High-affinity sodium–vitamin C co-transporters (SVCT) expression in embryonic mouse neurons
Version of Record online: 20 DEC 2001
Journal of Neurochemistry
Volume 78, Issue 4, pages 815–823, 2001
How to Cite
Castro, M., Caprile, T., Astuya, A., Millán, C., Reinicke, K., Vera, J. C., Vásquez, O., Aguayo, L. G. and Nualart, F. (2001), High-affinity sodium–vitamin C co-transporters (SVCT) expression in embryonic mouse neurons. Journal of Neurochemistry, 78: 815–823. doi: 10.1046/j.1471-4159.2001.00461.x
- Issue online: 20 DEC 2001
- Version of Record online: 20 DEC 2001
- Received February 5, 2001; revised manuscript received May 24, 2001; accepted May 25, 2001.
- ascorbic acid;
- dehydroascorbic acid;
The sodium–vitamin C co-transporters SVCT1 and SVCT2 transport the reduced form of vitamin C, ascorbic acid. High expression of the SVCT2 has been demonstrated in adult neurons and choroid plexus cells by in situ hybridization. Additionally, embryonic mesencephalic dopaminergic neurons express the SVCT2 transporter. However, there have not been molecular and kinetic analyses addressing the expression of SVCTs in cortical embryonic neurons. In this work, we confirmed the expression of a SVCT2-like transporter in different regions of the fetal mouse brain and in primary cultures of neurons by RT-PCR. Kinetic analysis of the ascorbic acid uptake demonstrated the presence of two affinity constants, 103 µm and 8 µm. A Km of 103 µm corresponds to a similar affinity constant reported for SVCT2, while the Km of 8 µm might suggest the expression of a very high affinity transporter for ascorbic acid. Our uptake analyses also suggest that neurons take up dehydroascorbic acid, the oxidized form of vitamin C, through the glucose transporters. We consider that the early expression of SVCTs transporters in neurons is important in the uptake of vitamin C, an essential molecule for the fetal brain physiology. Vitamin C that is found at high concentration in fetal brain may function in preventing oxidative free radical damage, because antioxidant radical enzymes mature only late in the developing brain.