Abstract
The role of n-6 polyunsaturated fats upon the formation of the mutagenic DNA adduct malondialdehydedeoxyguanosine (M1dG) in blood was investigated in male volunteers (n = 13) who consumed diets high in saturated and polyunsaturated fats, and polyunsaturated fat plus a-tocopherol supplemention (400 IU per day). On day 14 there was a significant difference in adduct levels between diets with saturated fats giving higher levels than polyunsaturated fats but this effect had disappeared by day 20 indicating that there is a relatively rapid adjustment to the effects on DNA damage of changes in dietary fat. a-Tocopherol showed a small benefit by day 20. Five females participated in the PUFA study and had higher mean adduct levels than men but there was no correlation with hormonal status. Overall, PUFA had a limited beneficial effect on M1dG levels that warrants further investigation.
Highlights
There is a vast body of evidence, from both epidemiological and dietary intervention studies [1,2,3], suggesting that diet is an important factor with regard to many health problems including the incidence of many cancers, identification of the most important aspects are often elusive
lipid peroxidation (LPO) is initiated by the attack of free-radicals on membrane lipids leading to reactive products that may be linked to tumour initiation
Of the 19 plasma fatty acids measured, the major ones were linoleic, arachidonic, palmitic and stearic acid which together made up 80% of the total fatty acid profile on the polyunsaturated fatty acids (PUFA) diet and 73% on the saturated fat (SFA) diet
Summary
There is a vast body of evidence, from both epidemiological and dietary intervention studies [1,2,3], suggesting that diet is an important factor with regard to many health problems including the incidence of many cancers, identification of the most important aspects are often elusive. Lipid peroxidation (LPO) and arachidonic acid metabolism have all been linked, amongst other factors, to colorectal carcinogenesis in a number of studies [7,8,9]. Malondialdehyde (MDA) is known to be a major product of LPO and has been shown to be mutagenic in bacterial [10, 11] and mammalian cells [12] due to the formation of the malondialdehyde-deoxyguanosine adduct, M1dG [13]. Another study has suggested that a diet high in n-6 polyunsaturated fatty acids (PUFA) elevates M1dG adducts in human blood DNA, with women showing a slighter higher increase than men, [15] compared with a diet rich in monounsaturated fats. Nair et al [16] examined etheno adducts in a subset of these
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