Oxidative stress is now linked to a number of diseases including cardiovascular disease and cancer. The damaging effects of oxidation are thought to contribute greatly to age-related deterioration of tissues and organs. Because of the link between oxidation and disease, nutrients that possess antioxidant properties are of interest to researchers. Many plant compounds such as flavonoids and carotenoids, as well as certain vitamins and minerals are known to possess antioxidant properties in vivo. While most plant antioxidants are water soluble, vitamin E and carotenoids are different in that they are both fat soluble, and this gives then unique properties in disease prevention. Being hydrophobic allows vitamin E and carotenoids to associate with lipid components in cells such as the cell membrane, where they may inhibit lipid peroxidation. Epidemiological studies suggest that both carotenoids and vitamin E intakes are inversely associated with some cancers and heart disease, respectively.
To investigate the effects of vitamin E and carotenoids on lipid peroxidation, 105 healthy study volunteers were randomly assigned to receive 25 g/d of spread containing 43 mg of α-tocopherol equivalents and 0.45 mg of carotenoids (50% lutein, 25% β-carotene, 10% α-carotene and 15% lycopene) (spread A), 111 mg of α-tocopherol equivalents and 1.24 mg of carotenoids (spread B) or 1.3 mg of d-α-tocopherol with no carotenoids (spread C). After 15 weeks, those individuals consuming spread A had a 31% increase in α-tocopherol plasma levels as well as a small increase in plasma carotenoid levels. This resulted in a significant increase in LDL oxidation resistance, probably due to a 17% rise in antioxidant capacity. The results for those consuming spread B were even greater, suggesting that vitamin E and carotenoids had a dose dependent effect on lipid peroxidation.
In addition spread B caused a 15% decrease in the lipid peroxidation marker F2α-isoprene after 15 weeks, but this effect was not seen with spread A or spread C. Those consuming spread B also had greater increases in plasma levels of vitamin E and carotenoids. The rise in the plasma levels of carotenoids was greater than expected from previous studies, and this can be explained because the absorption of carotenoids from a fat spread would be greater than from vegetables. Evidence suggests that large increases in plasma vitamin E and carotenoid levels are not possible from dietary sources because a substantial increase in fruit and vegetables would be required. Of the carotenoids, only lycopene plasma levels did not rise, and this is likely due to the higher intakes of lycopene in the subjects normal diets that masked the 2 to 4% rise caused by the supplement spread.
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