Nanoscale Aluminum Oxide–Bioaccumulation and Toxicological Features Based on Alimentary Intake

Abstract

Repeat oral administration of aluminum oxide (Al2O3) nanoparticles for 10 days at a total dose of 21 895 mg/kg of body weight causes the death of 50% of individuals in the exposed group. At the same time, the death rate amounts to 25% when exposed to microparticles. Aluminum concentrations after exposure to nanomaterial are increased relative to the control levels by 4.40, 1.23, and 1.48 times in the brain, liver, and blood of exposed animals, respectively. For micromaterial, these indexes are higher by 3.59 and 1.82 times in the brain and blood, respectively. The aluminum concentration under exposure to a nanomaterial is 1.23 times higher in the brain and 1.41 times higher in the liver than under exposure to a micromaterial. When exposed to nanodispersed Al2O3, acute liver congestion, eosinophilic gastroenteritis, lymphoid hyperplasia, and an increase in white pulp up to 70% were observed. When exposed to microparticles, pathomorphological changes were found only in spleen tissues as lymphoid hyperplasia and an increase in white pulp up to 50%. Intratracheal instillation of nano- and microparticles of Al2O3 leads to injuries of alveolar macrophages. When exposed to nanoparticles, the proportion of injuries and their number are 2.50 and 8 times higher, respectively, and the injury diameter is 2.25 times smaller. A high rate of animal death, features of bioaccumulation, pathomorphological changes in organ tissues during oral exposure, and injuries of alveolar macrophages during intratracheal exposure to Al2O3 nanoparticles proves the greater degree of toxicity of the nanomaterial via alimentary intake compared to the microdispersed analog.