Redox Properties of Human Erythrocytes Are Adapted for Vitamin C Recycling.
Level 5 - mechanism / opinion, no new human data
In vitro laboratory/bench study on human erythrocytes
PubMed 34938201 · doi:10.3389/fphys.2021.767439
What was done
In vitro experiments were conducted on isolated human erythrocytes to investigate how dehydroascorbate (DHA, the oxidized form of ascorbic acid) uptake affects red blood cell redox metabolism. Authors evaluated plasma membrane electron transport (PMET) activity mediated by DCytb, cellular reactive oxygen species (ROS) levels, and glutathione dynamics (GSH depletion and GSSG efflux) under varying conditions including the presence of glucose (5 mM), 2-deoxy-glucose (2-DG), and the MRP transporter inhibitor MK-571.
What was found
DHA uptake enhanced PMET activity and decreased cellular ROS levels, with both effects markedly increased in the presence of physiological glucose concentrations (no baseline or fold-change numbers provided in abstract). Reduction of DHA to ascorbic acid depleted intracellular GSH and caused GSSG efflux. GSSG efflux was inhibited by MK-571 with an IC50 of 5 μM. Both GSH depletion and GSSG efflux were completely reversed by 5 mM glucose and partially rescued by 2-deoxy-glucose.
Why it matters
This study delineates the biochemical pathways human erythrocytes use to recycle oxidized vitamin C, linking GLUT1 transport and DCytb activity to glucose-driven antioxidant maintenance.
Limits
The study is entirely in vitro; donor sample size (n), demographics, and preparation details are not reported in the abstract. In vivo relevance, physiological kinetics in whole blood, and clinical translation were not assessed.
Cited by
- supports Red blood cells transport dehydroascorbic acid only and generate ascorbate via intracellular recycling, rather than transporting ascorbate directly.