Alcohol consumption is a recognized cancer risk factor. A causal link has been established between alcohol drinking and cancers of the oral cavity, pharynx, esophagus, colon, rectum, liver, larynx and breast. Despite the clear association between alcohol consumption and cancer, the underlying mechanisms of alcohol-induced carcinogenesis remain unclear. Various mechanisms may come into play depending on the type of cancer, however convincing evidence supports the concept that acetaldehyde, ethanol's major metabolite is, at least partially, responsible for alcohol's carcinogenic effects. Acetaldehyde can react with DNA forming adducts. DNA adducts can serve as biomarkers of carcinogen exposure and potentially of cancer risk. The major DNA adduct of acetaldehyde is N2-ethylidenedeoxyguanosine which can be quantified as its reduced form N2-ethyl-dG by LC-ESI-MS/MS. To investigate the potential use of N2-ethyl-dG as a biomarker of alcohol induced DNA damage, we quantified this adduct in DNA from the oral and esophageal tissues of Rhesus monkeys exposed to ethanol drinking over their lifetime and compared the levels to those measured in tissue samples from control animals. N2-Ethyl-dG levels in the esophageal and oral DNA of exposed animals were 1.5 fold (p = 0.03) and 2.5 fold (p = 0.01) the levels measured in the control animals respectively.These results support the hypothesis that acetaldehyde plays a common role in oral and esophageal alcohol-induced carcinogenesis and confirm the quantitation of N2-ethyl-dG as a promising tool for the investigation of alcohol induced DNA damage.

Effects of alcohol consumption on levels of N<sup>2</sup>-ethylidenedeoxyguanosine in DNA from oral and esophageal tissues from Rhesus monkeys

246th National Meeting (2013)

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Effects of alcohol consumption on levels of N2-ethylidenedeoxyguanosine in DNA from oral and esophageal tissues from Rhesus monkeys

Effects of alcohol consumption on levels of N²-ethylidenedeoxyguanosine in DNA from oral and esophageal tissues from Rhesus monkeys