Title of article
Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid
Author/Authors
de Kok، نويسنده , , T.M.C.M and Zwingman، نويسنده , , I and Moonen، نويسنده , , E.J and Schilderman، نويسنده , , P.A.E.L and Rhijnsburger، نويسنده , , E and Haenen، نويسنده , , G.R.M.M and Kleinjans، نويسنده , , J.C.S، نويسنده ,
Issue Information
روزنامه با شماره پیاپی سال 2003
Pages
8
From page
351
To page
358
Abstract
It has been hypothesized that oxygen radicals generated by peroxidation of dietary linoleic acid may induce genetic damage and thereby increase cancer risk. We examined the effect of dietary supplementation with linoleic acid on the levels of oxidative DNA damage in peripheral lymphocytes and on the blood plasma antioxidant potential. Thirty volunteers received during 6 weeks either a high dose of linoleic acid (15 g/day), an intermediate dose of linoleic acid (7.5 g/day) or an isocaloric supplement without linoleic acid (15 g palmitic acid/day). After the intervention, no significant increase in oxidative DNA damage, measured as relative amounts of 7,8-dihydro-8-oxo-2′-deoxyguanosine (8-oxodG) in DNA from peripheral lymphocytes, was observed in both high and intermediate linoleic acid-supplemented groups (increase of respectively 13 and 21%; P>0.05). Also, the differences between levels of oxidative DNA damage in the high or intermediate linoleic acid-supplemented group and the control group receiving palmitic acid (23% decrease) were not significant. Furthermore, no statistically significant differences were found between the total antioxidant capacities of blood plasma from the different experimental groups. Plasma levels of malondialdehyde, an important end-product of lipid peroxidation, were not increased after supplementation, nor were effects found on the plasma concentrations of retinol, α-tocopherol and β-carotene. Despite the experimental design that excludes several forms of bias introduced in studies based on modulation of dietary composition, our results provide no indication of increased oxidative stress or genetic damage as a result of increased dietary intake of linoleic acid. Therefore, we see no scientific basis to reconsider the public health policy to stimulate the intake of polyunsaturated fatty acids aimed at the reduction of coronary heart diseases.
Keywords
Palmitic acid , dietary intervention , Total equivalent antioxidant capacity , Oxidative DNA damage , MDA , linoleic acid
Journal title
Food and Chemical Toxicology
Serial Year
2003
Journal title
Food and Chemical Toxicology
Record number
2117398
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