TiO2 P25 nanoparticles induce mitochondrial damage and increased glutathione synthesis in SH-SY5Y neural cells

Abstract

The increasing occurrence of TiO₂ nanoparticles in the environment leads to a higher risk of their entry into the human body. Because the nanomaterials can cross the blood-brain barrier, the knowledge of their effect in neural cells is also crucial. However, the exact mechanism of toxicity remains unclear. Therefore, our objective was to evaluate the biological effect of TiO₂ nanoparticles in neural cells. Therefore, we aimed to evaluate the biological effect of TiO₂ nanoparticles in neural cells. We used neuroblastoma SH-SY5Y cells treated with 25 nm TiO₂ nanoparticles (TiO₂ P25; 1-100 μg·mL^-1; 24-72 h). We measured dehydrogenase activity, glutathione metabolism, DNA damage and mitochondrial respiration. After treatment of SH-SY5Y cells with TiO₂ P25, we found a dose- and time-dependent decrease in dehydrogenase activity together with nuclear changes. Interestingly, 100 μg·mL^-1 TiO₂ P25 caused a significant increase of glutathione levels (p < 0.001) linked with increased glutamate-cysteine ligase expression after both 24 and 48 h. Furthermore, as the first study at all, we observed the significant decreases of mitochondrial respiration in SH-SY5Y cells caused by treatments with 10 and 100 μg·mL^-1 TiO₂ P25 after 48 and 72 h. In conclusion, our study brings new finding of occurrence of decreased mitochondrial respiration without glutathione depletion in SH-SY5Y cells contributing to the understanding of TiO₂ P25 toxicity in neural cells.

Keywords: Glutathione; Mitochondrial damage; Nanotoxicity; Neuronal cells; TiO(2) P25 nanoparticles.