Vitamin collagen synthesis

Signs of vitamin C deficiency in scurvy include skin changes, fragifity of blood capillaries, gum decay, tooth loss, and bone fracmre, many of which can be attributed to deficient collagen synthesis. 

In vitamin C avitaminosis, or scurvy, the joints become painful and the gums bleed and deteriorate, resulting in tooth loss. Gangrene and infections may also occur, and wounds do not heal properly. These symptoms all result from impaired collagen synthesis and... 

Nature makes some important compounds from simple sugars. Vitamin C—ascorbic acid—is one of these. Like glutathione, it protects us from stray oxidants as well as being involved in primary redox pathways (we mentioned earlier its role in collagen synthesis). Its reduced and oxidized forms are these. 

Deficiency of ascorbate in the diet of animals that are unable to synthesise it gives rise to defects in collagen synthesis which in man results in the condition known as scurvey. No deficiency disease associated with the radical repair mechanism of action of the vitamin has been reported. 

More than 90% of the body s supply of vitamin A is stored in the liver. The hepatic parenchymal cells are involved in its uptake, storage, and metabolism. Retinyl esters are transferred to hepatic fat-storing cells (also called Ito cells or lipocytes) from the parenchymal cells. The capacity of these fat-storing cells may determine when vitamin A toxicosis becomes symptomatic. During the development of hepatic fibrosis (e.g., in alcoholic liver disease), vitamin A stores in Ito cells disappear and the cells differentiate to myofibroblasts. These cells appear to be the ones responsible for the increased collagen synthesis seen in fibrotic and cirrhotic livers. 

A. The patient exhibits the classic symptoms of scurvy, a deficiency in vitamin C. In addition to being an important biological antioxidant, ascorbic acid is required for the hydroxylation of proUne and lysine residues of procollagen in the synthesis of collagen. A deficiency leads to defects in collagen synthesis, which adversely affects the intercellular cement substances in connective tissue, bones, and dentin. 

Quite apart from its antioxidant effects, we need vitamin C for a wide variety of biochemical reactions that help to maintain our normal physiological function. The best known requirement for vitamin C is as a cofactor (a necessary accessory for enzyme function) in collagen synthesis. 

Such a diverse array of functions lends vitamin C an aura of magic. Yet in each of these cases, vitamin C behaves in exactly the same way at the molecular level, as repetitively as flipping a coin, even if the outcomes are opposed. To see how, let us take a single example in a little more detail. Collagen synthesis illustrates not only how vitamin C works, but also throws light on its antioxidant properties, as well as its more dangerous side. 

Although ascorbate (vitamin C) is an oxidation-reduction coenzyme that functions in collagen synthesis and other reactions, it also plays a role in free radical defense. Reduced ascorbate can regenerate the reduced form of vitamin E through donating electrons in a redox cycle (Fig. 24.19). It is water-soluble and circulates unbound in blood and extracellular fluid, where it has access to the lipid-soluble vitamin E present in membranes and lipoprotein particles. 

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