Maturational loss of the vitamin C transporter in erythrocytes.
Level 5 - mechanism / opinion, no new human data
In vitro laboratory study in human erythrocytes and a mouse cell culture model (mechanism-based research)
PubMed 17586466 · doi:10.1016/j.bbrc.2007.06.072
What was done
Researchers measured radiolabeled ascorbate uptake and performed immunoblotting for the ascorbate transporter SVCT2 in human erythrocytes. They also tracked SVCT2 protein levels and ascorbate transport rates across erythroid differentiation stages using a Friend virus-infected mouse erythroblast cell culture model.
What was found
Human erythrocytes demonstrated very low rates of radiolabeled ascorbate uptake, matching an absence of SVCT2 protein on immunoblots. In the mouse erythroblast model, SVCT2 was present during early erythroblast stages but was lost upon nuclear extrusion during transition to the reticulocyte stage. Specific ascorbate transport rates directly correlated with SVCT2 presence throughout maturation. No specific numerical values or transport rates were reported in the abstract.
Why it matters
This study provides a mechanistic explanation for why mature red blood cells maintain ascorbate levels equivalent only to plasma rather than actively concentrating it like nucleated cells.
Limits
The abstract reports no quantitative transport rates, kinetic parameters, or sample sizes. Observations in mouse erythroid culture models may not fully capture every feature of human in vivo erythropoiesis.
Cited by
- supports Red blood cells transport dehydroascorbic acid only and generate ascorbate via intracellular recycling, rather than transporting ascorbate directly.