Molecular mechanism of kidney injury of mice caused by exposure to titanium dioxide nanoparticles

Numerous studies have demonstrated that damage of kidney of mice can be caused by exposure to titanium dioxide nanoparticles (TiO(2) NPs). However, the molecular mechanism of TiO(2) NPs-induced nephric injury remains unclear. In this study, the mechanism of nephric injury in mice induced by an intragastric administration of TiO(2) NPs was investigated. The results showed that TiO(2) NPs were accumulated in the kidney, resulting in nephric inflammation, cell necrosis and dysfunction. Nucleic factor-κB was activated by TiO(2) NPs exposure, promoting the expression levels of tumor necrosis factor-α, macrophage migration inhibitory factor, interleukin-2, interleukin-4, interleukin-6, interleukin-8, interleukin-10, interleukin-18, interleukin-1β, cross-reaction protein, transforming growth factor-β, interferon-γ and CYP1A1, while heat shock protein 70 expression was inhibited. These findings implied that TiO(2) NPs-induced nephric injury of mice might be associated with alteration of inflammatory cytokine expression and reduction of detoxification of TiO(2) NPs.