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Vitamin C metabolism refers to the network of biochemical processes involved in the absorption, transport, utilization, and catabolism of Vitamin C (L-ascorbic acid), an essential water-soluble vitamin for humans. Vitamin C acts as a critical antioxidant and as a cofactor for multiple enzymes, including those involved in collagen and carnitine biosynthesis, catecholamine and peptide hormone synthesis, and epigenetic regulation. Vitamin C is absorbed in the intestine (primarily via SVCT1), distributed to tissues via specific transporters (such as SVCT2), and maintained by renal reabsorption. Humans lack the ability to synthesize vitamin C due to mutations in the L-gulono-1,4-lactone oxidase gene, making dietary intake essential. Deficiency causes scurvy and contributes to broader pathophysiology in connective tissue, immune function, and redox balance. The process encompasses several enzymes and transporters, some of which may be considered direct therapeutic targets in disease contexts[1][2][3][5][6].
Vitamin C metabolism involves its antioxidant role (free radical scavenging, supports detoxification), its function as an enzyme cofactor (hydroxylation, demethylation, amidation, oxidation-reduction reactions), its pro-oxidant activity at pharmacologic IV doses (cytotoxicity to cancer cells), and its ability to enhance iron absorption (reduces ferric to ferrous iron).
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