Vitamin E primarily serves as a free radical scavenger to protect fatty acids from oxidation; deficiency predisposes cell membranes to oxidative injury. The cells that are most susceptible include neurons with long axons (due to large membrane surface area) and erythrocytes (due to high oxygen exposure).
Clinical features
Neurologic dysfunction
Demyelination of the posterior column and spinocerebellar tract → ↓ proprioception and vibration sensation; ataxia (mimics Friedreich ataxia)
Neurologic symptoms are similar to vitamin B12 deficiency, except that vitamin E deficiency does not lead to hypersegmented neutrophils, megaloblastic anemia, and increased methylmalonic acid levels.
Hemolytic anemia: deficiency results in increased fragility of erythrocytes and membrane breakdown
