Assessment Of Vitamin E Nutritional Status

The most commonly used index of vitamin E nutritional status is the plasma concentration of a-tocopherol; because it is transported in plasma lipoproteins, it is best expressed per mole of cholesterol or per milligram of total plasma lipids (Horwitt et al., 1972; Winbauer et al., 1999). The reference range is

Table 4.3 Indices of Vitamin E Nutritional Status

Deficient Low

Acceptable

Desirable

Plasma tocopherol, |xmol/L <12 12-16

>16

>30

Plasma tocopherol, |imol/g plasma <1.1 1.1-1.86

>1.86

>3.4

total lipid

Plasma tocopherol, mmol/mol <2.2 2.2-2.25

>2.25

>4.0

cholesterol

Erythrocyte fragility — —

<0.05

Ratio of hemolysis by

H2O2:H2O

Sources: From data reported by Horwitt et al., 1972; Sauberlich et al., rissey and Sheehy, 1999.

1974; Mor-

12 to 37 ^mol per L; ranges associated with inadequate and desirable status are shown in Table 4.3; an optimum concentration for protection against cardiovascular disease and cancer is >30 ^mol per L (Morrissey and Sheehy, 1999).

Erythrocytes are incapable of de novo lipid synthesis, 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 induced by either hydrogen peroxide or dialuric acid. This gives a means of assessing the functional adequacy of vitamin E intake, albeit one that will be masked by adequate selenium intake and may be affected by other, unrelated factors. Plasma concentrations of a-tocopherol greater than 14 ^mol per L are adequate to prevent significant hemolysis; less than 2.2 mmol per mol of cholesterol or 1.1 ^mol per g of total plasma lipid is associated with increased susceptibility of erythrocytes to induced hemolysis in vitro.

Overall antioxidant status, as opposed to specifically vitamin E status, can be assessed by a variety of measures of lipid peroxidation, including measurement of:

1. Plasma total thiobarbituric acid-reacting substances (TBARS);

2. F2 isoprostanes, the isomers of prostaglandin F2 that are formed by radical-catalyzed peroxidation of arachidonic acid in membranes.

3. The exhalation of pentane arising from the catabolism of the products of peroxidation of «6 polyunsaturated fatty acids or ethane arising from «3 polyunsaturated fatty acids. Intravenous infusion of a lipid mixture rich in linoleic acid stresses antioxidant capacity and results in increased breathpentane; this is more marked in subjects withlow vitamin E status, and the administration of vitamin E reduces the exhalation of pentane (Tappel and Dillard, 1981;Lemoyne etal., 1988; Van Gossumetal., 1988).

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