Aaa. El-fattah et al., Vitamin E protects the brain against oxidative injury stimulated by excessive aluminum intake, BIOC MOL B, 46(6), 1998, pp. 1175-1180
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.