Titanium dioxide nanoparticles impair lung mitochondrial function

Abstract

Titanium dioxide nanoparticles (TiO 2 NPs) are used in an increasing number of human products such as cosmetics, sunscreen, toothpaste and paints. However, there is clear evidence about effects associated to TiO 2 NPs exposure, which include lung inflammation and tumor formation and these effects are related to reactive oxygen species (ROS) formation. The ROS generation could be attributed to a mitochondrial dysfunction. Even though, it has been shown that TiO 2 NPs exposure can induce some alterations in mitochondria including cytochrome c release to cytosol, change in mitochondrial permeability and decrease of mitochondrial membrane potential (Δ Ψ m), there is no information about the changes in mitochondrial function induced by TiO 2 NPs. We hypothesized that TiO 2 NPs effects are associated with mitochondrial dysfunction and redox unbalance. To test our hypothesis we isolated mitochondria from lung tissue of rats and exposed them to 10 (g TiO 2 NPs (particle size < 25 nm)/mg protein for 1 h. Our results showed that TiO 2 NPs decreases NADH levels and impairs Δ Ψ m and mitochondrial function accompanied by ROS generation during mitochondrial respiration.