Brain oxidative stress and selective behaviour os aluminium in specific areas of rat brain: potential effects in a 6-OHDA-indiced model of Parkinson's disease

The ability of aluminium to affect the oxidant status of specificareas of the brain (cerebellum, ventral midbrain, cortex, hip-pocampus, striatum) was investigated in rats intraperitoneallytreated with aluminium chloride (10 mg Al 3+ /kg/day) for10 days. The potential of aluminium to act as an etiologicalfactor in Parkinson’s disease (PD) was assessed by studyingits ability to increase oxidative stress in ventral midbrain andstriatum and the striatal dopaminergic neurodegeneration in-duced by 6-hydroxydopamine in an experimental model of PD.The results showed that aluminium caused an increase inoxidative stress (TBARS, protein carbonyl content, and pro-tein thiol content) for most of the brain regions studied, whichwas accompanied by a decrease in the activity of some anti-oxidant enzymes (superoxide dismutase, catalase, glutathi-one peroxidase). However, studies in vitro confirmed theinability of aluminium to affect the activity of those enzymes.The reported effects exhibited a regional-selective behaviourfor all the cerebral structures studied. Aluminium also en-hanced the ability of 6-hydroxydopamine to cause oxidativestress and neurodegeneration in the dopaminergic system,which confirms its potential as a risk factor in the developmentof PD.