Abstract
Extensive applications of ZnO NPs (zinc oxide nanoparticles) in daily life have created concern about their biotoxicity. Zinc oxide nanoparticles induce oxidative stress, inflammation, and apoptosis in neurons. Edaravone applies antioxidant agent and anti-inflammatory impacts in the different cells, as evaluated in both in vitro and in vivo experimental models. This study is designed to explore, how edaravone would avert mitochondrial impairment in human neuronal cells against ZnO NPs-induced toxicity. Accordingly, we analyzed here whether a pretreatment (for 24 h) with edaravone (10-100 μM) would enhance mitochondrial protection in the human neuroblastoma cells SH-SY5Y against ZnO NPs-induced toxicity. We found that edaravone at 25 μM averted the ZnO NPs-induced decrease in the amounts of adenosine triphosphate (ATP), just as on the activity of the complexes I and V. Also, edaravone induced an antioxidant activity by diminishing the levels of lipid peroxidation, protein carbonylation, and protein nitration in the mitochondrial membranes. Edaravone blocked the ZnO NPs-induced transcription factor nuclear factor-κB (NF-κB) upregulation. The inhibition of the heme oxygenase-1 (HO-1) enzyme by zinc protoporphyrin IX (ZnPP IX, 10 μM) smothered the preventive impacts brought about by edaravone with respect to mitochondrial function and inflammation. After this examination, it can be concluded that edaravone caused cytoprotective impacts in an HO-1-dependent manner in SH-SY5Y cells against ZnO NPs-induced toxicity.