Vitamin C (Ascorbinsäure): the pathway in the body · Biomarker & Blood Analysis

Vitamin C (Ascorbinsäure) is part of the pathway “Vitamin C”. This page shows the whole pathway; the station of Vitamin C (Ascorbinsäure) is highlighted.

Where this laboratory value sits: Vitamin C in food — Ascorbic acid. Chemically, vitamin C is ascorbic acid. In the body it is present mainly as ascorbate, the charged form of the acid. Humans cannot make it themselves. All ascorbate in the body therefore comes from food. Source 1, 2

In brief

Vitamin C (ascorbic acid) is a water-soluble vitamin that humans cannot make themselves. It donates electrons and thereby keeps iron and copper in enzymes in working order, for example in the prolyl 4-hydroxylase of collagen formation. The kidney excretes any excess.

The pathway step by step

Each station states what the compound does there. Three signs: ↑ supplies — builds up or makes available · ↓ depletes — inhibits, consumes or withholds · ↕ both, depending on amount. Behind it stands what the statement rests on: established physiology, observed in studies, or contested. The signs do not grade; they name the direction.

1. Vitamin C in food → Into the gut cell SVCT1 · Sodium The transporter SVCT1 moves ascorbate together with sodium into the cells of the small intestinal wall. The oxidised form, dehydroascorbate, enters via sugar transporters. With large amounts the transporter is saturated. Source 2↑ supplies SVCT1 actively moves ascorbate into the gut cell, driven by sodium. With small amounts most of it thus reaches the blood; as the amount rises, the transporter becomes fully occupied. established physiology Source 2
   ⚖ When the balance tips

   too much — If SVCT1 is fully occupied, additional ascorbate does not enter the gut cell any faster; the rest remains in the gut contents and leaves the body with the stool.

   too little — If little ascorbate arrives in the gut, SVCT1 works below saturation and moves a large share of it into the gut cell.

   established physiology · Source 2

2. Into the gut cell → Ascorbate in the blood From the gut cell, ascorbate passes into the blood and through it reaches all tissues. Gut and kidney keep its amount in plasma within a narrow range. Source 2↑ supplies The blood distributes ascorbate to the tissues, which concentrate it via SVCT2. The amount in plasma stays within a narrow range, because gut and kidney regulate absorption and loss through the saturation of their transporters. established physiology Source 2
   ⚖ When the balance tips

   too much — If plasma ascorbate rises above the saturation of the kidney transporters, the kidney rapidly excretes the excess; only with administration into a vein are far higher plasma amounts reached briefly.

   too little — If little ascorbate comes in from the gut, it falls in plasma; the tissues that have concentrated it release their store only slowly.

   established physiology · Source 2

3. Ascorbate in the blood → Kidney SVCT1 · Sodium The kidney filters ascorbate from the blood and retrieves it via the same transporter, SVCT1. What is not retrieved leaves the body in the urine. Once retrieval is saturated, the excess is excreted. Source 2↕ both, depending on amount The kidney determines how much ascorbate stays in the body: below the saturation of SVCT1 it retrieves almost all of it, above it it excretes the excess. In this way it caps the amount in plasma. established physiology Source 2
   ⚖ When the balance tips

   too much — If retrieval is saturated, additional ascorbate leaves the body in the urine; part of it is first broken down to oxalate, which is likewise excreted via the kidney.

   too little — If there is little ascorbate in the blood, SVCT1 in the kidney retrieves nearly all that is filtered, and hardly any ascorbate is lost in the urine.

   established physiology · Source 2, 1

4. Ascorbate in the cell → Ascorbate as cofactor Many enzymes carry iron or copper in their active centre. Ascorbate donates an electron and keeps the metal in the form in which the enzyme can work. This keeps enzymes of collagen, carnitine and noradrenaline formation working. Source 3, 4, 5↑ supplies Ascorbate supplies the electrons for the prolyl and lysyl hydroxylases of collagen formation, for two steps of carnitine formation and for dopamine β-hydroxylase, which makes noradrenaline from dopamine. established physiology Source 3, 4, 5
   ⚖ When the balance tips

   too much — Once the metal centres of the enzymes are reduced, more ascorbate brings no further turnover; the enzymes then work as fast as substrate and oxygen allow.

   too little — If little ascorbate is available, the iron or copper more often remains stuck in the oxidised form; hydroxylases and monooxygenases then convert less.

   established physiology · Source 3, 4

5. Ascorbate in the cell → Ascorbyl radical When ascorbate donates an electron, the ascorbyl radical forms briefly. Two of these particles react with each other: one becomes ascorbate again, the other dehydroascorbate. An NADH-dependent enzyme can also convert it back directly. Source 1↕ both, depending on amount The ascorbyl radical is comparatively unreactive. An NADH-dependent enzyme returns it directly to ascorbate; when two radicals react with each other, one becomes ascorbate again, the other moves on as dehydroascorbate. established physiology Source 1
   ⚖ When the balance tips

   too much — If a lot of ascorbyl radical forms at once, it reacts mostly with itself, and more dehydroascorbate accumulates that must be recovered.

   too little — If little ascorbyl radical forms, hardly any ascorbate is used up, and little dehydroascorbate accumulates.

   established physiology · Source 1

6. Ascorbyl radical → Dehydroascorbate Dehydroascorbate carries no more electrons. Enzymes that use glutathione or thioredoxin can turn it back into ascorbate. If this does not happen quickly, dehydroascorbate breaks down irreversibly. Source 1↕ both, depending on amount Dehydroascorbate is the turning point: glutathione and thioredoxin reductase turn it back into ascorbate, with electrons that ultimately come from NADPH. If this does not happen quickly, it breaks down irreversibly. established physiology Source 1
   ⚖ When the balance tips

   too much — If more dehydroascorbate accumulates than can be returned, the rest breaks down to diketogulonic acid; at the same time recovery uses up more glutathione.

   too little — If little dehydroascorbate is present, hardly any glutathione or NADPH is needed for recovery.

   established physiology · Source 1

7. Dehydroascorbate → Diketogulonic acid If dehydroascorbate is not converted back, it breaks down in water to 2,3-diketogulonic acid and further to smaller acids such as oxalate, which the body excretes. This path cannot be reversed. Source 1↓ depletes With breakdown to 2,3-diketogulonic acid the vitamin is lost for good; no ascorbate forms from it again. Part of it ends up as oxalate, which is excreted via the kidney. established physiology Source 1
   ⚖ When the balance tips

   too much — If a lot of ascorbate is turned over and not recovered, more oxalate also forms, and the kidney excretes more of it.

   too little — If dehydroascorbate is recovered promptly, little breaks down, and hardly any diketogulonic acid or oxalate forms from vitamin C.

   established physiology · Source 1

8. Proline in collagen → Hydroxyproline Prolyl 4-hydroxylase · Iron, α-Ketoglutarate Prolyl 4-hydroxylase attaches an OH group to proline. The enzyme contains iron and uses up α-ketoglutarate; ascorbate keeps the iron in its reactive form. Without these OH groups the collagen chain remains unstable. Source 3↑ supplies The OH groups on proline make the collagen helix stable at body temperature. Ascorbate is not used up in every cycle, but when the enzyme's iron oxidises without proline. established physiology Source 3
   ⚖ When the balance tips

   too much — Once the hydroxylase iron is reduced, more ascorbate brings no additional OH groups; how many hydroxyprolines form is set by the chain.

   too little — If little ascorbate is available, the hydroxylase iron stays oxidised and the enzyme stops; the chains carry less hydroxyproline, fold less well and are released from the cell more slowly.

   established physiology · Source 3

9. Hydroxyproline → Collagen triple helix Only with the OH groups do three collagen chains wind stably around each other. This form gives collagen its tensile strength; it is found in skin, vessel walls, bone and tendons. Cross-linking into fibres also needs ascorbate. Source 3↑ supplies The stable triple helix is the precondition for collagen to be released from the cell and cross-linked into fibres. The lysyl hydroxylases prepare cross-linking sites for this; they too need ascorbate. established physiology Source 3
   ⚖ When the balance tips

   too much — Once hydroxylation is complete, more ascorbate brings no firmer helix; how much collagen is present is then set by the formation and breakdown of the chains.

   too little — If the chains carry little hydroxyproline, the helix stays unstable at body temperature; the cell retains or degrades the chains, and fewer tensile fibres form.

   established physiology · Source 3

Further stations

• Vitamin C in food — Ascorbic acid Chemically, vitamin C is ascorbic acid. In the body it is present mainly as ascorbate, the charged form of the acid. Humans cannot make it themselves. All ascorbate in the body therefore comes from food. Source 1, 2↑ supplies Food is the only source: humans lack the last enzyme of synthesis from glucose, L-gulonolactone oxidase. All ascorbate at work in the tissues therefore comes from intake. established physiology Source 1, 2
  ⚖ When the balance tips

  too much — If a lot of vitamin C arrives at once, the transporters in the gut saturate; the share that reaches the blood becomes smaller as the amount rises.

  too little — If little vitamin C arrives over a longer period, the stores in the tissues empty gradually, because the body cannot make it itself.

  established physiology · Source 2

• Ascorbate in the cell — via SVCT2 The transporter SVCT2 carries ascorbate together with sodium into cells. There it donates electrons and is itself converted in the process. Cells concentrate it far above the amount in the blood. Source 1, 2↑ supplies SVCT2 concentrates ascorbate in cells far above the amount in the blood, especially in the brain, adrenal glands and white blood cells. There it is available as an electron donor for enzymes. established physiology Source 2, 1
  ⚖ When the balance tips

  too much — If SVCT2 is saturated, ascorbate in the cell hardly rises further despite a higher amount in the blood; the cell thus keeps its content within a limited range.

  too little — If there is little ascorbate in the blood, SVCT2, thanks to its high binding strength, keeps drawing ascorbate into the cells, so the content there falls more slowly than in the blood.

  established physiology · Source 2

• Proline in collagen — Connective tissue unit Collagen is the most abundant protein in connective tissue. The amino acid proline occurs at regular intervals along its long chains. Prolyl 4-hydroxylase acts on these prolines. Source 3↑ supplies The regularly spaced prolines are the targets of prolyl 4-hydroxylase. Only when enough of them are hydroxylated do three chains come together into a stable triple helix. established physiology Source 3
  ⚖ When the balance tips

  too much — If many collagen chains are made, prolyl 4-hydroxylase must process correspondingly more prolines and uses up more α-ketoglutarate and oxygen in doing so.

  too little — If few collagen chains are made, the hydroxylases have less substrate, and correspondingly less hydroxyproline forms.

  established physiology · Source 3

Cofactors in this pathway

• Sodium — Drives the transporters SVCT1 and SVCT2, which carry ascorbate into cells; without sodium no transport Source 2In the ORY catalogue as a laboratory value: Natrium (intrazellulär)
• Iron — Metal centre of prolyl 4-hydroxylase, which ascorbate keeps reactive; without ascorbate it oxidises Source 3In the ORY catalogue as a laboratory value: Eisen
• Copper — Metal centre of monooxygenases to which ascorbate supplies electrons, such as dopamine β-hydroxylase Source 4In the ORY catalogue as a laboratory value: Kupfer (Cu)
• α-Ketoglutarate — Consumed by prolyl 4-hydroxylase in each hydroxylation and converted to succinate in the process Source 3In the ORY catalogue as a laboratory value: Alpha-Ketoglutarat (2-Oxoglutarat)
• Glutathione — Reduces dehydroascorbate back to ascorbate and is itself oxidised in the process Source 1, 6In the ORY catalogue as a laboratory value: Glutathion (GSH)
• Selenium — Component of thioredoxin reductase, which reduces dehydroascorbate to ascorbate; as selenocysteine in the active centre Source 6In the ORY catalogue as a laboratory value: Selen
• Niacin (NADPH) — NADPH supplies thioredoxin reductase with the electrons for recycling; without it the cycle stalls Source 6

Sources

1. Linster CL, Van Schaftingen E. Vitamin C. Biosynthesis, recycling and degradation in mammals. FEBS J 2007 · PubMed 17222174
2. Padayatty SJ, Levine M. Vitamin C: the known and the unknown and Goldilocks. Oral Dis 2016 · PubMed 26808119
3. Salo AM, Myllyharju J. Prolyl and lysyl hydroxylases in collagen synthesis. Exp Dermatol 2021 · PubMed 32969070
4. Prigge ST, Mains RE, Eipper BA et al. New insights into copper monooxygenases and peptide amidation: structure, mechanism and function. Cell Mol Life Sci 2000 · PubMed 11028916
5. Rebouche CJ. Ascorbic acid and carnitine biosynthesis. Am J Clin Nutr 1991 · PubMed 1962562
6. May JM, Mendiratta S, Hill KE, Burk RF. Reduction of dehydroascorbate to ascorbate by the selenoenzyme thioredoxin reductase. J Biol Chem 1997 · PubMed 9278416

Whole pathway: Vitamin C

Related pathways

• 8-OHdG — Eisen, Kupfer (Cu)
• Iodine — Natrium (intrazellulär), Eisen
• Nitrosative stress — Eisen, Glutathion (GSH)
• Thyroid hormones — Natrium (intrazellulär), Eisen
• Borrelia — Eisen, Selen

As of 2026-09-16. Draft written by Claude to schema v2; sources checked in PubMed; expert review pending
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