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Sodium-dependent vitamin C transporters are integral membrane proteins responsible for the active uptake of vitamin C (ascorbic acid) into cells, essential for human health because humans cannot synthesize vitamin C. The two main isoforms, SVCT1 (encoded by *SLC23A1*) and SVCT2 (encoded by *SLC23A2*), are members of the nucleobase-ascorbate transporter (NAT) family within the solute carrier (SLC23) superfamily[1][2][3][4][6]. These transporters co-transport sodium and vitamin C in a 2:1 stoichiometry, using the sodium gradient across the plasma membrane to drive the uptake of ascorbate against its concentration gradient[1][3][4][5]. SVCT1 is primarily involved in vitamin C absorption and re-absorption in epithelial tissues such as intestine and kidney, controlling systemic levels[1][2][4][7]. SVCT2 is widely expressed, facilitating vitamin C uptake in tissues with high metabolic needs such as brain and placenta[1][2][4]. In contrast, the oxidized form of vitamin C (dehydroascorbic acid) is taken up via glucose transporters (GLUT1, GLUT3, and GLUT4)[2][6]. Dysfunction or genetic variation in these transporters can impair vitamin C bioavailability and increase risk for diseases associated with oxidative stress, metabolic disorders, neurological deficits, and certain cancers[7][8]. Currently, no therapeutic inhibitors or activators are in clinical use, but transporter expression can affect efficacy of pharmacological vitamin C therapy[7][8].
Symport/co-transport: vectorial uptake of vitamin C (ascorbic acid) together with sodium ions (2:1 Na+:ascorbate)[1][3][4]; Transport of reduced ascorbic acid (not dehydroascorbic acid, which is transported by GLUTs)[2][6]
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