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354 JAMC• 6 FÉVR. 2001; 164 (3) dant and, at physiological concentrations, probably does not produce reactive intermediaries. It protects lowdensity lipoproteins from oxidation, reduces harmful oxidants in the stomach and promotes iron absorption. Its antioxidant role in vivo is, however, unclear. Plasma ascorbic acid concentrations may be low in chronic or acute oxidant states such as in diabetes, in smokers, or following acute pancreatitis or myocardial infarction. Ascorbic acid is easily oxidized to the unstable dehydroascorbic acid. Dehydroascorbic acid is not normally detectable in plasma but may occur transiently during oxidant stress. Ascorbic acid is transported into the cell by sodium-dependent vitamin C transporters SVCT1 and SVCT2, one or both of which are found in most tissues. 6 Dehydroascorbic acid is transported by glucose transporters GLUT1 and GLUT3, and, in insulin-sensitive tissues, also by GLUT4. When exposed to bacteria, neutrophils oxidize extracellular ascorbic acid to form dehydroascorbic acid, which is transported into the neutrophil and rapidly reduced to ascorbic acid by the protein glutaredoxin (Fig. 1). As a result of this recycling of extracellular ascorbic acid, the neutrophil internal concentration of ascorbic acid increases 10-fold. 7 Ascorbic acid may quench oxidants generated during phagocytosis and, thus, protect the neutrophil and surrounding tissues from oxidative damage. Brain, adrenal cortex, liver, spleen, pancreas and kidney tissues concentrate vitamin C for unknown reasons.

When given orally, ascorbic acid is well absorbed at lower doses, but absorption decreases as the dose increases. Thus, median …