Aluminum Oxide Nanoparticles Upregulate ED1 Expression in Rat Olfactory Bulbs by Repeated Intranasal Instillation

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Respiratory route is one of the major exposure routes to nanoparticles. The environmental agent aluminum is intensively investigated for the association with development of neurodegeneration. To evaluate potential neurotoxicity induced by aluminum oxide (Al2O3) nanoparticles, male rats were intranasally instilled with 0.1 or 1 (Al) mg/kg nanoAl2O3 or aluminum chloride (AlCl3) every two days for 60 days, using pure water as vehicle control. Neurotoxicity effects were determined by behavioural studies and immunohistochemistry staining of ED1 and beta-amyloid precursor protein (Aβ). Neither of nanoAl2O3 treated groups showed significant alterations in Morris water maze tests, however, increased escape latency were observed in 1mg/kg AlCl3 treated rats. Further, upregulation of ED1 expression were showed in olfactory bulb of 1 mg/kg nanoAl2O3 and AlCl3 exposed rats. Massive Aβ expressions were observed in whole brain of 1mg/kg (Al) AlCl3 treated rats. ED1 expression is a marker of microglia/macrophages activation, suggesting stimulus of Al2O3 nanoparticles to microglia/macrophages located in olfactory bulb and perivascular areas. In these studies, Al2O3 nanoparticles didnt show any alterations on spacial learning behaviours of rats and expression of Aβ of neuron, therefore, display lower neural effects than AlCl3.

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July 2013

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