Bismuth oxide nanoparticles induced oxidative stress-related inflammation in SH-SY5Y cell Line

Abstract

Bismuth (III) oxide nanoparticles' (Bi2O3-NPs) unique physicochemical properties have attracted attention in biological, industrial, technological and medical fields. Concurrently, increasing numbers of studies revealing their potential toxic effects and possible toxicity mechanisms are ongoing. In this study, we assessed the toxic potentials of Bi2O3-NPs in human SH-SY5Y neuroblastoma cell line. After Bi2O3-NPs characterization using TEM, the cytotoxic potentials were evaluated by MTT and LDH assays. The induction of reactive oxygen species production was evaluated by H(2)DCFDA. In order to evaluate the oxidative damages, the changes in antioxidant catalase and superoxide dismutase and glutathione levels were determined. The cellular death pathway and the role of immune response were studied by measuring the mRNA expression levels of related genes. Our results showed that Bi3O3-NPs decreased the cell viability through disruption on mitochondrial activity(IC50:77.57 mu g/mL) and membrane integrity (LDH%50:16.97 mu g/mL). At 50 mu g/mL Bi2O3-NPs, the production of reactive oxygen species (ROS) was induced significantly as well as the catalase and superoxide dismutase levels. In immune response, the mRNA expression levels of interleukin (IL)-6 increased more than 1.5-fold in all doses; whereas, TNF-alpha, NF-kappa B and MAPK8 expressions remained unchanged. Consequently, Bi2O3-NPs induced oxidative stress-related inflammation via activation of pro-inflammatory cytokine, IL-6.