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