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Ascorbic acid cellular transport

Molecular classification
Transporter, Membrane transporter, Solute carrier family, Nucleobase-ascorbate transporter family/NAT family for SVCTs, Facilitated diffusion transporter (GLUTs for dehydroascorbate)
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Overview

Cellular transport of ascorbic acid (vitamin C) is primarily mediated by sodium-dependent vitamin C transporters, SVCT1 and SVCT2, encoded by the SLC23A1 and SLC23A2 genes. SVCT1 is mainly expressed in epithelial tissues (kidney, intestine) and is responsible for maintaining whole-body vitamin C levels. SVCT2 is expressed more broadly (including the brain) and is crucial for distributing vitamin C to individual tissues. Both function as sodium-ascorbate symporters with a 2:1 sodium-to-ascorbate stoichiometry, enabling active uptake of ascorbic acid against a concentration gradient. For the oxidized form (dehydroascorbic acid), cellular entry occurs via facilitated diffusion through glucose transporters (GLUT1, GLUT3, GLUT4), important in some tissues. These transporters are essential for antioxidant protection, redox balance, and diverse roles in metabolism and disease, including cancer, neurological disorders, and scurvy[1][2][3][4].

Other names
SVCT1SVCT2SLC23A1SLC23A2SVCT = Sodium-dependent vitamin C transportergenes: SLC23A1, SLC23A2
02

Mechanism of action

Active, sodium-coupled co-transport of ascorbic acid (reduced form) via SVCT transporters Facilitated diffusion of dehydroascorbic acid (oxidized form) via GLUTs, followed by intracellular reduction

03

Biological functions

Cellular uptake of vitamin C (ascorbic acid and dehydroascorbic acid)Maintenance of vitamin C homeostasisRedox biology and antioxidant defenseBrain and organ function (SVCT2 is highly expressed in brain, retina, placenta, etc.)
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Disease associations

Cancer (altered expression associated with tumor biology)Neurodegenerative disease (due to role in brain ascorbate transport)Potential roles in cardiovascular disease (via antioxidant regulation)Other (inflammation, scurvy when deficient, oxidative stress conditions)
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Safety considerations

None directly related to normal function; excessive vitamin C supplementation considered generally safe but pharmacological doses (especially intravenous) may carry risks such as kidney stones in susceptible individuals or interactions with certain chemotherapiesGenetic deficiencies or variants in transporter genes could predispose to subclinical vitamin C deficiency
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Interacting drugs

Vitamin C (ascorbic acid, pharmacological high-dose ascorbate)

1 more in the full profile.

07

Biomarkers

SVCT1/SVCT2 protein or mRNA levels for tissue vitamin C uptake capacity (potential though not widely used)Plasma ascorbate concentration as surrogate markerSLC23A1 and SLC23A2 polymorphisms (associated with altered vitamin C transport efficiency)

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