Figure 8.57. Outline of ascorbic acid biosynthesis.
Table 8.5 Metabolie Roles of Ascorbic Acid (Vitamin C)
4 - Hydroxyphenyl-pyruvatedioxygenase hydroxylase
Trimethyl lysine hydroxylase
Cytochrome P450 isozymes
Hydroxy late dopamine phenethyl chain Amidate carboxyl end of peptide hormones Hydroxylate phenylalanine
Posttranslational Hydroxylation of proline Posttranslational hydroxylation of lysine Hydroxylation of trimethyl lysine
Oxidation of 4-butyrobetaine aldehyde Oxidation of steroids
Synthesis of norephrine
Biosynthesis of peptide hormones Synthesis of tyrosine of collagen of collagen
Corticosteroid biosynthesis from glucose (Fig. 8.57). The pathway follows the standard route to glucuronic acid. The aldose carbon is reduced to an alcohol and, following normal carbohydrate-naming convention, the former carbon 6 of D-glucuronic acid becomes carbon 1 of L-gulonic acid. Cyclic L-gulonolactone forms and is oxidized to L-ascorbicacid. Humans and primates lack gu-lonolactone oxidase.
3.13.2 Uptake. Ascorbic acid is absorbed from the intestine by a sodium-dependent active transport system that is saturable. As the concentration of vitamin C increases in the intestinal tract, the absorption changes to passive diffusion. Once in systemic circulation, there are specific transporters based on cell types.
3.13.3 Metabolic Roles. Ascorbic acid is an electron donor required for a variety of oxida-tive processes. It is readily regenerated by glutathione, NAD, and NADP and thus has a long biological half-life. Currently, there are eight known human enzymes that require ascorbic acid, and they are listed in Table 8.5. The precise metabolic roles have not been completely elucidated, but it appears that in the met-alloenzymes, ascorbate reduces the active metal site. In addition to these specific enzymes, ascorbic acid seems to function as a free-radical scavenger in the aqueous phase of plasma and cells.
3.1 3.4 Ascorbic Acid Deficiency. Scurvy is the classical disease associated with ascorbate deficiency. It is a disease of the connective tissue and probably is caused by inadequate crosslinking attributed to a lack of hydroxy-lated proline and lysine. Many consider scurvy to be an advanced stage of ascorbate deficiency. Chronic deficiencies may also (1) increase risk for malignancies, as evidenced by oxidized DNA markers and increased concentrations of reactive oxygen species; (2) decreased immune function, as evidenced by less vitamin in neutrophils and lymphocytes; (3) cardiovascular disease caused by the inflammatory response on the blood vessel walls; and (4) cataract formation caused by decreased concentrations of ascorbate in the ocular tissues.
3.1 3.5 Hypervitaminosis C. The vitamin is considered very safe. At one time, many of the over-the-counter products contained significant amounts of sodium ascorbate, which would be contraindicated in people on low sodium diets. Today's products are virtually sodium free unless labeled otherwise. Nevertheless, there are intermittent reports of adverse reactions associated with high doses. Therefore, there are Tolerable Upper Intake Levels, but these are very high relative to the RDAs. The UL to RDA ratio averages about 20.
3.1 3.6 Dietary Reference Intakes.
Children (1-8 years) Boys (9-18 years) Girls (9-18 years) Men (19-70+years) Women (19-70+) Pregnancy Lactation RDA
Children (1-8 years) Boys (9-18 years) Girls (9-18 years) Men (19-70+years) Women (19-70+) Pregnancy Lactation UL Infants
Children (1-8 years) Boys and Girls (913 years) Adolescents (14-18
years) Adults (19+ years) Pregnancy Lactation
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