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. 2021 May 15;13(5):1685. doi: 10.3390/nu13051685

Table 3.

Principal findings of postnatal vitamin C deficiency in the brain—findings from guinea pigs.

VitC Strain Time-Point Principal Findings Ref
Depletion Dunkin Hartley PD2–3 wks Increased lipid peroxidation (MDA), increased protein carbonyls, induced DNA-based excision. [24]
Severe deficiency Dunkin Hartley PD7–11 wks No effects on the investigated hippocampal structures or synaptic plasticity markers and BDNF in cortex, hippocampus or striatum. [184]
Deficiency No additional apparent differences compared to severe deficiency.
Pre- and postnatal deficiency Dunkin Hartley PD2–7 No effect on lipid peroxidation (MDA, 8-F2-isoprostane); GSH not different. [221]
PD10 Reduced hippocampal volume and reduced proliferation in hippocampal granular layer. [74]
PD27 Reduced hippocampal volume and increased proliferation in granular layer and subgranluar zones.
PD70 Increased lipid peroxidation (MDA). Hippocampal volume reduction. Persistent decrease in hippocampal volume despite vitC repletion after birth. [74,79]
Deficiency Dunkin Hartley PD7–9 wks No effect on lipid peroxidation (MDA) or redox markers (SOD, GSH). Reduced neuron numbers in hippocampus. Deviated serotonin metabolites and reduced synaptophysin. Reduced spatial memory competence. [185,266]

BDNF: brain-derived neurotrophic factor; deficiency: low vitC supplementation; depletion: no vitC supplementation; GSH: glutathione; MDA: malondialdehyde; PD: postnatal day; SOD: superoxide dismutase; wks: weeks.