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Abstract
The present study was performed to determine aluminum uptake, retention, and neurotoxic
effects in the presence of dietary citrate. Six-week-old female Swiss-Webster mice
were fed semipurified diets containing 3.5% sodium citrate and either 3 μg Al/g diet
(3 Al) or 1,000 μg Al/g diet (1,000 Al) as AlCl3. After 5 to 7 weeks of feeding these diets, changes in behavior were assessed using
the National Institute of Environmental Health Sciences Neurobehavioral Test Battery.
Liver and bone Al concentrations in the 1,000 Al group were higher than in the 3 Al
group at both the 5- and 7-week time points. Spinal cord Al concentrations in the
1,000 Al group were 200% higher at 5 weeks (P < .01) than in controls, and brain nuclear fraction Al concentrations in the 1,000
Al group were 150% higher at 5 and 7 weeks (P < .01) than in the 3 Al group. The Neurobehavioral Test Battery showed lower grip
strength and greater startle responsiveness in the 1,000 Al group compared with the
3 Al group at both the 5- and 7-week time points. Based on reports that Al can act
as a pro-oxidant, we examined Al-induced brain lipid and protein oxidative damage;
neither was evident in the Al-intoxicated mice. In summary, feeding of Al and citrate
to mice resulted in Al accumulation in the central nervous system, and this accumulation
was associated with overt signs of neurotoxicity. Brain protein and lipid oxidative
damage was not associated with early manifestation of Al toxicity.
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Article info
Publication history
Accepted:
November 2,
1992
Received:
August 10,
1992
Identification
Copyright
© 1993 Published by Elsevier Inc.