Vitamin C, or ascorbic acid, is an important antioxidant. It also participates in numerous cellular functions such as peptide amidation, myelin formation, synaptic potentiation, and protection against glutamate toxicity. Although it circulates in the plasma in micromolar concentrations, it reaches millimolar concentrations in most tissues. These high concentrations are thought to be generated and maintained by SVCT2, a Na⁺-dependent transporter¹.

SVCT2 belongs to the SLC23 family of nucleobase-ascorbate transporters (NAT), that consists of SLCT1, SLCT2 and SLCT3 transporters². The NAT family shares a structure that contains fourteen transmembrane segments that are organized into a pair of “7 + 7” inverted repeats. The intertwined repeats constitute two distinctive domains, namely the core domain and the gate domain².

Neurons in the central nervous system (CNS) contain some of the highest ascorbic acid concentrations in mammalian tissues, and therefore targeted deletion of SVCT2 in mice causes widespread cerebral hemorrhage and death on post-natal day one. SCVT2 is also related to neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s. The expression of SVCT2 is relatively widespread, where it serves to either deliver ascorbic acid to tissues with high demand of vitamin C for enzymatic reactions or to protect metabolically highly active cells or protect specialized tissues from oxidative stress³.