Vitamin E requirements
It is difficult to establish vitamin E requirements, partly because deficiency is more or less unknown, but also because the requirement depends on the intake of PUFAs. It is generally accepted, albeit with little experimental evidence, that an acceptable intake of vitamin E is 0.4 mg α-tocopherol equivalent/g dietary PUFA.
The plasma concentration of α-tocopherol is used to assess vitamin E status; since most vitamin E is trans-ported in plasma lipoproteins, it is the concentration per gram total plasma lipid, or better per mole cholesterol, that is useful, rather than the simple concentration.
Erythrocytes are incapable of de novo lipid synthe-sis, so peroxidative damage resulting from oxygen stress has a serious effect, shortening red cell life and possibly precipitating hemolytic anemia in vitamin E deficiency. This has been exploited as a method of assessing status by measuring the hemolysis of red cells induced by dilute hydrogen peroxide relative to that observed on incubation in water. This gives a means of assessing the functional adequacy of vitamin E intake, albeit one that will be affected by other, unre-lated, factors. Plasma concentrations of α-tocopherol below 2.2 mmol/mol cholesterol or 1.1 μmol/g total plasma lipid are associated with increased susceptibil-ity of erythrocytes to induced hemolysis in vitro.
An alternative method of assessing functional anti-oxidant status, again one that is affected by both vitamin E and other antioxidants, is by measuring the exhalation of pentane arising from the catabolism of the products of peroxidation of n-6 PUFAs or ethane arising from n-3 PUFAs.
There is good epidemiological evidence that intakes of vitamin E are associated with a lower risk of ath-erosclerosis and ischemic heart disease. High concen-trations of vitamin E will inhibit the oxidation of PUFAs in plasma lipoproteins, and it is this oxidation that is responsible for the development of atheroscle-rosis. The plasma concentrations of α-tocopherol that appear to be beneficial would require an intake of 17–40 mg/day, which is above what could be achieved by eating normal diets. Individual interven-tion trials of vitamin E supplements have generally been disappointing, and metaanalysis shows a signifi-cant increase in all-cause mortality among people taking vitamin E (and other antioxidant) supple-ments. This presumably reflects the fact that the stable tocopheroxyl radical can penetrate deeper into tissues and plasma lipoproteins, and increase radical damage. However, it is also possible that the plasma concentra-tion of α-tocopherol is a surrogate marker for some other protective factor in the diet.
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