NO - Besoin d'assistance

Mechanisms and Biomarkers (WG 4) page 52
__________________________________________________________________________________________
as demonstrated by the consistent literature. As regards human intervention studies, generally
supplements at high concentrations are used rather than dietary doses or rich foods. Thus
definitive conclusions can not be drawn without considering the limits of interpretation of
such works. However the most relevant literature on the evidence on vitamin E, vitamin C,
and β-carotene against the major biomarkers of oxidative stress (lipid peroxidation and DNA
damage) are reported.
Lipid peroxidation
Vitamin E - The most consistent data with respect to micronutrient antioxidants and
atherosclerosis appear to relate to α-tocopherol, which is the quantitatively most important
antioxidant present in LDLs, followed by retinyl stearate, γ-tocopherol, β-carotene, and
lycopene (Esterbauer et al., 1990).
There is good evidence that α-tocopherol has significant protective effect against LDL
oxidation. Apart from in vitro studies, several in vivo studies demonstrated that vitamin E
supplementation increased the resistance of LDLs to oxidative modification, nevertheless the
doses used were generally very high, also higher than those usually contained in α-tocopherol
supplements. Furthermore, in many studies small numbers of subjects were supplemented and
most had no randomized control groups.
Supplementation with 1200-1600 mg/day vitamin E led to a ≈50% decrease in susceptibility
of LDL to oxidation (Reaven et al., 1993; Princen et al., 1992; Reaven and Witztum, 1993;
Fuller et al., 1998; Reaven et al., 1996; Dieber-Rotheneder et al., 1991).
A significant effect was reported also using lower amounts (Princen et al., 1992; Dieber-
Rotheneder et al., 1991; Jialal and Grundy, 1992; Astley et al., 1999; Simons et al., 1996;
Suzukava et al., 1995), however always greatly exceeding the RDA. 400 IU/day α-tocopherol
for 8 weeks (Marangon et al., 1999) prolonged LDL lag time of lipid peroxide formation and
conjugated dienes after copper-catalyzed LDL oxidation, decreased urinary F2-isoprostanes.
The supplementation of 50 smokers with 280 mg α-tocopherol acetate daily for 10 weeks
determined a reduction of plasma concentrations of lipid peroxides, thiobarbituric acid
reactive substances and conjugated dienes (Brown et al., 1994). There was also a significant
reduction in erythrocyte lipid peroxidation. In a similar study (Porkkala-Sarataho et al., 1998)
200 mg α-tocopheryl acetate/day elevated oxidation resistance of VLDL+LDL, prolonging
the lag time by 34% when assessed with a copper-induced method and by 109% when
assessed with a hemin + hydrogen peroxide-induced method. The same dose (200 mg/day)