Supplementation with vitamin E but not with vitamin C lowers lipid peroxidation in vivo in mildly hypercholesterolemic men

• Published in: Free radical research Vol. 35; no. 6; pp. 967 - 978
• Main Authors: Kaikkonen, Jari, Porkkala-Sarataho, Elina, Morrow, Jason D., Roberts, L. Jackson, Nyyssönen, Kristiina, Salonen, Riitta, Tuomainen, Tomi-Pekka, Ristonmaa, Ulla, Poulsen, Henrik E., Salonen, Jukka T.
• Format: Journal Article
• Language: English
• Published: England Informa UK Ltd 01.01.2001; Taylor & Francis
• Subjects: Aged; Analysis of Variance; Antioxidants; Ascorbic Acid - blood; Ascorbic Acid - pharmacology; Clinical trials; Dietary Supplements; F2-Isoprostanes - blood; Gas Chromatography-Mass Spectrometry; Humans; Hypercholesterolemia - metabolism; isoprostane; Lipid peroxidation; Lipid Peroxidation - drug effects; Male; Middle Aged; Smoking; Vitamin C; Vitamin E; Vitamin E - blood; Vitamin E - pharmacology
• ISSN: 1071-5762; 1029-2470
• DOI: 10.1080/10715760100301461

Although the use of vitamin E supplements has been associated with a reduction in coronary events, assumed to be due to lowered lipid peroxidation, there are no previous long-term clinical trials into the effects of vitamin C or E supplementation on lipid peroxidation in vivo. Here, we have studied the long-term effects of vitamins C and E on plasma F2-isoprostanes, a widely used marker of lipid peroxidation in vivo. As a study cohort, a subset of the "Antioxidant Supplementation in Atherosclerosis Prevention" (ASAP) study was used. ASAP is a double-masked placebo-controlled randomized clinical trial to study the long-term effect of vitamin C (500 mg of slow release ascorbate daily), vitamin E (200 mg of d-α-tocopheryl acetate daily), both vitamins (CellaVie®), or placebo on lipid peroxidation, atherosclerotic progression, blood pressure and myocardial infarction (n = 520 at baseline). Lipid peroxidation measurements were carried out in 100 consecutive men at entry and repeated at 12 months. The plasma F2-isoprostane concentration was lowered by 17.3% (95% CI 3.9-30.8%) in the vitamin E group (p = 0.006 for the change, as compared with the placebo group). On the contrary, vitamin C had no significant effect on plasma F2-isoprostanes as compared with the placebo group. There was also no interaction in the effect between these vitamins. In conclusion, long-term oral supplementation of clinically healthy, but hypercholesterolemic men, who have normal vitamin C and E levels with a reasonable dose of vitamin E lowers lipid peroxidation in vivo, but a relatively high dose of vitamin C does not. This observation may provide a mechanism for the observed ability of vitamin E supplements to prevent atherosclerosis.