Ascorbate function and metabolism in the human erythrocyte.
Level 5 - mechanism / opinion, no new human data
Narrative review of biochemical and cellular mechanisms without primary human trial data.
PubMed 9405334 · doi:10.2741/a262
What was done
This narrative review describes the biochemical mechanisms of ascorbic acid (vitamin C) transport, intracellular recycling, and antioxidant function in human erythrocytes and blood plasma.
What was found
The abstract reports no numerical data or effect sizes. Mechanistically, erythrocytes match plasma ascorbate concentrations, rapidly import dehydroascorbic acid (DHA) via the GLUT1 transporter, and reduce DHA to ascorbate via direct reaction with glutathione as well as enzymatic reduction involving glutaredoxin and thioredoxin reductase. The resulting intracellular ascorbate slowly leaves erythrocytes, maintaining plasma ascorbate levels and preserving alpha-tocopherol (vitamin E) in red cell membranes and low-density lipoproteins against lipid peroxidation.
Why it matters
It outlines how erythrocytes serve as a continuous recycling reservoir for vitamin C to prevent oxidative damage and lipid peroxidation in vascular beds.
Limits
The abstract contains only mechanistic descriptions from a narrative review and presents no primary experimental numbers, sample sizes, controlled human trials, or clinical endpoints.
Cited by
- supports Red blood cells transport dehydroascorbic acid only and generate ascorbate via intracellular recycling, rather than transporting ascorbate directly.