ABSTRACT
Journal of Clinical Nutrition 2009;90:540–6.

ABSTRACT
Background: The neonatal brain is particularly vulnerable to imbalances in redox homeostasis because of rapid growth and immature antioxidant systems. Vitamin C has been shown to have a key function in the brain, and during states of deficiency it is able to retain higher concentrations of vitamin C than other organs. However, because neurons maintain one of the highest intracellular concentrations of vitamin C in the organism, the brain may still be more sensitive to deficiency despite these preventive measures.

Objective: The objective was to study the potential link between chronic vitamin C deficiency and neuronal damage in newborn guinea pigs.

Design: Thirty 6- to 7-d-old guinea pigs were randomly assigned to 2 groups to receive either a vitamin C–sufficient diet or the same
diet containing a low concentration of vitamin C (but adequate to prevent scurvy) for 2 mo. Spatial memory was assessed by the
Morris Water Maze, and hippocampal neuron numbers were quantified by stereologic techniques.

Results: The results showed a reduction in spatial memory (P , 0.05) and an increased time to first platform hit (P , 0.05) in de-
ficient animals compared with controls. The deficient animals had a lower total number of neurons in hippocampal subdivisions (dentate gyrus, cornu ammonis 1, and cornu ammonis 2–3) than did the normal controls (P , 0.05).

Conclusions: Our data show that vitamin C deficiency in early postnatal life results in impaired neuronal development and a functional decrease in spatial memory in guinea pigs. We speculate that this unrecognized effect of vitamin C deficiency may have clinical implications for high-risk individuals, such as in children born from vitamin C–deficient mothers.

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