Vitamin E (α-tocopherol; VE) is known to be regenerated from VE radicals by vitamin C (L-ascorbic acid; VC) in vitro. However, their in vivo interaction in various tissues is still unclear. Therefore, we alternatively examined the in vivo interaction of VC and VE by measurement of their concentrations in various tissues of senescence marker protein-30 (SMP30) knockout (KO) mice as a VC synthesis deficiency model. Male SMP30-KO mice were divided into four groups (VC+/VE+, VC+/VE–, VC–/VE+ and VC–/VE–), fed diets with or without 500 mg/kg VE and given water with or without 1·5 g/l VC ad libitum. Then, VC and VE concentrations in the plasma and various tissues were determined. Further, gene expression levels of transporters associated with VC and VE, such as α-tocopherol transfer protein (α-TTP) and sodium-dependent vitamin C transporters (SVCTs), were examined. These results showed that the VE levels in the VC-depleted (VC–/VE+) group were significantly lower than those in the VC+/VE+ group in the liver and heart; the VC levels in the VE-depleted (VC+/VE–) group were significantly lower than those in the VC+/VE+ group in the kidneys. The α-TTP gene expression in the liver and kidneys was decreased by VC and/or VE depletion. Moreover, SVCT1 gene expression in the liver was decreased by both VC and VE depletion. In conclusion, these results indicate that VC spares VE mainly in the liver and heart and that VE spares VC in the kidneys of SMP30-KO mice. Thus, interaction between VC and VE is likely to be tissue specific.

Ascorbic acid (vitamin C) has major effects on the intestinal uptake and utilisation of Fe in humans. The objective of the present study was to investigate the impact of Fe on the acquisition of ascorbic acid. The strategy was to study the cellular uptake and transport of ascorbic acid in the presence of Fe and also to observe the expression of the Na-dependent vitamin C transporter 1 (SVCT1) protein in human intestinal Caco-2 cells. SVCT1 is involved in the cellular uptake of ascorbic acid and is therefore a candidate for playing a role in the regulation of Fe utilisation. Caco-2 cells were cultured on transmembrane inserts in a three-compartment system followed by treatment with various combinations of FeCl2·4H2O (10–20 μmol/l) and sodium ascorbate (150 μmol/l). ELISA and Western blot analyses revealed that both SVCT1 and ferritin expressions were up-regulated in the presence of ascorbic acid in the basal compartment underneath the cells (10 and 22 %, respectively). Furthermore, when cells deficient in ascorbic acid were exposed to Fe, SVCT1 expression increased significantly (23·7 %). The increase in SVCT1 expression correlated with an increase in ascorbic acid uptake (285 %) in Fe-treated cells, as indicated by the SVCT1 inhibitor quercetin. We conclude that Fe plays an important role in regulating the uptake of ascorbic acid in human intestinal Caco-2 cells. This new angle could change the conceptual thinking of Fe and ascorbic acid utilisation and assist in the treatment and prevention of ascorbic acid-deficiency syndromes such as scurvy.