Ascorbic acid has been found to be involved in a number of biochemical processes. Function of vitamin C is related to its reversible oxidation and reduction characteristics; however, the exact role of this vitamin in the living system is not completely understood, since a coenzyme form has not yet been reported. In addition to the relationship of ascorbic acid to hydroxylase enzymes, Franceschi (1992) suggests that vitamin C is required for differentiation of connective tissue such as muscle, cartilage and bone derived from mesenchyme (embryonic cells capable of developing into connective tissue). It is proposed that the collagen matrix produced by ascorbic acid-treated cells provides a permissive environment for tissue-specific gene expression. A common finding in all studies is that vitamin C can alter the expression of multiple genes as cells progress through specific differentiation programs (Ikeda et al., 1997).
The most clearly established functional role for vitamin C involves collagen biosynthesis. Beneficial effects result from ascorbic acid in the synthesis of "repair" collagen. Alteration of basement membrane collagen synthesis and its integrity in mucosal epithelium during vitamin C restriction might explain the mechanism by which the capillary fragility is induced in scurvy as well as the increased incidences of periodontal disease under vitamin C deprivation. Failure of wounds to heal and gum and bone changes, resulting from vitamin C undernutrition, are direct consequences of reduction of insoluble collagen fibers.
Biochemical and physiological functions of vitamin C have been reviewed (Sauberlich, 1990; Moser and Bendich, 1991; Padh, 1991; Gershoff, 1993). The functional importance of vitamin C, other than the previously mentioned role in collagen synthesis, includes the following:
(a) Due to the ease with which ascorbic acid can be oxidized and reversibly reduced, it is probable that it plays an important role in reactions involving electron transfer in the cell. Almost all terminal oxidases in plant and animal tissues are capable of directly or indirectly catalyzing the oxidation of L-ascorbic acid. Such enzymes include ascorbic acid oxidase, cytochrome oxidase, phenolase, and peroxidase. In addition, its oxidation is readily induced under aerobic conditions by many metal ions and quinones.
(b) Metabolic oxidation of certain amino acids, including tyrosine.
(c) Ascorbic acid has a role in metal ion metabolism due to its reducing and chelating properties. It can result in enhanced absorption of minerals from the diet and their mobilization and distribution throughout the body. Ascorbic acid promotes non-heme iron absorption from food (Olivares et al., 1997) and acts by reducing the ferric iron at the acid pH in the stomach and by forming complexes with iron ions that stay in solution at alkaline conditions in the duodenum. Also, a sufficient vitamin C status is the prerequisite for the C-1 hydroxylation of vitamin D3 and its storage form 25(OH)D to the active form 1,25(OH)2D (Suter, 1990).
(d) Carnitine is synthesized from lysine and methionine and is dependent on two hydroxylases, both containing ferrous iron and L-ascorbic acid. Vitamin C deficiency can reduce the formation of carnitine, which can result in accumulation of triglycerides in blood and physical fatigue and lassitude associated with scurvy (Ha et al., 1994).
(e) Interrelationships of vitamin C to B vitamins are known, as tissue levels and urinary excretion of vitamin C are affected in animals with deficiencies of thiamin, riboflavin, pantothenic acid, folic acid and biotin.
(f) Vitamin C has been demonstrated to inhibit nitrosamines, which are potent carcinogens. The vitamin is effective in detoxifying high nitrate diets for ruminants (Aseltine, 1990).
(g) Vitamin C is involved in controlling synthesis of glucocorticoids (corticosteroids) in the adrenal gland. The protective effects of vitamin C (also vitamin E) on health may partially be a result of reducing circulating levels of glucocorticoids (Nockels, 1990). During stress, glucocorticoids, which suppress the immune response, are elevated. Vitamin C reduces adrenal glucocorticoid synthesis, helping to maintain immunocompetence. In addition, ascorbate can regenerate the reduced form of alpha-tocopherol, perhaps accounting for observed sparing effects of these vitamins (Jacob, 1995). In the process of sparing fatty acid oxidation, tocopherol is oxidized to the tocopheryl free radical. Ascorbic acid can donate an electron to the tocopheryl free radical, regenerating the reduced antioxidant form of tocopherol.
(h) Ascorbic acid is found in up to a tenfold concentration in seminal fluid as compared to serum levels. Decreasing levels have caused nonspecific sperm agglutination. In a review of ascorbic acid and fertility, Luck et al. (1995) suggest how three of ascorbic acid's principal functions, namely its promotion of collagen synthesis, its role in hormone production, and its ability to protect cells from free radicals, may explain its reproductive actions.
(i) Ascorbic acid is reported to have a stimulating effect on phagocytic activity of leukocytes, function of the reticuloendothelial system and formation of antibodies. Tissue defense mechanisms against free-radical damage generally include vitamin C, vitamin E, and beta-carotene as the major vitamin antioxidant sources. In addition, several metalloenzymes that include glutathione peroxidase (selenium), catalase (iron), and superoxide dismutase (copper, zinc and manganese) are also critical in protecting the internal cellular constituents from oxidative damage. The dietary and tissue balance of all these nutrients is important in protecting tissue against free radical damage. Both in vitro and in vivo studies showed that the antioxidant vitamins generally enhance different aspects of cellular and noncellular immunity. The antioxidant function of these vitamins could, at least in part, enhance immunity by maintaining the functional and structural integrity of important immune cells. A compromised immune system will result in reduced animal production efficiency through increased susceptibility to diseases, thereby leading to increased animal morbidity and mortality.