Chronic vitamin C deficiency promotes redox imbalance in the brain but does not alter sodium-dependent vitamin C transporter 2 expression.
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.
Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C 1870, Denmark. maypa@sund.ku.dk.
Maya D
MD
Paidi
Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C 1870, Denmark. jannes@sund.ku.dk.
Janne G
JG
Schjoldager
Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C 1870, Denmark. jopl@sund.ku.dk.
Jens
J
Lykkesfeldt
Faculty of Health and Medical Sciences, University of Copenhagen, Frederiksberg C 1870, Denmark. ptn@sund.ku.dk.
Pernille
P
Tveden-Nyborg
D000818:Animals; D001205:Ascorbic Acid / Q000008:administration & dosage / Q000097:blood; D001206:Ascorbic Acid Deficiency / Q000503:physiopathology*; D001921:Brain / Q000378:metabolism* / Q000503:physiopathology; D002908:Chronic Disease; D005260:Female; D005786:Gene Expression Regulation; D006168:Guinea Pigs; D050356:Lipid Metabolism; D008315:Malondialdehyde / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress; D060347:Sodium-Coupled Vitamin C Transporters / Q000235:genetics / Q000378:metabolism*
D060347:Sodium-Coupled Vitamin C Transporters; D008315:Malondialdehyde; D001205:Ascorbic Acid