Summary Vitamin E inhibits oxidative processes in living tissues. We produced vitamin E-deficient mice by feeding them a vitamin E-deficient diet to verify the influence of chronic vitamin E deficiency on cognitive function. We measured cognitive function over a 5-d period using the Morris water maze task, as well as antioxidant enzyme activity and lipid peroxidation in discrete brain regions, and total serum cholesterol content. Threeand six-mo-old vitamin E-deficient and age-matched control mice were used. In addition, 24-mo-old mice were used as an aged-model. In the 3-mo-old mice, cognitive function in the vitamin E-deficient (short-term vitamin E-deficient) group was significantly impaired compared to age-matched controls. Although the lipid peroxidation products in the cerebral cortex, cerebellum and hippocampus did not significantly differ in 3-mo-old mice, the levels in the 6-mo-old vitamin E-deficient (long-term vitamin E-deficient) mice were significantly increased compared to age-matched controls. Serum cholesterol content was also significantly increased in the short-and long-term vitamin E-deficient mice compared to their respective age-matched controls. These results indicate that chronic vitamin E deficiency may slowly accelerate brain oxidation. Thus, vitamin E concentrations may need to be monitored in order to prevent the risk of cognitive dysfunction, even under normal conditions.

Obesity is a serious public health issue in developed countries, and is known to increase the risk of several diseases such as diabetes, cardiovascular events and arteriosclerosis. These phenomena are closely correlated with oxidative damage. Recently, several lines of evidence have demonstrated that neurodegenerative diseases such as Alzheimer’s and Parkinson’s are also related to oxidative damage. To clarify the relationship between obesity and oxidative brain injury, we investigated brain antioxidant networks in high-fat (HF) diet-treated mice in the presence or absence of tocotrienols (T3s) and bran. Co-treatment with T3s and bran significantly inhibited bodyweight gain in HF diet-treated mice. Serum and cortex T3 levels, and brain antioxidant enzyme activities and protein expressions did not differ among the groups except for SOD protein expression in the cerebellum. Brain p-mTOR and p-Akt protein expressions, which are related to autophagy, did not differ among the groups. These results indicate that treatment with T3s for eight weeks had showed an anti-obesity effect in HF diet-treated mice. However, significant alterations in T3 levels were not observed in the serum and brain of mice.

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