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Sodium-dependent vitamin C transporter 1 and Sodium-dependent vitamin C transporter 2 (SLC23A1 (for Sodium-dependent vitamin C transporter 1), SLC23A2 (for Sodium-dependent vitamin C transporter 2))

Target
SLC23A1 (for Sodium-dependent vitamin C transporter 1), SLC23A2 (for Sodium-dependent vitamin C transporter 2)
Molecular classification
Transporter, Solute carrier (SLC) family, Nucleobase-ascorbate transporter (NAT) family
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Overview

Sodium-dependent vitamin C transporter 1 (SLC23A1, SVCT1) and Sodium-dependent vitamin C transporter 2 (SLC23A2, SVCT2) are integral membrane proteins responsible for the active uptake of ascorbic acid (vitamin C) into cells, using the sodium gradient across the plasma membrane[1][2][3]. SVCT1 is primarily expressed in epithelial tissues such as the intestine, liver, and kidney, mediating intestinal absorption and renal reabsorption of ascorbate, and is characterized by high-capacity, moderate-affinity transport[1][3]. SVCT2 is broadly expressed, notably in brain, placenta, spleen, and other tissues, and is a high-affinity transporter critical for tissue ascorbate distribution and overall cellular antioxidant capacity; its absence is incompatible with life in mice[1][2][3]. Both transporters are essential for maintaining physiological levels of vitamin C, and their dysfunction is associated with severe deficiency states, increased oxidative stress, and perinatal mortality.

Other names
SVCT1 (for SLC23A1)SVCT2 (for SLC23A2)Ascorbate transporter 1/2Sodium-dependent ascorbate transporter 1/2
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Mechanism of action

For inhibitors: Blockade of sodium-dependent cotransport of ascorbate, reducing cellular vitamin C uptake. Diclofenamic acid: Inhibits ascorbate transport activity.

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Biological functions

Cellular uptake of ascorbic acid (vitamin C)Maintenance of intracellular and tissue ascorbate concentrationsRenal reabsorption of ascorbate (SLC23A1)Tissue distribution of ascorbate (SLC23A2)
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Disease associations

Other (Essential nutrient homeostasis; disruption causes scurvy, developmental/neonatal lethality in knockout mice, associated with disease risk via vitamin C deficiency)
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Safety considerations

Genetic deficiency or pharmacologic inhibition could cause severe vitamin C deficiency, neonatal death, and organ dysfunctionCompromised transporter activity results in perinatal mortality, increased oxidative stress, and impaired ascorbate reabsorption
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Interacting drugs

Diclofenamic acid (experimental SVCT inhibitor)

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