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Companion Animals: Vitamin E
Properties and Metabolism

Vitamin E activity in foods and feedstuffs is derived from a series of compounds of plant origin, the tocopherols and tocotrienols. The term vitamin E, according to the International Union of Pure and Applied Chemistry-International Union of Biochemistry (IUPAC-IUB) Commission on Biochemical Nomenclature, is used as a generic descriptor for all tocol and tocotrienol derivatives that qualitatively exhibit the biologic activity of alpha-tocopherol (IUPAC-IUB, 1973). Both the tocols (tocopherols) and tocotrienols consist of a hydroquinone nucleus and an isoprenoid side chain. Characteristically, tocols have a saturated side chain, whereas the tocotrienols have an unsaturated side chain containing three double bonds. There are four principal compounds of each of these two sources of vitamin E activity (alpha, beta, gamma, delta), differentiated by the presence of methyl (-CH3) groups at positions 5, 7 or 8 of the chroman ring (Figure 1). Alpha-tocopherol, the most biologically active of these compounds, is the predominant vitamin E active compound in feedstuffs and the form used commercially for supplementation of animal diets. The biological activity of the other tocols is limited (Table 1).
Figure 1
Table 1

There are three asymmetric carbon atoms in the tocopherol molecule located at the 2, 4', and 8' positions. The d-form of alpha-tocopherol has all of the methyl groups in these positions facing in one direction and is referred to as the RRR-form. This is the form found in plants. The dl- or chemically synthesized form of alpha-tocopherol has an equal mixture of the R and S configurations at each of the three positions, (i.e., it contains eight stereoisomers) and is referred to as the all-rac (for racemic) form of the compound.

Commercially there is no truly "natural" tocopherol product available since the d-alpha-tocopherol commercial products are obtained from the original raw material only after several chemical processing steps. Hence, it should be referred to as "natural-derived" and not natural. In addition, the international unit (IU) is the standard of vitamin E activity, and consequently it is the same regardless of the source.

Typically, deodorizer distillates produced during the purification and manufacture of vegetable oils are utilized in the production of d-alpha-tocopherol or tocopheryl acetate. These deodorizer distillates contain a mixture of alpha-, beta-, gamma- and delta-tocopherols, and this mixture is extracted and purified. In the final process, ultra-vacuum molecular distillation is performed and the end material methylated to produce an alpha-tocopherol concentrate. This material may then be acetylated. The acetate ester is used because it is more stable in processing and storage of foods and feeds than the alcohol (tocopherol) form.

All-rac-alpha-tocopherol acetate is the most common vitamin E form used to supplement animal feeds. This form of vitamin E is manufactured by condensing trimethyl hydroquinone and isophytol and conducting ultra-vacuum molecular distillation, producing a highly purified form of alpha-tocopherol. This material may then be acetylated. As previously stated, all-rac-alpha-tocopherol is a mixture of eight stereoisomers (four enantiomeric pairs) of alpha-tocopherol acetate. The enantiomeric pairs, racemates, have been shown to be present in equimolar amounts (Cohen et al., 1981; Weiser and Vecchi, 1981, 1982; Scott et al., 1982). This finding indicates that the manufacturing processes employed lead to all-rac-alpha-tocopherol acetate with similar proportions of all eight stereoisomers (Weiser and Vecchi, 1982).

Alpha-tocopherol is a yellow oil that is insoluble in water but soluble in organic solvents (Illus. 1). Tocopherols are extremely resistant to heat but readily oxidized. Natural vitamin E is subject to destruction by oxidation, which is accelerated by heat, moisture, rancid fat, copper, and iron. Alpha-tocopherol is an excellent naturally occurring antioxidant that protects carotene and other oxidizable materials in the feed and in the body. However, in the process of acting as an anti-oxidant, it is oxidized and becomes biologically inactive.
Illustration 1

The naturally occurring tocopherol form is subject to destruction in the digestive tract to some extent, while the acetate ester is not. Much of the acetate is readily split off in the intestinal wall and the alcohol is absorbed, thereby permitting the vitamin to function as a biological antioxidant. Any acetate form absorbed into the body is converted to the alcohol form.

Vitamin E absorption is related to fat digestion and is facilitated by bile and pancreatic lipase (Sitrin et al., 1987). Whether presented as free alcohol or as esters, most vitamin E is absorbed as the alcohol. Esters are largely hydrolyzed in the intestinal wall, and the free alcohol enters the intestinal lacteals and is transported via the lymph to the general circulation.

The animal appears to have preference for tocopherol versus other tocols. Rates and amounts of absorption of the various tocopherols and tocotrienols are in the same general order of magnitude as their biological potencies. Alpha-tocopherol is absorbed best, with gamma-tocopherol absorption slightly less than that of alpha-forms but with a more rapid excretion. It can be generally assumed that most of the vitamin E activity within plasma and other animal tissues is alpha-tocopherol (Ullrey, 1981). Vitamin E in plasma is attached mainly to lipoproteins in the globulin fraction within cells and occurs mainly in mitochondria and microsomes. The vitamin is taken up by the liver and is released in combination with low-density lipoprotein (LDL) cholesterol.

Vitamin E does not cross the placenta in any appreciable amounts; however, it is concentrated in colostrum (Van Saun et al., 1989). With respect to neonatal ruminants (Hidiroglou et al., 1969; Van Saun et al., 1989) and baby pigs (Mahan, 1991), several investigators have reported limited placental transport of alpha-tocopherol, making neonates highly susceptible to vitamin E deficiency. This may be related to either a decreasing efficiency in placental vitamin E transfer as gestation proceeds, a dilution effect as a result of rapid fetal growth or possibly a decrease in available maternal vitamin E. With limited placental transfer of vitamin E, newborns must rely heavily on ingestion of colostrum as a source of vitamin E. Van Saun et al. (1989) reported decreased fetal serum vitamin E concentrations with increasing fetal age. Additionally, these authors reported less of a decline in fetal serum vitamin E concentration during gestation in fetuses from vitamin E-adequate dams.

There is inefficient placental transfer of vitamin E but high levels of the vitamin have been shown in calves (Nockels, 1991) and lambs (Njeru et al., 1994) after consumption of colostrum. Nockels (1991) reported alpha-tocopherol levels in plasma from beef calves prior to colostrum consumption, and for several days thereafter. Precolostral plasma vitamin E levels averaged 0.2 µg per ml and increased to 3.3 µg per ml at five to eight days of age. Njeru et al. (1994) fed ewes dl-alpha-tocopherol acetate at graded levels (0, 15, 30 and 60 IU per head daily) to study placental and mammary gland transfer. Supplemental vitamin E had no effect on serum alpha-tocopherol of lambs prior to nursing, averaging 0.35 µg per ml. By day 3, lamb serum tocopherol increased to 1.41, 1.84, 2.43 and 4.46 µg per ml, respectively, for the four supplemental dietary levels of vitamin E (Table 2). Vitamin E at the given levels of supplementation increased colostral alpha-tocopherol at a linear rate of 3.3, 6.8, 8.0, and 9.6 µg per ml, respectively. The importance of providing colostrum rich in vitamin E is quite apparent, as both calves and lambs are born with low levels of the vitamin (Nockels, 1991; Njeru et al., 1994). Low blood vitamin E may lead to diminished disease resistance and immune response in the neonate (Nockels, 1991).

Less than 1% of the dam’s tocopherol intake is secreted in the milk (Millar et al., 1973), however, colostrum tocopherol concentration is directly affected by maternal intake (Whitting and Loosli, 1948). Levels of vitamin E in the colostrum are considerably higher than in milk.

The detailed mechanism of tocopherol uptake and retention by tissues is unknown, but relatively little storage occurs. The liver is not a storage organ for vitamin E. It contains only a small fraction of total body stores, in contrast to vitamin A, for which about 95% of the body reserves are in the liver. Small amounts of vitamin E will persist tenaciously in the body for a long time. However, stores are exhausted rapidly by polyunsaturated fatty acids (PUFA) in the tissues, the rate of disappearance being proportional to the intake of PUFA. A major excretory route of absorbed vitamin E is bile, in which tocopherol appears mostly in the free form. Tocopherol entering the circulatory system becomes distributed throughout the body with the majority localizing in the fatty tissues. Subcellular fractions from different tissues vary considerably in their tocopherol content, with the highest levels found in membranous organelles, such as microsomes and mitochondria, that contain highly active oxidation-reduction systems (McCay et al., 1981; Taylor et al., 1976)

 
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