The Biochemical Pathway of Vitamin C Explained

December 24, 2025 •

3 min read

Over 95% of circulating vitamin C is transported in its reduced form, ascorbate, highlighting its critical role in the body. Understanding the biochemical pathway of vitamin C involves examining its absorption, distribution, metabolic functions as an antioxidant and cofactor, and eventual degradation and excretion.

Quick Summary

This article details the biochemical processing of vitamin C, including intestinal uptake, transport to tissues, key cellular functions, and catabolism. It covers how the body manages this essential nutrient, from absorption to eventual excretion or oxidative breakdown.

Key Points

Absorption Mechanism: Vitamin C is absorbed via both active transport (SVCT1) at low doses and passive diffusion at high doses in the small intestine.
Tissue Distribution: The SVCT2 transporter ensures high concentrations of vitamin C are maintained in vital tissues like the brain and adrenal glands.
Metabolic Recycling: Oxidized dehydroascorbic acid (DHA) is efficiently reduced back to ascorbate intracellularly, primarily using glutathione and specific reductases.
Cofactor Functions: As an electron donor, vitamin C is a vital cofactor for enzymes critical to collagen synthesis, carnitine production, and neurotransmitter metabolism.
Antioxidant Activity: The reversible redox couple of ascorbate and DHA allows vitamin C to effectively neutralize damaging free radicals and protect cells from oxidative stress.
Degradation and Excretion: Unrecycled DHA is irreversibly hydrolyzed to 2,3-diketogulonic acid, which is ultimately degraded to oxalate and excreted in the urine.

Absorption: The Body's Intake of Vitamin C

The human body relies entirely on dietary sources for vitamin C, also known as L-ascorbic acid, as a genetic mutation renders us unable to synthesize it internally. The journey of vitamin C begins in the small intestine, where its absorption is a dose-dependent process. At physiological concentrations, active transport via sodium-dependent vitamin C transporters (SVCT1) is the primary mechanism. At higher doses, absorption efficiency decreases, and passive diffusion plays a role. The oxidized form, dehydroascorbic acid (DHA), is absorbed using glucose transporters (GLUTs) and quickly reduced back to ascorbate inside the cell.

Transport and Distribution

After absorption, vitamin C enters the bloodstream and is transported as ascorbate. SVCT1 and SVCT2 transporters facilitate cellular uptake, resulting in much higher intracellular concentrations compared to plasma. SVCT2 is particularly important for maintaining high vitamin C levels in tissues like the brain and adrenal glands. These high tissue concentrations suggest crucial roles in functions like hormone synthesis.

Metabolism: Antioxidant and Cofactor Functions

Vitamin C's metabolic activity stems from its ability to donate electrons, acting as both an antioxidant and an enzymatic cofactor.

Vitamin C's Role in Redox Reactions

As an antioxidant, vitamin C neutralizes reactive oxygen species. It becomes semidehydroascorbate when donating an electron, which can then dismutate into ascorbate and DHA. Intracellular enzymes and glutathione (GSH) reduce DHA back to ascorbate, allowing for recycling.

Enzymatic Cofactor Activity

Vitamin C is a cofactor for enzymes by keeping metal ions in a reduced state. This is essential for:

Collagen Synthesis: It's required for hydroxylases that modify proline and lysine, necessary for collagen's structure. Deficiency leads to scurvy.
Carnitine Biosynthesis: Vitamin C supports the synthesis of L-carnitine, important for fatty acid transport into mitochondria.
Neurotransmitter Synthesis: It aids in producing catecholamines like norepinephrine.
Tyrosine Metabolism: It acts as a cofactor for an enzyme involved in tyrosine breakdown.

Catabolism and Excretion of Vitamin C

Unrecycled vitamin C is degraded into inactive metabolites and eliminated via the kidneys. DHA can undergo irreversible hydrolysis to 2,3-diketogulonic acid. This is further metabolized into products including oxalic acid, threonic acid, and carbon dioxide, with oxalate being a significant urinary excretion product. At normal intake, kidney reabsorption is efficient, minimizing loss. However, with high intake exceeding tissue saturation, excess vitamin C is excreted in urine.

Comparison of Vitamin C Recycling vs. Degradation


Feature	Recycling Pathway	Degradation Pathway
Starting Molecule	Oxidized DHA and semidehydroascorbate	Unrecycled DHA
Key Reaction	Reduction back to ascorbate	Irreversible hydrolysis of DHA
Main Enzymes	Glutaredoxin, NADPH-dependent reductases, and glutathione (GSH)	Spontaneous and enzymatic cleavage
Outcome	Restoration of the active vitamin C (ascorbate) pool	Loss of active vitamin C and formation of inactive metabolites
Physiological Significance	Maintains a stable intracellular vitamin C supply, supporting antioxidant and cofactor functions.	Eliminates excess or oxidized vitamin C from the body, preventing accumulation.
Key Products	Ascorbate	2,3-diketogulonic acid, oxalate, threonic acid, CO2

Conclusion: The Integrated Pathway of an Essential Nutrient

The biochemical pathway of vitamin C involves efficient absorption, transport, metabolic functions as an antioxidant and cofactor, and controlled excretion. This complex process, driven by specific transporters and enzymatic reactions, is vital for maintaining human health and highlights the importance of dietary intake of this essential nutrient.

Optional outbound Markdown link

For more information on the history and functions of vitamin C, visit the National Institutes of Health Office of Dietary Supplements.

Frequently Asked Questions

Humans cannot synthesize vitamin C because we lack the enzyme L-gulonolactone oxidase, which is necessary to catalyze the final step of its synthesis pathway.

SVCT1 and SVCT2 are crucial sodium-dependent transporters that facilitate the absorption of vitamin C (ascorbate) into intestinal cells and distribute it throughout various body tissues.

The oxidized form, dehydroascorbic acid (DHA), is recycled back to active ascorbate using intracellular systems involving glutathione (GSH) and NADPH-dependent reductases.

Excess vitamin C that saturates bodily tissues is primarily excreted through the kidneys. Unrecycled dehydroascorbic acid is degraded into inactive products like oxalic acid and then eliminated in the urine.

Vitamin C acts as a cofactor for hydroxylase enzymes that add hydroxyl groups to proline and lysine amino acids within collagen chains. This modification is essential for the formation of the stable, triple-helical structure of mature collagen.

If not recycled, vitamin C is irreversibly metabolized into products including 2,3-diketogulonic acid, oxalic acid, and threonic acid, which are then excreted.

The oxidized form of vitamin C, DHA, utilizes glucose transporters (GLUTs) to enter cells. This process can be inhibited by high levels of glucose, especially in individuals with diabetes.