Vitamin B12 is a dark-red, hygroscopic, needle-shaped crystal, freely soluble in water and alcohol but insoluble in acetone, chloroform and ether. Cyanocobalamin has a molecular weight of 1,355. Oxidizing and reducing agents and exposure to sunlight tend to destroy its activity. Losses of vitamin B12 during feed processing are usually not excessive because vitamin B12 is stable at temperatures lower than 482†F (250†C).
On average 3% of dietary cobalt is converted to vitamin B12, and only 1% to 3% of the vitamin B12 synthesized in the rumen is absorbed from the small intestine (Girard, 1998a). In ruminants, as in most species, the distal small intestine (ileum) is the primary absorptive site for vitamin B12. Substantial amounts of vitamin B12 are secreted into the duodenum and reabsorbed in the ileum, a process that is presumably subject to regulation based on the vitamin B12 status of the animal.
Absorption of vitamin B12 requires the presence of the intrinsic factor, a glycoprotein synthesized by the parietal cells of the gastric mucosa (McDowell, 2000). Pernicious anemia in humans is caused by a lack of the intrinsic factor. Recently, a second factor, transcobalamin II, has been identified in the intestinal villus (Quadros et al., 2000). Vitamin B12 absorption also occurs by diffusion, but only at very high concentrations (Ellenbogen and Cooper, 1991). In ruminants, vitamin B12 absorption requires the following: (a) adequate quantities of dietary vitamin B12 or cobalt; (b) a functional abomasum for digestion of food proteins and release of vitamin B12 and the production of intrinsic factor; (c) a functional pancreas (trypsin secretion) for protein digestion and release of bound vitamin B12 ; (d) a functional ileum. Intrinsic factor has been demonstrated in the cow but not the sheep. Factors that diminish vitamin B12 absorption include deficiencies of protein, iron and vitamin B6; thyroid removal/ hypothyroidism; and dietary tannic acid. Cobalamin analogs may compose up to 50% of the total plasma vitamin B12 in cattle, but are undetectable in sheep (Halpin et al., 1984).
Storage of vitamin B12 occurs principally in the liver. Other storage sites include the kidney, heart, spleen and brain. Andrews et al. (1960) reported that the proportion of liver cobalt that occurs as vitamin B12 varies with the cobalt status of the animal. In cattle or sheep grazing cobalt-adequate pastures, most of the cobalt in the liver is in the form of vitamin B12. However, in cobalt deficiency only about 33% of liver cobalt is in the form of vitamin B12. This indicates that during cobalt deficiency vitamin B12 is depleted more rapidly than other forms of cobalt in the liver.
Unlike the other water-soluble vitamins, vitamin B12 is stored in significant amounts in the liver and other tissues, providing a reserve in times of cobalt depletion. Kominato (1971) reported a tissue half-life of 32 days, indicating considerable tissue storage. Cattle and sheep with normal liver stores can tolerate a cobalt-deficient diet for several months without showing vitamin B12 deficiency signs.
In ruminants, both cobalt and vitamin B12 are excreted primarily in the feces, with smaller amounts excreted in urine (Smith and Marston, 1970). Lactating cows fed normal diets excrete 86% to 87.5% of all excreted cobalt in the feces (mainly associated with bile acids), 0.9% to 1.0% in the urine, and 11.5% to 12.5% in milk.
