Abstract
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.
Highlights
Vitamin E (α-tocopherol; vitamin E (VE)) is a lipid-soluble antioxidant acting as a peroxyl radical scavenging molecule that inhibits lipid peroxidation in biological membranes
The interaction between vitamin C (VC) and VE with respect to their concentrations, the gene expression of their transporters and GSH level in various tissues were examined using SMP30KO mice
Based on the intake of mice, the converted doses of VC and VE in a human (60 kg body weight) were estimated approximately 1000 mg/d VC and 300 mg/d VE according to the FDA guidance
Summary
Vitamin E (α-tocopherol; VE) is a lipid-soluble antioxidant acting as a peroxyl radical scavenging molecule that inhibits lipid peroxidation in biological membranes. The OH group on the chromanol of VE is no longer available after reacting with a free radical and needs to be regenerated to maintain its antioxidant status[1]. VE can intercept lipid peroxyl radicals at the membrane surface as well as inside the membrane, and water-soluble agents that regenerate VE can access the chromanol group when it is located at the surface[2]. Chylomicrons containing VE eventually reach the liver and are incorporated into hepatocytes by endocytosis. The VE component is selectively secreted from the liver by α-tocopherol transfer protein. Α-tocopherol transfer protein selectively binds VE and moves to the cell membrane[4].
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