Studies in mice have suggested that both dietary Al excess and dietary Mn deficiency promote oxidative tissue damage. To determine if these factors can interact to produce functional nervous system damage, female mice (N = 10-12 per group) were fed diets with control or low Mn (35 or 3 μg Mn/g diet) and/or control or high Al (25 or 1000 μg Al/g diet, Al as Al lactate) content for a 90-day period. No overt signs of neurotoxicity were observed in any group. Excess Al produced a threefold Al accumulation in both liver and brain, a slight acceleration of growth, decreased motor activity, decreased grip strength, and decreased startle responsiveness. Manganese deprivation led to liver, brain, and femur Mn depletion and reduced liver MnSOD activity but no neurobehavioral changes. No interactive effects between Al excess and Mn deficiency were observed. Neither Al excess nor Mn deficiency altered brain or liver lipid peroxidation measures. This study suggests that (1) subchronic dietary Al at doses of 1000 μg Al/g diet produces elevated brain Al and altered neurobehavioral indices in adult mice; (2) brain lipid peroxidation is not altered by this treatment; (3) dietary Mn deficiency doess not influence Al neurotoxicity in adult mice.
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