Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid
de Kok TM, Zwingman I, Moonen EJ, Schilderman PA, Rhijnsburger E, Haenen GR, Kleinjans JC
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 12 citas
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- Diseño
- Ensayo controlado aleatorizado (indexado por PubMed)
- Estudiado en
- Personas
- Resultado principal
- Solo mecanismos
- Consumo medido con
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Quién lo pagó
- Financiación
- Financiación no declarada
Publicación
- Publicado
- 2002-12-28 · Food Chem Toxicol · vol. 41 · número 3 · págs. 351–358
- Editorial
- Elsevier BV
- Citado
- 23 citas · más que el 51% de estudios similares · 0.2× el promedio de su campo
- Referencias
- 50 trabajos
- Acceso
- De pago
- Áreas de investigación
- Antioxidant Activity and Oxidative Stress · Fatty Acid Research and Health · Carcinogens and Genotoxicity Assessment
- Palabras clave
- linoleic acid, dietary supplementation, oxidative DNA damage, 8-hydroxy-2'-deoxyguanosine, lipid peroxidation, malondialdehyde, antioxidant capacity, polyunsaturated fatty acids, palmitic acid, peripheral blood lymphocytes, cancer risk, coronary heart disease prevention
- MeSH
- lymphocytes, humans, dna damage, reactive oxygen species, malondialdehyde, beta carotene, vitamin a, linoleic acid, palmitic acid, alpha-tocopherol, antioxidants, analysis of variance, oxidation-reduction, lipid peroxidation, dose-response relationship, drug, dietary supplements, adult, female
7 autores
- Theo M. C. M. de Kok🇳🇱 · autor de correspondenciaMaastricht University
- I. Zwingman🇳🇱Maastricht University
- Edwin J C Moonen🇳🇱Maastricht University
- Pauline A. E. L. Schilderman🇳🇱Maastricht University
- Els H. Rhijnsburger🇳🇱Maastricht University
- Guido R.M.M. Haenen🇳🇱Maastricht University
- Jos C. S. Kleinjans🇳🇱Maastricht University
Resumen
El texto original del estudio, en el idioma en que se publicó.
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, alpha-tocopherol and beta-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.
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