Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid
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...
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description | 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. |
doi_str_mv | 10.1016/S0278-6915(02)00237-5 |
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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.</description><identifier>ISSN: 0278-6915</identifier><identifier>EISSN: 1873-6351</identifier><identifier>DOI: 10.1016/S0278-6915(02)00237-5</identifier><identifier>PMID: 12504167</identifier><identifier>CODEN: FCTOD7</identifier><language>eng</language><publisher>Oxford: Elsevier Science</publisher><subject>Adult ; alpha-tocopherol ; alpha-Tocopherol - blood ; Analysis of Variance ; antioxidant activity ; Antioxidants - metabolism ; beta Carotene - blood ; beta-carotene ; Biological and medical sciences ; blood serum ; dietary fat ; Dietary Supplements ; DNA damage ; DNA Damage - drug effects ; Dose-Response Relationship, Drug ; fat intake ; Female ; Food toxicology ; genotoxicity ; Humans ; linoleic acid ; Linoleic Acid - administration & dosage ; Linoleic Acid - blood ; Linoleic Acid - pharmacokinetics ; Linoleic Acid - toxicity ; Lipid Peroxidation ; Lymphocytes - metabolism ; malondialdehyde ; Malondialdehyde - blood ; Medical sciences ; Oxidation-Reduction ; oxidative stress ; palmitic acid ; Palmitic Acid - administration & dosage ; Reactive Oxygen Species ; toxicity testing ; Toxicology ; vitamin A ; Vitamin A - blood</subject><ispartof>Food and chemical toxicology, 2003-03, Vol.41 (3), p.351-358</ispartof><rights>2003 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c390t-eb465ce49ca1cd6100d83fee86d0b7e36f9c59ac54f8e73442c15c890f0a87b93</citedby><cites>FETCH-LOGICAL-c390t-eb465ce49ca1cd6100d83fee86d0b7e36f9c59ac54f8e73442c15c890f0a87b93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=14441684$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12504167$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kok, T.M.C.M. de</creatorcontrib><creatorcontrib>Zwingman, I</creatorcontrib><creatorcontrib>Moonen, E.J</creatorcontrib><creatorcontrib>Schilderman, P.A.E.L</creatorcontrib><creatorcontrib>Rhijnsburger, E</creatorcontrib><creatorcontrib>Haenen, G.R.M.M</creatorcontrib><creatorcontrib>Kleinjans, J.C.S</creatorcontrib><title>Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid</title><title>Food and chemical toxicology</title><addtitle>Food Chem Toxicol</addtitle><description>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.</description><subject>Adult</subject><subject>alpha-tocopherol</subject><subject>alpha-Tocopherol - blood</subject><subject>Analysis of Variance</subject><subject>antioxidant activity</subject><subject>Antioxidants - metabolism</subject><subject>beta Carotene - blood</subject><subject>beta-carotene</subject><subject>Biological and medical sciences</subject><subject>blood serum</subject><subject>dietary fat</subject><subject>Dietary Supplements</subject><subject>DNA damage</subject><subject>DNA Damage - drug effects</subject><subject>Dose-Response Relationship, Drug</subject><subject>fat intake</subject><subject>Female</subject><subject>Food toxicology</subject><subject>genotoxicity</subject><subject>Humans</subject><subject>linoleic acid</subject><subject>Linoleic Acid - administration & dosage</subject><subject>Linoleic Acid - blood</subject><subject>Linoleic Acid - pharmacokinetics</subject><subject>Linoleic Acid - toxicity</subject><subject>Lipid Peroxidation</subject><subject>Lymphocytes - metabolism</subject><subject>malondialdehyde</subject><subject>Malondialdehyde - blood</subject><subject>Medical sciences</subject><subject>Oxidation-Reduction</subject><subject>oxidative stress</subject><subject>palmitic acid</subject><subject>Palmitic Acid - administration & dosage</subject><subject>Reactive Oxygen Species</subject><subject>toxicity testing</subject><subject>Toxicology</subject><subject>vitamin A</subject><subject>Vitamin A - blood</subject><issn>0278-6915</issn><issn>1873-6351</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0Etv1DAQwHELUdGl8BEAX0D0EJiJH3GOq_KqVMGhVBytWWfcGuWxjRNovz3Z7oqe5vIbW_MX4hXCBwS0Hy-hrFxhazTvoTwFKFVVmCdiha5ShVUGn4rVf3Isnuf8GwAqrOwzcYylAY22Wolf657a-5yyHKIc7lJDU_rD8tP3tWyoo2uWFCce5c3cUS-bxBON9zLP223LHffTwode_k3TjWxTP7ScgqSQmhfiKFKb-eVhnoirL59_nn0rLn58PT9bXxRB1TAVvNHWBNZ1IAyNRYDGqcjsbAObipWNdTA1BaOj40ppXQY0wdUQgVy1qdWJeLd_dzsOtzPnyXcpB25b6nmYs0dnldO1WaDZwzAOOY8c_XZM3XKMR_C7ov6hqN_l8lD6h6J-t_f68MG86bh53DokXMDbA6AcqI0j9SHlR6f1wpxe3Ju9izR4uh4Xc3VZAipAUCUqVP8Aea-IGA</recordid><startdate>20030301</startdate><enddate>20030301</enddate><creator>Kok, T.M.C.M. de</creator><creator>Zwingman, I</creator><creator>Moonen, E.J</creator><creator>Schilderman, P.A.E.L</creator><creator>Rhijnsburger, E</creator><creator>Haenen, G.R.M.M</creator><creator>Kleinjans, J.C.S</creator><general>Elsevier Science</general><scope>FBQ</scope><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7U7</scope><scope>C1K</scope></search><sort><creationdate>20030301</creationdate><title>Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid</title><author>Kok, T.M.C.M. de ; Zwingman, I ; Moonen, E.J ; Schilderman, P.A.E.L ; Rhijnsburger, E ; Haenen, G.R.M.M ; Kleinjans, J.C.S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c390t-eb465ce49ca1cd6100d83fee86d0b7e36f9c59ac54f8e73442c15c890f0a87b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Adult</topic><topic>alpha-tocopherol</topic><topic>alpha-Tocopherol - blood</topic><topic>Analysis of Variance</topic><topic>antioxidant activity</topic><topic>Antioxidants - metabolism</topic><topic>beta Carotene - blood</topic><topic>beta-carotene</topic><topic>Biological and medical sciences</topic><topic>blood serum</topic><topic>dietary fat</topic><topic>Dietary Supplements</topic><topic>DNA damage</topic><topic>DNA Damage - drug effects</topic><topic>Dose-Response Relationship, Drug</topic><topic>fat intake</topic><topic>Female</topic><topic>Food toxicology</topic><topic>genotoxicity</topic><topic>Humans</topic><topic>linoleic acid</topic><topic>Linoleic Acid - administration & dosage</topic><topic>Linoleic Acid - blood</topic><topic>Linoleic Acid - pharmacokinetics</topic><topic>Linoleic Acid - toxicity</topic><topic>Lipid Peroxidation</topic><topic>Lymphocytes - metabolism</topic><topic>malondialdehyde</topic><topic>Malondialdehyde - blood</topic><topic>Medical sciences</topic><topic>Oxidation-Reduction</topic><topic>oxidative stress</topic><topic>palmitic acid</topic><topic>Palmitic Acid - administration & dosage</topic><topic>Reactive Oxygen Species</topic><topic>toxicity testing</topic><topic>Toxicology</topic><topic>vitamin A</topic><topic>Vitamin A - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kok, T.M.C.M. de</creatorcontrib><creatorcontrib>Zwingman, I</creatorcontrib><creatorcontrib>Moonen, E.J</creatorcontrib><creatorcontrib>Schilderman, P.A.E.L</creatorcontrib><creatorcontrib>Rhijnsburger, E</creatorcontrib><creatorcontrib>Haenen, G.R.M.M</creatorcontrib><creatorcontrib>Kleinjans, J.C.S</creatorcontrib><collection>AGRIS</collection><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Toxicology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>Food and chemical toxicology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kok, T.M.C.M. de</au><au>Zwingman, I</au><au>Moonen, E.J</au><au>Schilderman, P.A.E.L</au><au>Rhijnsburger, E</au><au>Haenen, G.R.M.M</au><au>Kleinjans, J.C.S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid</atitle><jtitle>Food and chemical toxicology</jtitle><addtitle>Food Chem Toxicol</addtitle><date>2003-03-01</date><risdate>2003</risdate><volume>41</volume><issue>3</issue><spage>351</spage><epage>358</epage><pages>351-358</pages><issn>0278-6915</issn><eissn>1873-6351</eissn><coden>FCTOD7</coden><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, 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.</abstract><cop>Oxford</cop><cop>New York, NY</cop><pub>Elsevier Science</pub><pmid>12504167</pmid><doi>10.1016/S0278-6915(02)00237-5</doi><tpages>8</tpages></addata></record> |
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subjects | Adult alpha-tocopherol alpha-Tocopherol - blood Analysis of Variance antioxidant activity Antioxidants - metabolism beta Carotene - blood beta-carotene Biological and medical sciences blood serum dietary fat Dietary Supplements DNA damage DNA Damage - drug effects Dose-Response Relationship, Drug fat intake Female Food toxicology genotoxicity Humans linoleic acid Linoleic Acid - administration & dosage Linoleic Acid - blood Linoleic Acid - pharmacokinetics Linoleic Acid - toxicity Lipid Peroxidation Lymphocytes - metabolism malondialdehyde Malondialdehyde - blood Medical sciences Oxidation-Reduction oxidative stress palmitic acid Palmitic Acid - administration & dosage Reactive Oxygen Species toxicity testing Toxicology vitamin A Vitamin A - blood |
title | Analysis of oxidative DNA damage after human dietary supplementation with linoleic acid |
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