Background: Aluminium (Al) is known to have neurotoxic effects that can result in oxidative damage to a range of cellular biomolecules. These effects appear to be of significance in the developmental stages of the brain. We therefore investigated the oxidative and histopathological damage induced by Al during growth and development of the chick brain.
Material/Methods: We used a chick embryonic development model, with Al treatment of 500 µg Al sulphate in 0.1 ml saline injected into the egg air chambers at the beginning of their incubation period. The effects on chick-brain growth and development were then assessed at term (day 21). Determination of malondialdehyde and glutathione levels were used as relevant biological measures for increased oxidative stress in terms of lipid peroxidation and biochemical oxidative damage, respectively. Furthermore, we also monitored neuronal degeneration as estimated stereologically using the Cavalieri brain volume estimation tool.
Results: This Al treatment showed significantly increased MDA levels and decreased GSH levels, as indicators of increased biochemical oxidative damage. This was accompanied by significantly decreased brain volume, as a measure of neuronal degeneration during brain development in this chick embryonic development model.
Conclusions: Exposure to Al during chick embryonic development results in increased oxidative stress in the brain that is accompanied by neuronal degeneration.

Keywords: Oxidative Stress - drug effects, Malondialdehyde - metabolism, Lipid Peroxidation - drug effects, Glutathione - metabolism, Embryo, Nonmammalian - drug effects, Chick Embryo, Brain - metabolism, Alum Compounds - pharmacology