Excessive dietary aluminum (Al) has been proposed to be a factor contributing to several neurological disorders in humans. Six 8-week-old female Swiss Webster mice were fed for 10 weeks purified diets containing 100 (control, 100 Al), 500 (500 Al) or 1000 (1000 Al) μg Al/g diet. Brain and liver lipid peroxidation was determined by evaluating the production of 2-thiobarbituric acid reactive substances (TBARS) in brain and liver homogenates in the presence or absence of 50 μM ferrous iron. TBARS production in the absence of iron in brain homogenates from mice fed the 1000 Al diet was higher (30%) than that in the 100 Al control group (3.1 vs. 2.4 nmol TBARS/mg protein). The addition of ferrous iron increased TBARS production in brain homogenates from all 3 dietary groups. The iron-induced TBARS production was 26% higher in the 1000 Al brain homogenates than in the 100 Al group (4.9 vs. 3.9 nmol TBARS/mg protein). Brain TBARS production in the presence and absence of iron was similar between the 100 and 500 Al groups. TBARS production in liver homogenates measured either with or without iron was similar for the 3 groups. These results show that, in mice, dietary Al intoxication leads to increased brain TBARS production, suggesting that enhanced lipid peroxidation may be one possible mechanism underlying the neurological damage associated with increased tissue Al. © 1990.
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