Vitamin C or ascorbic acid, usually found on citrus fruits, is the only glucose-derive vitamin which can come from the uronic acid pathway in some animals. In humans, other primates, and guinea pigs, there is an absence of L-gulonolactone oxidase which unables them to synthesize ascorbic acid, hence it is essential and must be supplied in the body. Its functions are; first, to be an O2 radical quencher or an antioxidant like Vitamin A and E; second, a coenzyme in some hydroxylation reactions and tyrosine degradation; third, increase in intestinal Fe absorption, prevention of common colds which moderate the symptoms and shorten the duration of the illness; and lastly, it is also an anti-infective vitamin (Madarcos, 2013).
In the presence of ascorbate, the peptide-bound proline and lysine in the precursor procollagen are hydroxylated by prolyl and lysl hydroxylase for the synthesis of collagen, therefore the deficiency of Vitamin C will possibly result to impaired collagen connective tissue functions. There will be poor wound healing in the skin, osteoporosis due to defective organic matrix formation in the bone, fragility in the capilliaries and anemia due impaired intestinal Fe absorption and bleeding diathesis.
Ascorbic acid also has a role on the synthesis of catecholamines and also the degradation of tyrosine. It acts as a cofactor of the hydroxylation reaction of dopamine to epinephrine and the conversion of p-hydroxyphenylpyruvate to homogentisate – a step on tyrosine degradation, consequently. It also has a role in the synthesis of carnitine which also acts as a cofactor for the series of its chemical reactions. Carnitine serves to transport long chain fatty acids from the cytoplasm into the mitochondrion during the β-oxidation process thus; Vitamin C deficiency will result into fatigue due to decreased ATP synthesis from decreased rate of fatty acid oxidation.
In the presence of ascorbate, the peptide-bound proline and lysine in the precursor procollagen are hydroxylated by prolyl and lysl hydroxylase for the synthesis of collagen, therefore the deficiency of Vitamin C will possibly result to impaired collagen connective tissue functions. There will be poor wound healing in the skin, osteoporosis due to defective organic matrix formation in the bone, fragility in the capilliaries and anemia due impaired intestinal Fe absorption and bleeding diathesis.
Ascorbic acid also has a role on the synthesis of catecholamines and also the degradation of tyrosine. It acts as a cofactor of the hydroxylation reaction of dopamine to epinephrine and the conversion of p-hydroxyphenylpyruvate to homogentisate – a step on tyrosine degradation, consequently. It also has a role in the synthesis of carnitine which also acts as a cofactor for the series of its chemical reactions. Carnitine serves to transport long chain fatty acids from the cytoplasm into the mitochondrion during the β-oxidation process thus; Vitamin C deficiency will result into fatigue due to decreased ATP synthesis from decreased rate of fatty acid oxidation.
Figure 6. Hemorrhage and swollen gums of a patient with scurvy. Lippincott’s Illustrated Reviews: Biochemistry 5th ed. (p. 377), by R. A. Harvey & D. R. Ferrier, 2011, Philadelphia: Lippincott Williams & Wilkins, a Wolters Kluwer business. Copyright 201 by Lippincott Williams & Wilkins, a Wolters Kluwer business.
A deficiency of ascorbic acid will also result in scurvy, a disease characterized by sore and spongy gums, loose teeth, fragile blood vessels, swollen joints, and anemia (Figure 6). Many of the deficiency symptoms can be explained by a deficiency in the hydroxylation of collagen, resulting in defective connective tissue (Harvey & Ferrier, 2011)