Brain oxidative stress and selective behaviour of aluminium in specific areas of rat brain: potential effects in a 6-OHDA-induced model of Parkinson’s disease
Article first published online: 24 MAR 2009
© 2009 The Authors. Journal Compilation © 2009 International Society for Neurochemistry
Journal of Neurochemistry
Volume 109, Issue 3, pages 879–888, May 2009
How to Cite
Sánchez-Iglesias, S., Méndez-Álvarez, E., Iglesias-González, J., Muñoz-Patiño, A., Sánchez-Sellero, I., Labandeira-García, J. L. and Soto-Otero, R. (2009), Brain oxidative stress and selective behaviour of aluminium in specific areas of rat brain: potential effects in a 6-OHDA-induced model of Parkinson’s disease. Journal of Neurochemistry, 109: 879–888. doi: 10.1111/j.1471-4159.2009.06019.x
- Issue published online: 7 APR 2009
- Article first published online: 24 MAR 2009
- Received October 7, 2008; revised manuscript received February 20, 2009; accepted February 20, 2009.
- antioxidant enzymes;
- lipid peroxidation;
- Parkinson’s disease;
- protein oxidation
J. Neurochem. (2009) 109, 879–888.
The ability of aluminium to affect the oxidant status of specific areas of the brain (cerebellum, ventral midbrain, cortex, hippocampus, striatum) was investigated in rats intraperitoneally treated with aluminium chloride (10 mg Al3+/kg/day) for 10 days. The potential of aluminium to act as an etiological factor in Parkinson’s disease (PD) was assessed by studying its ability to increase oxidative stress in ventral midbrain and striatum and the striatal dopaminergic neurodegeneration induced by 6-hydroxydopamine in an experimental model of PD. The results showed that aluminium caused an increase in oxidative stress (TBARS, protein carbonyl content, and protein thiol content) for most of the brain regions studied, which was accompanied by a decrease in the activity of some antioxidant enzymes (superoxide dismutase, catalase, glutathione peroxidase). However, studies in vitro confirmed the inability of aluminium to affect the activity of those enzymes. The reported effects exhibited a regional-selective behaviour for all the cerebral structures studied. Aluminium also enhanced the ability of 6-hydroxydopamine to cause oxidative stress and neurodegeneration in the dopaminergic system, which confirms its potential as a risk factor in the development of PD.