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dc.contributor.authorMeagher, Emma A.
dc.contributor.authorBarry, Orla Patricia
dc.contributor.authorLawson, John A.
dc.contributor.authorRokach, Joshua
dc.contributor.authorFitzGerald, Garret Gerald A.
dc.date.accessioned2017-12-05T21:16:26Z
dc.date.available2017-12-05T21:16:26Z
dc.date.issued2001-03
dc.identifier.citationMeagher, E. A., Barry, O. P., Lawson, J. A., Rokach, J., & FitzGerald, G. A. (2001). Effects of vitamin E on lipid peroxidation in healthy persons. Journal of the American Medical Association, 285(9), 1178-1182.en_US
dc.identifier.urihttp://hdl.handle.net/11141/2202
dc.descriptionAdult, Aldehydes, Antioxidants, Dietary Supplements, Dinoprost, Dose-Response Relationship, Drug Double-Blind Method Female Humans Lipid, Peroxidation, Male, Oxidative, Stress Reference, Values,Vitamin Een_US
dc.description.abstractContext: Oxidative stress may play a role in the development or exacerbation of many common diseases. However, results of prospective controlled trials of the effects of antioxidants such as vitamin E are contradictory. Objective: To assess the effects of supplemental vitamin E on lipid peroxidation in vivo in healthy adults. Design: Randomized, double-blind, placebo-controlled trial conducted March 1999 to June 2000. Setting: A general clinical research center in a tertiary referral academic medical center. Participants: Thirty healthy men and women aged 18 to 60 years. Interventions: Participants were randomly assigned to receive placebo or α-tocopherol dosages of 200, 400, 800, 1200, or 2000 IU/d for 8 weeks (n=5 in each group), followed by an 8-week washout period. Main Outcome Measures: Three indices of lipid peroxidation, urinary 4-hydroxynonenal (4-HNE) and 2 isoprostanes, iPF2n-III and iPF2α-VI, measured by gas chromatography/mass spectrometry and compared among the 6 groups at baseline, 2, 4, 6, and 8 weeks, and 1, 3, and 8 weeks after discontinuation. Results: Circulating vitamin E levels increased in a dose-dependent manner during the study. No significant effect of vitamin E on levels of urinary 4-HNE or either isoprostane was observed. Mean (SEM) baseline vs week 8 levels of iPF2α-III were 154 (20.1) vs 168 (22.3) pg/mg of creatinine for subjects taking placebo; 165 (19.6) vs 234 (30.1) pg/mg for those taking 200 IU/d of vitamin E; and 195 (26.7) vs 213 (40.6) pg/mg for subjects taking 2000 IU/d. Corresponding iPF2α-VI levels were 1.43 (0.6) vs 1.62 (0.4) ng/mg of creatinine for subjects taking placebo; 1.64 (0.3) vs 1.24 (0.8) ng/mg for those taking 200 IU/d of vitamin E; and 1.83 (0.3) vs 1.94 (0.9) ng/mg for those taking 2000 IU/d. Baseline vs week 8 levels of 4-HNE were 0.5 (0.04) vs 0.4 (0.05) ng/mg of creatinine for subjects taking placebo; 0.4 (0.06) vs 0.5 (0.02) ng/mg with 200 IU/d of vitamin E; and 0.2 (0.02) vs 0.2 (0.1) ng/mg with 2000 IU/d. Conclusions: Our results question the rationale for vitamin E supplementation in healthy individuals. Specific quantitative indices of oxidative stress in vivo should be considered as entry criteria and for dose selection in clinical trials of antioxidant drugs and vitamins in human disease.en_US
dc.language.isoen_USen_US
dc.rights© 2001 American Medical Associationen_US
dc.rights.urihttp://jamanetwork.com/journals/jama/pages/instructions-for-authors#SecDepositingResearchArticlesinApprovedPublicRepositoriesen_US
dc.titleEffects of vitamin E on lipid peroxidation in healthy personsen_US
dc.typeArticleen_US


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