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)