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Environ Toxicol Pharmacol. 2013 Nov;36(3):1242-52. doi: 10.1016/j.etap.2013.10.008. Epub 2013 Oct 23.

Oxidative stress precedes mitochondrial dysfunction in gerbil brain after aluminum ingestion.

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Special Hospital for Addictions, Teodora Drajzera 44, Belgrade, Serbia.


Several studies suggest that aluminum (Al) intake might increase an individual's risk of developing Alzheimer disease. The dynamic of changes in acetylcholinesterase (AChE), cytochrome c oxidase (COX), Complex I, superoxide dismutase (SOD) and catalase (CAT) activities, and the lipid peroxide (MDA), superoxide anion (O₂(-)) and thiol (SH) group levels in gerbil's brain after aluminum ingestion were analyzed. Gerbils that orally received aluminum chloride (LD₂₅ or LD₅₀) were sacrificed 2, 6 or 24 h later. Another group was subacutely treated (21 days; LD10). Controls received saline. Biochemical parameters were measured in cortex, hippocampus, thalamus and nucleus caudatus. Two hours after acute Al exposure AChE activity and SH group content were decreased and MDA and O₂(-) levels were elevated in all investigated brain structures. The changes of COX and CAT were structure specific. SOD was increased after 6 h. Changes of investigated parameters were also seen after subacute Al treatment. These results might suggest the presence of additional source of free radicals in early phase of Al poisoning.


Aluminum; Alzheimer's disease; Cytochrome c oxidase; Gerbils; Oxidative stress

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