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首页> 外文期刊>Nutrients >Chronic Vitamin C Deficiency Promotes Redox Imbalance in the Brain but Does Not Alter Sodium-Dependent Vitamin C Transporter 2 Expression
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Chronic Vitamin C Deficiency Promotes Redox Imbalance in the Brain but Does Not Alter Sodium-Dependent Vitamin C Transporter 2 Expression

机译：慢性维生素C缺乏症会促进大脑中的氧化还原失衡，但不会改变钠依赖性维生素C转运蛋白2的表达

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摘要

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.
机译：维生素C（VitC）在大脑中既有特异性抗氧化剂又有非特异性抗氧化剂。大脑维持很高的VitC浓度，即使在缺乏时也能够优先保留VitC。钠依赖的VitC转运蛋白（SVCT2）主要实现了脑中VitC水平的积累远高于血液中的积累。这项研究调查了慢性的出生前和出生后VitC缺乏症以及出生后VitC补充对幼年豚鼠脑SVCT2表达和氧化应激标志物的影响。生化分析表明，与对照组相比，VitC缺乏动物的大脑中总VitC显着降低，脱氢抗坏血酸百分比增加，脂质氧化（丙二醛）增加（p <0.0001）。补充VitC的动物与对照组无显着差异。在各组或大脑区域之间，SVCT2的基因或蛋白质表达均未检测到显着变化。总之，慢性产前和产后VitC缺乏症会增加脑氧化还原失衡，但不会增加SVCT2表达。我们的发现表明，VitC缺乏症可能引起大脑氧化还原失衡的负面影响，并为维生素C缺乏症期间大脑中VitC的调节提供新的见解。

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