← DatabaseEssential Vitamin
Vitamin C (Ascorbate)
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A water-soluble essential vitamin and physiological antioxidant that serves as an electron-donating cofactor for collagen-synthesizing and other dioxygenase enzymes; severe deficiency causes scurvy.
How it works
Vitamin C is an essential nutrient that humans, unlike most animals, cannot synthesize, so it must come from the diet, primarily fruits and vegetables. It is best known for its role in building collagen, the structural protein that holds skin, blood vessels, and connective tissue together. Severe, prolonged deficiency causes scurvy, with bleeding gums, poor wound healing, and fragile blood vessels, a condition that resolves when vitamin C is restored.
Beyond collagen, vitamin C acts as a donor of electrons, which lets it serve as an antioxidant and as a helper for several enzymes that build hormones and regulate gene activity. It also improves the absorption of plant-based (non-heme) iron from the gut. These roles explain why a steady dietary supply matters for normal physiology.
Where the evidence gets murkier is high-dose supplementation in people who are not deficient. Popular claims, such as preventing the common cold, are not well supported for most people, and the body tightly regulates blood levels, excreting the excess from large oral doses. So while preventing and treating deficiency is firmly established, the benefit of taking large amounts beyond dietary needs is generally weak or unproven.
Mechanism · Detailed Analysis
Molecular targetAscorbate is a reducing cofactor for a family of metal-dependent dioxygenase enzymes. It keeps the iron in prolyl- and lysyl-hydroxylases in the reduced ferrous state, enabling hydroxylation of collagen; it similarly supports dopamine beta-hydroxylase, peptidylglycine alpha-amidating monooxygenase, and the 2-oxoglutarate-dependent dioxygenases including HIF prolyl hydroxylases and TET and Jumonji demethylases.
Signaling & downstream effectsHydroxylation of proline and lysine residues stabilizes the collagen triple helix, so deficiency yields defective connective tissue and the clinical picture of scurvy. Support of monooxygenases contributes to catecholamine and peptide-hormone biosynthesis, while activity at HIF and chromatin-modifying dioxygenases links ascorbate to oxygen sensing and epigenetic regulation. As a freely diffusible electron donor it also scavenges aqueous reactive oxygen species and recycles oxidized vitamin E, and it reduces dietary ferric iron to the more absorbable ferrous form.
PharmacokineticsOral ascorbate is absorbed via sodium-dependent vitamin C transporters with saturable kinetics, so plasma and tissue levels are tightly controlled and fractional absorption falls as intake rises. Once transporters are saturated, additional oral intake is largely excreted in urine, capping achievable plasma concentrations; this ceiling is bypassed only by intravenous administration. The vitamin is water-soluble, not stored to a large extent, and turns over relatively quickly compared with fat-soluble vitamins.
CaveatsStrong evidence supports preventing and treating deficiency; for replete individuals, routine high-dose supplementation has not convincingly prevented common illnesses such as the cold in the general population. Very large oral doses can cause gastrointestinal upset and, in predisposed people, raise oxalate-related kidney-stone concerns. Regulatory status is as a recognized essential nutrient and dietary supplement; this entry is educational and not a treatment recommendation.
Published EvidenceLoading cited studies from PubMed…
Human Data ···
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Educational aggregation of public literature. Not medical advice and not a recommendation to use any compound. Many compounds here are not approved for human use. Consult a licensed clinician.