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.
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.
Sánchez-Iglesias
Sofía
S
Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Santiago de Compostela, Santiago de Compostela, Spain.
Méndez-Alvarez
Estefanía
E
Iglesias-González
Javier
J
Muñoz-Patiño
Ana
A
Sánchez-Sellero
Inés
I
Labandeira-García
José Luís
JL
Soto-Otero
Ramón
R
D018663:Adrenergic Agents / Q000494:pharmacology*; D000077410:Aluminum Chloride; D017607:Aluminum Compounds / Q000494:pharmacology*; D000704:Analysis of Variance; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects*; D001921:Brain / Q000033:anatomy & histology / Q000187:drug effects* / Q000502:physiology / Q000648:ultrastructure; D002374:Catalase / Q000378:metabolism; D002712:Chlorides / Q000494:pharmacology*; D004298:Dopamine / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000378:metabolism; D050356:Lipid Metabolism / Q000187:drug effects; D008297:Male; D008928:Mitochondria / Q000187:drug effects; D008995:Monoamine Oxidase / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D016627:Oxidopamine / Q000494:pharmacology*; D050050:Protein Carbonylation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013482:Superoxide Dismutase / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014446:Tyrosine 3-Monooxygenase / Q000378:metabolism
D018663:Adrenergic Agents; D017607:Aluminum Compounds; D002712:Chlorides; D017392:Thiobarbituric Acid Reactive Substances; D000077410:Aluminum Chloride; D016627:Oxidopamine; D002374:Catalase; D005979:Glutathione Peroxidase; D014446:Tyrosine 3-Monooxygenase; D013482:Superoxide Dismutase; D008995:Monoamine Oxidase; D004298:Dopamine