Vitamin E protects the brain against oxidative injury stimulated by excessive aluminum intake

The effect of feeding groups of mice with a diet containing 2000, 4000 and 6000 mu g aluminum (Al3-/g) for two weeks (subacute) or 2000 and 4000 mu g Al3+/g for eight weeks (subchronic) as well as the coadministration of vita min E (alpha-tocopherol) 500 mu g/g with Al3-, On the status of glutathione (GSH) and lipid peroxides as thiobarbituric acid reactive substances (TBAR S) in whole brain tissues were evaluated. Changes in TBARS were further eva luated in vitro following the incubation of brain homogenates of the Al3+-f ed mice in the presence of 50 mu M FeSO4. The results of subacute experimen ts revealed that the brain levels of GSH were significantly decreased only in the group of mice that received 6000 mu g Al3+/g diet (P<0.05) and this effect was partially ameliorated when vitamin E was coadministered with Al3 -. TEARS were significantly increased in vitro only in the presence of free iron ions and depended on the concentration of Al3+ in the diet. The effec t was opposed by the vitamin E intake. Following subchronic Al3+ intake, the GSH content of the brain was signific antly decreased only in the group of mice that received 4000 mu g Al3- /g d iet (P<0.01), while TBARS were significantly increased in the brain tissues in vivo as well as in the presence of free iron ions in vitro. However, co adminstration of vitamin E with Al3+ for eight weeks preserved GSH levels a nd decreased TEARS in the brain of mice in vivo and in the presence of free iron ions in vitro. It is concluded that the long term administration of v itamin E may prevent Al3+-stimulated oxidative injury in the brain.