Oxidative stress in the brain of mice caused by translocated nanoparticulate TiO2 delivered to the abdominal cavity.

In order to study the mechanisms underlying the effects of TiO(2) nanoparticles on the brain, ICR mice were injected with nanoparticulate anatase TiO(2) (5 nm) of various doses into the abdominal cavity daily for 14 days. We then examined the coefficient of the brain, the brain pathological changes and oxidative stress-mediated responses, and the accumulation of nanoparticulate anatase TiO(2) and levels of neurochemicals in the brain. The results showed that high-dose nanoparticulate anatase TiO(2) could induce some neurons to turn into filamentous shapes and others into inflammatory cells. The concentration of nanoparticulate anatase TiO(2) in the brain was increased as increases in nanoparticulate anatase TiO(2) dosages used. The oxidative stress and injury of the brain occurred as nanoparticulate anatase TiO(2) appeared to trigger a cascade of reactions such as lipid peroxidation, the decreases of the total anti-oxidation capacity and activities of antioxidative enzymes, the excessive release of nitric oxide, the reduction of glutamic acid, and the downregulated level of acetylcholinesterase activities. We concluded that TiO(2) nanoparticles injected at the abdominal cavity could be translocated into the brain and in turn caused the brain injury.