Acute effects of pulmonary exposure to zinc oxide nanoparticles on the brain in vivo

Although the applications for zinc oxide nanoparticles (ZnONP) are continually increasing, the neurotoxicity of this material remains unclear. This study investigated the acute effects of pulmonary exposure to ZnONP on the brain in terms of behavioral changes, oxidative stress, inflammation, and tau and autophagy expressions using rat subjects. Based on the test subjects’ performance in a Morris water maze and an elevated-plus maze, respectively, no major alterations occurred in spatial cognition or learning ability, or anxiety. Following exposure to 10 mg kg–1 of ZnONP, we observed that the level of 8-hydroxy-2ʹ-deoxyguanosine (8-OHdG)/dG significantly increased in the hippocampus, whereas those of interleukin (IL)-1β and IL-6 significantly decreased in the cerebellum and the cortex. Additionally, microglia were activated in the hippocampus. Tau protein expression was strong in the cerebellum and the hippocampus, but no significant expression of Beclin-1, light chain 3 (LC3) II/I, or ubiquitin was detected. Our results suggest that acute exposure to ZnONP induces oxidative stress, microglia activation, and tau protein expression in the brain, leading to neurotoxicity.