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Divisions of Toxicology and Cancer Risk Factors [T. H., J. N., H. B.] and Clinical Epidemiology [N. B., A. K.], German Cancer Research Center (Deutsches Krebsforschungszentrum), 69120 Heidelberg, Germany
Etheno-DNA adducts such as 1,N6-ethenodeoxyadenosine (
dA) and N2,3-ethenodeoxycytidine (
dC) are formed as result of oxidative stress and lipid peroxidation via reactive alkenals (J. Nair et al., Mutat. Res., 424:5969, 1999). High
-6 polyunsaturated fatty acid intake markedly increased levels of WBCs in female volunteers on a controlled diet (J. Nair et al., Cancer Epidemiol. Biomark. Prev., 6:591601, 1997). In healthy female volunteers we investigated possible correlations between dietary fatty acid intake (by questionnaire), concentration of linoleic acid (LA) and oleic acid (OA) in serum (n = 34), and etheno-DNA adduct levels in WBC (n = 42). Two groups of samples were selected according to dietary intake >15 g (group A) or <5 g (group B) LA/day. Serum samples were analyzed for free OA and LA by gas chromatography-mass spectroscopy and WBC-DNA for
dA and
dC adducts by immunoaffinity 32P postlabeling. On a group level, serum LA and OA concentrations were higher in group A than group B, whereas the LA/OA ratios were similar. The mean
dA and
dC levels did not significantly differ in groups A and B, but a third of the individuals had more than twice the mean adduct levels than the rest. Correlation analyses revealed a significant inverse correlation for
dA in WBC-DNA and vegetable or vitamin E consumption. We conclude that etheno-DNA adduct levels are not determined by LA intake alone but might depend on the ratio of
-6 polyunsaturated fatty acid:other fatty acids and of antioxidants consumed in the diet. This pilot study also indicated a protective effect of dietary vitamin E and vegetables against miscoding, lipid peroxidation-induced DNA lesions.
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