Ascorbic acid deficiency

Deficiency may occur in infants if no fruits or vegetables are added to their milk formulas. In alcoholics, and in elderly subjects who consume inadequate diets vitamin C deficiencies are frequent. Severe ascorbic acid deficiency is characterized by the syndrome known as scurvy. Its manifestations are generally based on a loss of collagen. Symptoms include hemorrhages, loosening of teeth. In children cellular changes in the long bones occur. 

Vitamin C is used for the treatment of ascorbic acid deficiency. Claims that high doses of up to 1 g daily had efficacy in shortening the duration... 

Abrupt discontinuation after prolonged use of large doses may produce rebound ascorbic acid deficiency. 

Hydroxyproline and hydroxylysine result from the hydroxylation by specific hydroxylases of proline and lysine residues after their incorporation into a-chains. The enzymes require ascorbic acid as a cofactor. [Note An ascorbic acid deficiency results in scurvy.] The hydroxyl group of the hydroxylysine residues of collagen may be enzymatically glycosy lated (most commonly, glucose and galactose are added sequentially to the triple helix). 

As indicated in Figure 2, when minces of tumor obtained from normal and ascorbic acid-deficient animals were incubated with C14-pro-line, much more radioactivity was incorporated into the collagen of the normal tissue. When the specific radioactivities of the isolated imino acids were examined (Table HI), several conclusions were possible. In the experiments with granuloma from normal animals and C14-proline, the values for hydroxyproline were not far from those of proline. With the scorbutic granulomas, the specific activity of the isolated proline was not greatly reduced, compared to that obtained from the normal granuloma. In contrast, the specific activity of the hydroxyproline isolated from the deficient tissues was markedly reduced. Similar results were obtained in the studies with tritiated proline. Thus, the specific activity of the proline isolated from the deficient granuloma was only moderately reduced, whereas the specific activity of the hydroxyproline was extremely low. This observation may be explained in terms of a dual-pathway mechanism of proline incorporation, considered below. 

Table VI. Stimulation of Hydroxylation of Proline 4>y Ascorbic Acid-Deficient Granuloma by in Vitro Addition of Ascorbic Acid...

Conklin, P.L., Saracco, S.A., Norris, S.R., and Last, R.L., 2000, Identification of ascorbic acid-deficient Arabidopsis thaliana mutants. Genetics 154 847-856. 

Hodges RE, Hood J, Canham JE, Sauberlich HE, and Baker EM (1971) Clinical manifestations of ascorbic acid deficiency in man. American Journal of Clinical Nutrition 24, 432-43. 

Iron being a redox-active metal, it most hkely exerts its toxic effects through the generation of hydroxyl radical or by generation of ferryl ion. In iron loaded condition, there is generation of radical species leading to hpid peroxidation. Lipid peroxidation of cellular membrane would have deleterious effects on their function and hence on the function of the cell. There is also irreversible oxidation of ascorbic acid. Deficiency of ascorbic acid can lead to a reduction in the amount of iron available for erythropoiesis. 

Barnes, M. J., Constable, B. J., Morton, L. F., and Kodicek, E. (1970). Studies in vivo on the biosynthesis of collagen and elastin in ascorbic acid-deficient guinea pigs. Biochan. j. 119, 575-585-... 

Leukocyte ascorbic acid concentrations are generally considered to provide a better reflection of tissue stores than other blood components. Supporting evidence for this belief includes observations such as (i) leukocyte ascorbate levels drop slowly during ascorbic acid deficiency. 

Reid-Briggs ascorbic acid deficient diet 99). 

We have used the growth effects and pathologies associated with L-ascorbic acid deficiency as a basis for the determination of the biological potency of related compounds (Table I). At a dietary concentration of 0.5 mM, L-ascorbic acid and dehydroascorbic acid were fully active, as well as some ester derivatives including the 6-myristate and 2-phosphate compounds. The insect may be metabolically like the guinea pig because both were able to utilize those esters (17), Carboxylesterases and phosphatases probably converted those derivatives to the free vitamin (18). The 6-bromo compound was less active and apparently cannot be metabolized to L-ascorbic acid or only poorly so. 

Another possible function of L-ascorbic acid in the cuticle is to promote collagen formation. No evidence for this has been obtained using insects, but L-ascorbic acid deficiency disease in penaeid shrimp, termed black death, was related to collagen hypohydroxylation (39,40). Melanized lesions of loose connective tissue occurred in endocuticle at intersegmental spaces. Perhaps insects also underhydroxylate collagen when deficient in ascorbic acid. 

Specific activity equals nmol of cytochrome Pj,so reducedfh1100 mg of microsomal protein at 27° C. The number of animals in each group is given in the figure. The diets of the various groups contained less than 1.0 mg ascorbic acid 1100 g of liver, ascorbic acid deficient diet for 15 d (point 1), 2.3 mg of ascorbic acid/100 g of liver, ascorbic acid deficient diet for 8 d (point 2), 7.4 mg of ascorbic acid/100 g of liver, 25 mg of ascorbic acid/d for 3 d (point 3), 13.5 mg of ascorbic acid/100 g of liver, 75 mg of ascorbic acid/d for 8 d (point 4), 27.0 mg of ascorbic acid/100 g of liver, chow guinea pig diet plus greens for 8 d (point 5). 

Cytochrome Pt,so and ascorbic acid were determined in the liver 15,000 X g supernatant fraction from guinea pigs (200-250 g) maintained on an ascorbic acid deficient diet for 20 d (open bar), normal chow diet (cross-hatched bar), or chow diet plus 1.0 mg/mL of ascorbic acid in the drinking water Id (solid bars). Animals were divided into groups according to their liver concentration of ascorbic acid 1 fimol of ascorbic acid 1100 mg of protein equals 19 mg/100 g wet weight of liver. Number in parentheses represents number of animals. 

Chow diet + 50 mg/d of ascorbic acid (8 d) Chow diet -j- 500 mg/d of ascorbic acid (8 d) Ascorbic acid deficient diet (8 d)... 

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