UCL Discovery

Abstract

A rat model of vitamin E (alpha-tocopherol) deficiency with similar "clinical," electrophysiological, and neuropathological abnormalities to those seen in man was used to investigate the effects of various amounts and forms of alpha-tocopheryl acetate (alphaTA) on neural and visual function. Electrophysiological techniques provide an objective, non-invasive measure of neural and visual function. These techniques were used in the animal model to determine the minimum dietary requirement of vitamin E necessary to prevent neural and visual abnormalities. They were also used to compare the biological activities of the natural (RRR-) and synthetic (all-rac-) forms of alpha-tocopherol in neural tissues. The results were as follows: (1) Significant differences in neural and visual function were observed between deficient and control rats after approximately 8 months. (2) An intake of 1.0 mg/kg all-rac- or 0.75 mg/kg RRR-alphaTA was observed to marginally protect nerves from vitamin E deficiency. (3) The biological activity of all-rac-alpha-tocopherol in neural tissues was approximately 75% of RRR-alpha-tocopherol. (4) The concentration of free malondialdehyde (an indicator of lipid peroxidation) was significantly increased in tissues from the deficient compared to the control animals. These results are consistent with a deficiency of alpha-tocopherol causing increased lipid peroxidation leading to abnormal neural electrophysiology. They could also be explained by more specific but as yet undefined function(s) of alpha-tocopherol in neural tissues.