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Vitamin C metabolism

Molecular classification
Enzyme, Transporter, Redox cofactor
01

Overview

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].

Other names
Ascorbate metabolismAscorbic acid metabolismVitamin C biosynthetic pathway (in animals/plants)Vitamin C catabolic pathway
02

Mechanism of action

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).

03

Biological functions

Antioxidant activityEnzyme cofactor for collagen, carnitine, catecholamine and peptide hormone biosynthesisGene expression and epigenetic regulation (through effects on TET and Jumonji enzymes)Immune system regulationIron absorption enhancementMaintenance of redox homeostasis
04

Disease associations

Scurvy (vitamin C deficiency)Cardiovascular diseaseCancer (effects on tumor growth or therapy resistance)Immune dysfunctionNeurodegenerative diseaseOther metabolic, fibrotic, and epigenetic disorders
05

Safety considerations

Deficiency leads to scurvy (collagen defects, poor wound healing, lethargy)Excess oral vitamin C can cause gastrointestinal disturbance (nausea, diarrhea)IV vitamin C at high doses may act as a pro-oxidant with theoretical risk in people with iron overload, kidney disorders, or G6PD deficiencyRenal stones may be promoted by excess ascorbate
06

Interacting drugs

Vitamin C formulations/supplements

2 more in the full profile.

07

Biomarkers

Plasma vitamin C levels (indicator of status)Leukocyte vitamin C levels (body stores)Genetic variants in SVCT1/SVCT2 (SLC23A1/SLC23A2 genes)

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