Vitamin K1 is a golden yellow, viscous oil. Naturally occurring sources of vitamin K are fat soluble; stable to heat; and labile to oxidation, alkali, strong acids, light and irradiation. Vitamin K1 is slowly degraded by atmospheric oxygen, but fairly rapidly destroyed by light. In contrast to naturally occurring sources of vitamin K, vitamin K3 salts of menadione are water soluble.
Vitamin K antagonists increase the need for this vitamin. Deficiency of this vitamin is produced by ingestion of the antagonist, dicumarol, or by feeding of sulfonamides (in monogastric species) at levels sufficient to inhibit intestinal synthesis of vitamin K. Supplementation of vitamin K will overcome the anticoagulation effect of dicumarol. Mycotoxins are also antagonists that may cause vitamin K deficiency.
Like all fat-soluble vitamins, vitamin K is absorbed in association with dietary fats and requires the presence of bile salts and pancreatic juice for adequate uptake from the alimentary tract. Absorption of vitamin K depends on its incorporation into mixed micelles, and optimal formation of these micellar structures requires the presence of both bile and pancreatic juice. Thus, any malfunction of the fat absorption mechanism (e.g., biliary obstruction) reduces availability of vitamin K. Unlike phylloquinone and the menaquinones, menadione salts are relatively water soluble, and, therefore, are absorbed satisfactorily from low-fat diets. Male animals are more susceptible to dietary vitamin K deprivation than females, apparently as a result of a stimulation of phylloquinone absorption by estrogens; the administration of estrogens increases absorption in both male and female animals (Jolly et al., 1977).
The lymphatic system is the major route of transport of absorbed phylloquinone from the intestine. Shearer et al. (1970) demonstrated the association of phylloquinone with serum lipoproteins, but little is known of the existence of specific carrier proteins. Ingested phylloquinone is absorbed by an energy-dependent process from the proximal portion of the small intestine (Hollander, 1973). In contrast to the active transport of phylloquinone, menaquinone is absorbed from the small intestine by a passive noncarrier-mediated process.
The measured efficiency of vitamin K absorption ranges from 10% to 70%, depending on the form of the vitamin administered. Some reports have indicated that menadione is completely absorbed, but phylloquinone is absorbed only at a rate of 50%. The complete absorption of menadione may be due to aqueous solubility of the menadione salts. Rats were found to excrete about 60% of ingested phylloquinone in the feces within 24 hours of ingestion, but only 11% of ingested menadione (Griminger and Donis, 1960; Griminger, 1984). However, 38% of ingested menadione, but only a small amount of phylloquinone, was excreted via the kidneys during the same period. The conclusion was that although menadione is well absorbed, it is poorly retained, while the opposite is true for phylloquinone.
Griminger and Brubacher (1966) showed that a major portion of the phylloquinone fed to chicks was absorbed and deposited in the liver intact and, as such, had equally as good biological activity upon prothrombin synthesis as menaquinone found in the chick's liver following feeding of menadione. Therefore, menaquinone is most likely produced if menadione is fed or if the intestinal microorganisms degrade the dietary K1 or K2 to menadione. Formation of menaquinone is not required for metabolic activity of vitamin K, since phylloquinone is equally active in synthesis of the vitamin K-dependent, blood-clotting proteins (Scott et al., 1982).
A number of studies have shown that phylloquinone is specifically concentrated and retained but menadione is poorly retained in the liver. Menadione is found to be widely distributed in all tissues and to be very rapidly excreted. Although phylloquinone is rapidly concentrated in liver, it does not have a long retention time in this organ (Thierry et al., 1970). The inability to rapidly develop a vitamin K deficiency in most species results, therefore, from the difficulty in preventing absorption of the vitamin from the diet or from intestinal synthesis rather than from a significant storage of the vitamin. Some breakdown products of vitamin K are excreted in the urine. One of the principal excretory products is a chain-shortened and oxidized derivative of vitamin K, which forms gamma-lactone and is probably excreted as a glucuronide.