Vitamin C is absorbed in a manner similar to carbohydrates (monosaccharides). Intestinal absorption in vitamin C-dependent animals appears to require a sodium- dependent active transport system. It is assumed that those species that are not susceptible to scurvy do have an absorption mechanism by diffusion (Spencer et al., 1963). Ascorbic acid is readily absorbed when small quantities are ingested, but limited intestinal absorption occurs when excess amounts of ascorbic acid are ingested. Bioavailability of vitamin C in foods is limited, but apparently 80% to 90% appears to be absorbed (Kallner et al., 1977). Site of absorption in the guinea pig is located in the duodenal and proximal small intestine, whereas the rat showed highest absorption in the ileum (Hornig et al., 1984).
In its metabolism ascorbic acid is first converted to dehydroascorbate by a number of enzymes or non-enzymatic processes and is then reduced in cells (Rose et al., 1986). Absorbed vitamin C readily equilibrates with the body pool of the vitamin. No specific binding proteins for ascorbic acid have been reported, and it is suggested that the vitamin is retained by binding to subcellular structures.
Ascorbic acid is widely distributed throughout the tissues, both in animals capable of synthesizing vitamin C as well as in those dependent on an adequate dietary amount of the vitamin. In experimental animals, highest concentrations of vitamin C are found in pituitary and adrenal glands, with high levels also found in liver, spleen, brain and pancreas. Vitamin C also tends to localize around healing wounds.
Ascorbic acid is excreted mainly in urine, with small amounts in sweat and feces. Urinary excretion of vitamin C depends on body stores, intake and renal function.
