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

Abstract

J. Neurochem. (2009) 109, 879–888. Abstract 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.

In vivo evaluation of a magnesium-based degradable intramedullary nailing system in a sheep model

“…For this reason, the quantities of rare earth elements should be to the minimum necessary in magnesium alloys, especially cerium, which leads to more adverse effects than neodymium or lanthanum [111,116,117]. Although adverse effects of aluminum (possible contribution to Alzheimer and Parkinson disease) [121][122][123] and rare earth elements were reported in the literature, only few suitable investigations about the toxicological values (maximum quantities / no observed adverse effect level (NOAEL)) exists. Yuen et al [124] have mentioned that the annual aluminum exposure limit for a 60 kg adult is 35.88 mg year 1 (type of exposure limit: NOAEL).…”

Amelioration of Aluminum- And Fluoride-Induced Behavioral Alterations Through Resveratrol in Rats.

“…Neuropathological, biochemical, and epidemiological studies suggest that Al contributes to the progression of several neurodegenerative diseases, including Alzheimer's disease and Parkinson's disease [23,24]. It is also showed that the SLM function was significantly impaired and significant karyopyknosis of hippocampal neurons.…”

Evaluation of the toxic potential of calcium carbide in the third instar larvae of transgenic Drosophila melanogaster (hsp70-lacZ)Bg9

“…In our present study a dose dependent significant decrease in the activity of acetylcholinestrase was observed. Aluminium has been reported to enhance brain oxidative stress in rat brain (Sánchez-Iglesias et al, 2009). In some studies it has been reported to alter the function of blood brain barrier (Banks and Kastin, 1989) and has been controversially indicated as a factor in Alzheimer's disease (Ferreira et al, 2008).…”