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Animal seizure models have demonstrated that pharmacological doses of vitamin E administered after a kainate-induced seizure, can almost completely restore function of glutamine synthase, the enzyme responsible for converting excitatory glutamate, into non-toxic glutamine, for transport between astrocytes and neurons ( in vitro data which suggests that vitamin E may be able to reduce activity of the ionotropic AMPA, kainate, and NMDA glutamate receptors, in addition to protecting mitochondrial membrane potential through its antioxidant function ( in vitro and in vivo evidence that vitamin E can reduce neuroinflammatory responses mediated by microglial cells (Li et al., 2001

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Additionally, vitamin C and E supplementation improved clinical symptoms and clinical scores in TAO patients by reducing oxidative stress markers (131)