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Mechanisms and Biomarkers (WG 4) page 56
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(corresponding to 500 mg ascorbic acid) for 2 months. Sanchez-Quesada et al. (1998)
demonstrated that oral supplementation with 1 g ascorbic acid protects LDL from the
increased susceptibility to oxidation that occurs after intense aerobic exercise. This inhibition
had been attributed to the antioxidant role of ascorbic acid in the seeding of LDL with
hydroperoxide, and to the regeneration of oxidized α-tocopherol contained in LDL after its
exercise-induced consumption.
Combined supplementation - Whether the capacity of each single antioxidant to reduce
susceptibility of LDL to oxidation is additive when antioxidants are given in combined
supplementation, has not been determined in depth. Jialal and Grundy (1993) studied the
effect of combined supplementation with α-tocopherol (800 IU/day) plus ascorbate
(1.0 g/day) and β-carotene (30 mg/day) on copper-catalysed LDL oxidation in a randomised,
placebo-controlled study over a 3-month period, and found that the combined
supplementation resulted in a twofold prolongation of the lag phase and a 40% decrease in the
oxidation rate. The combined antioxidant group was also compared with a group that received
800 IU of α-tocopherol only, but no significant differences between the two groups with
respect to LDL oxidation kinetics were observed. In a similar study with a daily supplement
of 18 mg β-carotene, 900 mg vitamin C and 200 mg vitamin E over a 6-month period, Abbey
et al. (1993) found a lengthened lag time before the onset of oxidation after antioxidant
supplementation (28% after 3 months and 35% after 6 months), but no difference in the rate
of oxidation. In addition there was a significant correlation between prolongation of the lag
phase and LDL α-tocopherol content, but no correlation with β-carotene content. Mackness et
al. (1993) supplemented 16 volunteers with selenium-ACE tablets (200 mg selenium, 18 mg
β-carotene, 180 mg vitamin C and 74 mg vitamin E daily) for 20 days and provided further
evidence that these substances can protect isolated LDL against Cu 2+ catalysed oxidation.
However, as in their experiments antioxidant supplements produced significant decreases in
the rate of conjugated diene formation but had no effect on the subsequent generation of lipid
peroxides, they suggested to be cautious in increasing antioxidant vitamin intake in order to
make LDL in the artery wall more resistant to oxidation. It seems therefore that natural
antioxidants such as vitamin E, are rapidly exhausted and may offer little long-term
protection. In contrast, Nyyssönen et al. (1994) supplemented 40 smokers with 400 mg
ascorbic acid, 100 µg organic selenium, 200 mg α-tocopherol, 30 mg β-carotene and found a
27% increase in lag time to oxidation of VLDL+LDL: the increase in the oxidation lag time