Ascorbic acid depletion enhances expression of the sodium-dependent vitamin C transporters, SVCT1 and SVCT2, and uptake of ascorbic acid in livers of SMP30/GNL knockout mice

2010 ◽  
Vol 496 (1) ◽  
pp. 38-44 ◽  
Author(s):  
Akiko Amano ◽  
Toshiro Aigaki ◽  
Naoki Maruyama ◽  
Akihito Ishigami
Endocrinology ◽  
2008 ◽  
Vol 149 (1) ◽  
pp. 73-83 ◽  
Author(s):  
Ximei Wu ◽  
Takuma Iguchi ◽  
Norio Itoh ◽  
Kousuke Okamoto ◽  
Tatsuya Takagi ◽  
...  

Glia ◽  
2009 ◽  
pp. NA-NA ◽  
Author(s):  
Burkhard Gess ◽  
Christina Lohmann ◽  
Hartmut Halfter ◽  
Peter Young

2007 ◽  
Vol 575 (1-3) ◽  
pp. 1-11 ◽  
Author(s):  
Takeshi Takarada ◽  
Eiichi Hinoi ◽  
Yuki Kambe ◽  
Koichi Sahara ◽  
Shintaro Kurokawa ◽  
...  

2013 ◽  
Vol 154 (42) ◽  
pp. 1651-1656 ◽  
Author(s):  
András Szarka ◽  
Tamás Lőrincz

Vitamin C requirement is satisfied by natural sources and vitamin C supplements in the ordinary human diet. The two major forms of vitamin C in the diet are L-ascorbic acid and L-dehydroascorbic acid. Both ascorbate and dehydroascorbate are absorbed along the entire length of the human intestine. The reduced form, L-ascorbic acid is imported by an active mechanism, requiring two sodium-dependent vitamin C transporters (SVCT1 and SVCT2). The transport of the oxidized form, dehydroascorbate is mediated by glucose transporters GLUT1, GLUT3 and possibly GLUT4. Initial rate of uptake of both ascorbate and dehydroascorbate is saturable with increasing external substrate concentration. Vitamin C plasma concentrations are tightly controlled when the vitamin is taken orally. It has two simple reasons, on the one hand, the capacity of the transporters is limited, on the other hand the two Na+-dependent transporters can be down-regulated by an elevated level of ascorbate. Orv. Hetil., 154 (42), 1651–1656.


2019 ◽  
Vol 122 (10) ◽  
pp. 1120-1129 ◽  
Author(s):  
Ryusei Uchio ◽  
Yoshitaka Hirose ◽  
Shinji Murosaki ◽  
Akihito Ishigami

AbstractVitamin C (VC) is a vital micronutrient for humans and some other mammals and also has antioxidant activity. Stress-induced elevation of glucocorticoid production is well known to cause immunosuppression. The present study evaluated the effect of high VC intake on glucocorticoid-induced immune changes in mice. Senescence marker protein 30 knockout mice with genetic VC deficiency were fed a diet containing the recommended VC content (20 mg/kg per d; 0·02 %VC group) or a high VC content (200 mg/kg per d; 0·2 %VC group) for 2 months, then dexamethasone was given by intraperitoneal injection. After administration of dexamethasone, the plasma ascorbic acid concentration decreased significantly in the 0·02 %VC group and was unchanged in wild-type C57BL/6 mice on a VC-deficient diet (wild-type group), while it was significantly higher in the 0·2 %VC group compared with the other two groups. In the 0·02 %VC and wild-type groups, dexamethasone caused a significant decrease in the cluster of differentiation (CD)4+ and CD8+ T cells among splenocytes as well as a significant decrease in IL-2, IL-12p40 and interferon-γ protein production by splenocytes and a significant decrease in T-cell proliferation among splenocytes. In the 0·2 %VC group, these dexamethasone-induced immunosuppression improved when compared with the other two groups. In addition, reduction in the intracellular levels of ascorbic acid, superoxide dismutase and glutathione in splenocytes by dexamethasone as well as elevation in thiobarbituric acid-reactive substances were significantly suppressed in the 0·2 %VC group. These findings suggest that high dietary VC intake reduces glucocorticoid-induced T-cell dysfunction by maintaining intracellular antioxidant activity.


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