoking kills over 1 000 000 people each year by causing lung cancer as well as many other neoplasmas. p53 mutations are frequent in tobaccorelated cancers and the mutation load is often higher in cancers from smokers than from nonsmokers. In lung cancers, the p53 mutational patterns are different between smokers and nonsmokers with an excess of G to T transversions in smoking-associated cancers. The prevalence of G to T transversions is 30% in smokers' lung cancer but only 12% in lung cancers of nonsmokers. A similar trend exists, albeit less marked, in laryngeal cancers and in head and neck cancers. This type of mutation is infrequent in most other tumors aside from hepatocellular carcinoma. At several p53 mutational hotspots common to all cancers, such as codons 248 and 273, a large fraction of the mutations are G to T events in lung cancers but are almost exclusively G to A transitions in non-tobacco-related cancers. Two important classes of tobacco smoke carcinogens are the polycyclic aromatic hydrocarbons (PAH) and the nicotine-derived nitrosamines. Recent studies have indicated that there is a strong coincidence of G to T transversion hotspots in lung cancers and sites of preferential formation of PAH adducts along the p53 gene. Endogenously methylated CpG dinucleotides are the preferred sites for G to T transversions, accounting for more than 50% of such mutations in lung tumors. The same dinucleotide, when present within CpGmethylated mutational reporter genes, is the target of G to T transversion hotspots in cells exposed to the model PAH compound benzo[a]pyrene-7,8-diol-9,10-epoxide. As summarized here, a number of other tobacco smoke carcinogens also can cause G to T transversion mutations. The available data suggest that p53 mutations in lung cancers can be attributed to direct DNA damage from cigarette smoke carcinogens rather than to selection of pre-existing endogenous mutations.

show abstract

Section: Adduct Detectionsupporting

confidence: 55%

Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

et al. 2002

View full text Add to dashboard Cite

show abstract

“…8,87,203 Samples of human urinary bladder and lung DNA, hydrolyzed and subjected to GC-NICI-MS analysis, were shown to contain 4-ABP-DNA adducts at levels that are in keeping with 32 P-postlabeling analysis of the same samples using appropriate standards. 204,205 Additionally, the levels of MDA-induced M 1 dG were determined to be as low as 52 and 6.2 adducts per 10 8 nucleosides in rat liver 83 and human leukocyte DNA, 192 respectively, by the GC/EC-NICI-MS method.…”

Section: Quantitative Analysis Of Dna Adductsmentioning

confidence: 99%

Mass spectrometry for the assessment of the occurrence and biological consequences of DNA adducts

2015

View full text Add to dashboard Cite

Exogenous and endogenous sources of chemical species can react, directly or after metabolic activation, with DNA to yield DNA adducts. If not repaired, DNA adducts may compromise cellular functions by blocking DNA replication and/or inducing mutations. Unambiguous identification of the structures and accurate measurements of the levels of DNA adducts in cellular and tissue DNA constitute the first and important step towards understanding the biological consequences of these adducts. The advances in mass spectrometry (MS) instrumentation in the past 2–3 decades have rendered MS an important tool for structure elucidation, quantification, and revelation of the biological consequences of DNA adducts. In this review, we summarized the development of MS techniques on these fronts for DNA adduct analysis. We placed our emphasis of discussion on sample preparation, the combination of MS with gas chromatography-or liquid chromatography (LC)-based separation techniques for the quantitative measurement of DNA adducts, and the use of LC-MS along with molecular biology tools for understanding the human health consequences of DNA adducts. The applications of mass spectrometry-based DNA adduct analysis for predicting the therapeutic outcome of anti-cancer agents, for monitoring the human exposure to endogenous and environmental genotoxic agents, and for DNA repair studies were also discussed.

show abstract

“…This technique, which has been used to measure dG-C8 adduct of 4-aminobiphenyl [81], is based upon alkaline hydrolysis of dG-C8-HAA adducts with formation of the parent HAA compounds. Following chemical derivatization with trifluoromethylbenzylbromide, the di(3,5-bistrifluoromethylbenzyl)HAA derivative is measured by gas chromatography-electron-capture detection or gas chromatography-negative chemical ionization mass spectrometry [82].…”

Section: Haa-dna Adducts Analyses In Vitro and In Experimental Animalmentioning

confidence: 99%

Formation and analysis of heterocyclic aromatic amine–DNA adducts in vitro and in vivo

Turesky

Vouros

2004

Journal of Chromatography B

114

View full text Add to dashboard Cite

Analysis of 4-aminobiphenyl-DNA adducts in human urinary bladder and lung by alkaline hydrolysis and negative ion gas chromatography-mass spectrometry.

Cited by 60 publications

References 18 publications

Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

Tobacco smoke carcinogens, DNA damage and p53 mutations in smoking-associated cancers

Mass spectrometry for the assessment of the occurrence and biological consequences of DNA adducts

Formation and analysis of heterocyclic aromatic amine–DNA adducts in vitro and in vivo

Contact Info

Product

Resources

About