mins are essential to maintain normal metabolic processes and homeostasis within the body. The amount of a specific vitamin required by an individual varies considerably and it is influenced by such factors as body size, growth rate, physical activity, and pregnancy. Most vitamins are stored minimally in human cells, but some are stored in liver cells to a greater extent. Vitamins A and D, for example, may be stored in sufficient amounts to maintain an individual without any intake for 5 to 10 months and 2 to 4 months, respectively. However, a deficiency of vitamin B compounds (except vitamin B12) may be noted within days, and the lack of vitamin C will manifest within weeks and may result in death in 5 to 6 months. The current recommended dietary allowance (RDA) of vitamin C is 75 mg for woman and 90 mg for men, based on the vitamin’s role as an antioxidant as well as protection from deficiency. High intakes of the vitamin are generally well tolerated, however, a Tolerable Upper Level (TUL) was recently set at 2 g based on gastrointestinal upset that sometimes accompanies excessive dosages. Several populations warrant special attention with respect to vitamin C requirements. These include patients with periodontal disease, smokers, pregnant and lactating women, and the elderly.

Humans require vitamin C in their diet. Fruits and vegetables are rich in vitamin C. While pro-longed storage of unprocessed fruits and vegetables leads to the loss of vitamin C, most means of food processing (boiling, steaming, freezing, canning) preserve vitamin C to a great extent. The intestinal absorption of vitamin C is 80-90% efficient. This efficiency rate, however, declines with increased intake. Vitamin C is actively co-transported with sodium against an electrochemical gradient into intestinal (small bowel) epithelial cells. Once in the cells, a concentration gradient is created by both brush border absorption and intracellular reduction of dehydro-L-ascorbic acid (DHAA) to ascorbate. Facilitated diffusion of ascorbate into the circulation is sodium independent and follows a concentration and electrochemical gradient. A similar transport mechanism is responsible for the near complete resorption of ascorbate in the kidneys. Ascorbate and, significantly, one of its metabolites, oxalate, are found in the urine only in excess states. The latter is pertinent, as it accounts for one of the few potential clinical toxicities of systemic vitamin C supplementation, oxalic acid renal stones.

Vitamin C readily undergoes reversible oxidation and reduction and plays an important role as a redox agent in biological systems.1 Its best understood function is in the synthesis of collagen, which promotes the formation of hydroxy-proline.2 Nonhydroxylated collagen is unstable and cannot form the triple helix required for normal structure of subcutaneous tissue, cartilage, bone, and teeth. The failure of cells to deposit collagen fibrils and intracellular cement substance leads to delayed wound healing. The inability of osteoblasts to form new bone matrix between cells prevents ossification, which may lead to bone fractures, and prevent bone healing. A lack of intracellular cement substance and an inability to form collagen fibrils results in capillary fragility characterized by petechial, purpuric, ecchymotic skin and mucosal lesions, and subperiosteal and visceral hemorrhages, which lead to anemia.3 The anemia that accompanies scurvy is of multifactorial origin. It results from acute blood loss related to hemorrhage, decreased absorption of iron, and the concurrent folate deficiency that is seen in patients with scurvy. 4 Molecular studies on platelets deficient in collagen-induced aggregation also suggest a possible role for platelet-related collagen receptors. These studies have shown the platelets, which lacked collagen-induced aggregation and adhesion, have significantly reduced levels of 62-kD membrane glycoprotein VI (GPVI). GPVI has been suggested to function as a platelet-related collagen receptor. 5 It has also been reported the serum from an idiopathic thrombocytopenic pupura patient contained an antibody against a platelet protein, which was later identified as GPVI.

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