© 1996 Oxford University Press
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Determination of DNA adducts of malonaldehyde in humans: effects of dietary fatty acid composition
Molecular Epidemiology Unit, Center for Nutrition and Toxicology, Department of Biosciences at NOVUM, Karolinska Institute S-141 57 Huddinge, Sweden
11Department of Applied Chemistry and Microbiology (Nutrition), University of Helsinki SF-00014 Helsinki, Finland
4To whom correspondence should be addressed
The effects of dietary fatty acid composition on the endogenous formation of DNA adducts of malonal-dehyde (MA), the major product of lipid peroxidation, were investigated in humans. A group of 59 healthy individuals of both sexes and different ages was initially fed a milk fat-based diet rich in saturated fatty acids for 14 days. Following this initial period, after which the group was considered homogeneous with respect to diet, 30 randomly chosen subjects were given a sunflower oil-based (rich in polyunsaturated fatty acids) (SO) diet and the remaining 29 individuals a low erucic acid rapeseed oil-based (rich in monounsaturated fatty acids) (RO) diet for 25 days. The fatty acid composition of plasma lipid fractions and the level of DNA adducts of MA in total white blood cells were then determined at the end of the SO and RO dietary periods. DNA adduct levels were measured by 32P-post-labelling using reversed-phase HPLC with on-line detection of radioactivity. Higher concentrations of polyunsaturated fatty acids in plasma triglycerides and higher levels of DNA adducts of MA were found in the subjects on the SO diet when compared with those in the RO dietary group. A large inter-individual variation in adduct levels was observed. The average adduct level in the SO diet group was 7.4 ± 8.7 adducts/107 nucleotides (n = 23). This level was 3.6-fold higher than that found in individuals in the RO diet group (P < 0.001). Our results, in conjunction with the mutagenic and carcinogenic properties of MA, thus suggest the interaction of lipid peroxidation products such as MA with DNA as one pausible mechanism explaining the involvement of dietary fat in carcinogenesis.
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