Ascorbic acid physiological functions

Ascorbic acid is a reasonably strong reducing agent. The biochemical and physiological functions of ascorbic acid most likely derive from its reducing properties—it functions as an electron carrier. Loss of one electron due to interactions with oxygen or metal ions leads to semidehydro-L-ascorbate, a reactive free radical (Figure 18.30) that can be reduced back to L-ascorbic acid by various enzymes in animals and plants. A characteristic reaction of ascorbic acid is its oxidation to dehydro-L-aseorbie add. Ascorbic acid and dehydroascor-bic acid form an effective redox system. 

Vitamin C occurs as L-ascorbic acid and dihydroascorbic acid in fruits, vegetables and potatoes, as well as in processed foods to which it has been added as an antioxidant. The only wholly undisputed function of vitamin C is the prevention of scurvy. Although this is the physiological rationale for the currently recommended intake levels, there is growing evidence that vitamin C may provide additional protective effects against other diseases including cancer, and the recommended dietary allowance (RDA) may be increased in the near future. Scurvy develops in adults whose habitual intake of vitamin C falls below 1 mg/d, and under experimental conditions 10 mg/d is sufficient to prevent or alleviate symptoms (Bartley et al., 1953). The RDA is 60 mg per day in the USA, but plasma levels of ascorbate do not achieve saturation until daily intakes reach around 100 mg (Bates et al., 1979). Most of the ascorbate in human diets is derived from natural sources, and consumers who eat five portions, or about 400-500 g, of fruits and vegetables per day could obtain as much as 200 mg of ascorbate. 

Physiological functions, of vitamins, 25 784 Physiology, of ascorbic acid, 25 766-773 Physisorbed water, 23 71-72 Physostigmine, 2 817-818 Phytane, 18 592... 

The reduction of adrenochrome (1) with ascorbic acid (59) was first reported in 1948,158 although the nature of the reaction products (which may be of physiological importance, cf. ref. 159) was not determined until several years later. It was shown by Heacock and Laidlaw in 1958 that reduction mixtures of this type contained at least three indolic products,147 one of which was isolated and shown to be 5,6-dihydroxy- -methylindole (28).147 The major component of aqueous adrenochrome-ascorbic acid reaction mixtures has recently been shown to be a secondary product (60) (which was isolated as its di- and tetra-acetyl derivatives) produced by the interaction of the o-dihydroxy group of 28 with the a-dicarbonyl function of dehydro-... 

Physiological Function. The mechanism by which L-ascorbic acid benefits an insect is unknown. The vitamin is found in many tissues where it probably plays a variety of roles related to its redox potential. Besides the possible general function of detoxifying superoxide and hydrogen peroxide, L-ascorbic acid may be involved in metabolic processes such as tyrosine metabolism, collagen formation, steroid synthesis, detoxification reactions, phagostimulation, or neuromodulation. At this time one can only speculate about the function of vitamin C in some specific tissues. 

Perhaps more than any other nutritional factor, ascorbic acid has been the focus of the questions, How much ascorbic acid is required in humans for optimum health and well-being and What factors can change this requirement There seem to be no simple answers to these questions, but good progress has been made in fundamentals related to this problem, such as measurement of pool sizes and turnover in humans as a function of environmental variables. The lack of such physiological data for children, women, and pregnant women needs to be corrected. 

Vitamin C (ascorbic acid, Fig. 2) is a water-soluble vitamin that dissociates at physiological pH. It is essential as a cofactor of several enzymes, including proline hydroxylase and lysine hydroxylase. Scurvy is known as the result of malnutrition with ascorbic acid. This vitamin deficiency is characterized by instable collagen. This results from insufficient hydroxylation of collagen molecules. Besides this, ascorbic acid has a function as an antioxidant. 

We still do not know how ascorbic acid acts in the body or how it prevents scurvy. Scurvy is clearly a molecular disease, in the sense that all its signs and symptoms should ultimately be referable to the biochemical and physiological consequences of the failure to make the ascorbic acid molecule. This is the next problem. Interest is now turning to the biochemical functions of ascorbic acid in the body and to the use of scurvy and ascorbic acid as reagents to probe deeper into other mysteries about how the body operates. 

The mechanisms by which vitamins prevent illnesses are not weU understood, and the amounts needed to lower risks for certain disease conditions may be higher than the current recommended levels for preventing nutritional deficiencies. For example, the Institute of Medicine recommends that to prevent neural tube birth defects, women of child-bearing age should consume 400 Xg of folic acid per day (but not more than 1000 Xg/day) from fortified foods and/or dietary supplements in addition to folates obtained from a varied diet. " < Ascorbic acid intakes of 80-200mg daily (8-20 times the amounts needed to prevent scurvy) may be necessary to enhance certain physiological functions and minimize specific disease risks. " ... 

Under physiological conditions, ascorbic acid is mainly used as a reductant in a variety of functions. It is essential in chloroplasts for the removal of photoproduced active oxygen species (Miyake and Asada, 1992). Ascorbate can also regenerate some membrane-bound radical quenchers such as a-tocopherol and zeaxanthin (Foyer et al, 1991). Ascorbate function is in addition extended to the removal of free radical oxygen species produced by air pollutants, certain herbicides, and other cytotoxic compounds derived from lipid peroxidation (Polle et al., 1990 Penel and Castillo, 1991 Luwe et al., 1993). 

If histamine degradation is a physiological function of vitamin C, it is necessary to delineate the tissue level of ascorbic acid required for this effect. In the rat, which is capable of synthesizing ascorbic acid, serum ascorbic acid rose from 1.10 mg/100 ml to 1.63 mg/100 ml within 30 min of immobilization stress, nearly a 50% increase (Nakano and Suzuki, 1984). Liver ascorbate in these animals fell significantly after 15 min of stress, then rose dramatically to over 60% of the initial value within the next 15 min, indicating elevated hepatic biosynthesis of the vitamin. Adrenal ascorbic acid stores fell to 50% of the initial value following immobilization stress, and these levels remained depressed at 4 hr post-stress. Blood histamine levels rose 80%, from 38 to 68 ng/ml, peaking at about 30 min post-stress (Nakano and Suzuki, 1984). Hence, in the rat, stress induced a rapid rise in serum ascorbate which was fueled by ascorbic acid mobilized from tissue stores and by hepatic synthesis of ascorbate. 

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