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. 2014 Apr 29;6(5):1809-22.
doi: 10.3390/nu6051809.

Chronic vitamin C deficiency promotes redox imbalance in the brain but does not alter sodium-dependent vitamin C transporter 2 expression

Maya D Paidi  1 , Janne G Schjoldager  2 , Jens Lykkesfeldt  3 , Pernille Tveden-Nyborg  4
Affiliations

Chronic vitamin C deficiency promotes redox imbalance in the brain but does not alter sodium-dependent vitamin C transporter 2 expression

Maya D Paidi et al. Nutrients. .

Abstract

Vitamin C (VitC) has several roles in the brain acting both as a specific and non-specific antioxidant. The brain upholds a very high VitC concentration and is able to preferentially retain VitC even during deficiency. The accumulation of brain VitC levels much higher than in blood is primarily achieved by the sodium dependent VitC transporter (SVCT2). This study investigated the effects of chronic pre-and postnatal VitC deficiency as well as the effects of postnatal VitC repletion, on brain SVCT2 expression and markers of oxidative stress in young guinea pigs. Biochemical analyses demonstrated significantly decreased total VitC and an increased percentage of dehydroascorbic acid, as well as increased lipid oxidation (malondialdehyde), in the brains of VitC deficient animals (p < 0.0001) compared to controls. VitC repleted animals were not significantly different from controls. No significant changes were detected in either gene or protein expression of SVCT2 between groups or brain regions. In conclusion, chronic pre-and postnatal VitC deficiency increased brain redox imbalance but did not increase SVCT2 expression. Our findings show potential implications for VitC deficiency induced negative effects of redox imbalance in the brain and provide novel insight to the regulation of VitC in the brain during deficiency.

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Figures

Figure 1
Figure 1
Quantitative PCR analysis of SVCT2 mRNA expression in brain. Quantitative PCR analysis of SVCT2 from three brain regions of guinea pigs between CTRL, REPL and DEF groups; Expressed values are mean of normalized ratio of SVCT2 to the reference gene S18 ± SD; target gene expression in HP (A); BC (B); and BFC (C), n = 10 for each group. Effect of diet between the three groups was assessed by one way ANOVA (p > 0.05).
Figure 2
Figure 2
Specificity of anti-SVCT2 in Western blot. (A) Specificity of anti-SVCT2 without pre-absorption of antibody with blocking peptide in guinea pig (Gp) brain lysates (HP, BFC, and BC, respectively) seen as a doublet above 60 kDa and in mouse (M) brain lysates as a single band at 60 kDa; (B) Show brain lysates of Gp and M with pre-absorption of antibody with blocking peptide. Block arrow show the non-specific band detected in western blots in a few guinea pig brain lysates. Western blot standard ladder (Std) and band lengths are displayed for both blots.
Figure 3
Figure 3
Western blot analysis of SVCT2 protein in brain. Densitometry analysis of western blot analysis of SVCT2 protein levels from three brain regions of guinea pigs HP (A); BC (B) and BFC (C); CTRL: control group, REPL: repleted group and DEF: deficient group. Representative pictures of the blots are depicted above each bar graph. Values are displayed as mean of normalized ratio to actin ± SD, the exact SVCT2 densitometry mean values (±SD) are provided in Table 3.
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