Vitamin C is efficiently absorbed in a manner similar to monosaccharides. Absorption occurs by both a sodium-dependent, active transport system at low concentrations and by diffusion at higher concentrations (Sauberlich, 1990; Tsukaguchi et al., 1999). Absorption occurs in the small intestine with an apparent 80% to 90% absorption rate (Kallner et al., 1977). Site of absorption in the guinea pig is in the duodenal and proximal small intestine, whereas the rat showed highest absorption in the ileum (Hornig et al., 1984). High levels of dietary iron, zinc, copper and pectin reduce the utilization of ascorbic acid, either by direct oxidation of vitamin C or by reducing its absorption (Sauberlich, 1990). Considerable quantities of ascorbic acid are secreted into the gastrointestinal tract and then re-absorbed as dehydroascorbate (Dabrowski, 1990).
Endogenous production of vitamin C is dependent on the presence or absence of the liver microsomal enzyme L-gluconolactone oxidase, which imparts the ability to synthesize ascorbic acid from monosaccharides (Lehninger, 1982). Humans, other primates, guinea pigs, invertebrates, some insects, fish, bats and birds lack this enzyme and cannot synthesize vitamin C (Sauberlich, 1990). Ruminants synthesize vitamin C.
A second important feature of vitamin C metabolism is the interconversion of L-ascorbic acid and dehydro-L-ascorbic acid. In its metabolism, ascorbic acid is converted to dehydroascorbate by enzymatic or nonenzymatic means and can be enzymatically reduced back to ascorbic acid in cells in a glutathione-dependent reaction (Rose et al., 1986; Sauberlich, 1990; Vethanayagam et al., 1999). Dehydroascorbic acid is the preferred form of vitamin C for uptake by erythrocytes, lymphocytes and neutrophils (Sauberlich, 1990). Recycling between dehydroascorbate and ascorbate is a prominent feature of vitamin C metabolism in erythrocytes and white blood cells, and appears to aid in maintaining antioxidant reserves (Mendiratta et al., 1998). The selenium enzyme glutathione peroxidase is involved in the regeneration of ascorbic acid from dehydroascorbic acid in bovine erythrocytes (Washburn and Wells, 1999). Ascorbic acid is also stabilized by the antioxidant enzymes superoxide dismutase and catalase (Miyake et al., 1999), which require copper, zinc, manganese and iron.
Ascorbic acid is widely distributed throughout the tissues. The highest concentrations are found in the adrenal glands, pituitary gland, pancreas, spleen and white blood cells, although quantitatively the largest pools of vitamin C are found in skeletal muscle, the lungs, brain and liver (Sauberlich, 1990). Vitamin C tends to be concentrated in tissues during wound healing. In calves the major reservoirs of ascorbic acid are in the lungs, liver and muscle tissue (Toutain et al., 1997). Based on radioisotope measurements of ascorbic acid kinetics, the lungs appear to be a smaller but rapidly mobilized vitamin C pool, while the liver and muscle are larger, more slowly mobilized reserves (Toutain et al., 1997).
Ascorbic acid is metabolized to 2,3-diketogulonic acid and oxalate and excreted in the urine (Sauberlich, 1990). When vitamin C intake far exceeds requirements, ascorbic acid is excreted in urine unchanged (Sauberlich, 1990). Urinary excretion of vitamin C depends on vitamin C status and renal function.
