Effects of Acute Exposure to Titanium Dioxide on Endothelial Function

Abstract

Nanotechnology, the manipulation and manufacturing of particles less than 100 nm in size, is at the forefront of scientific research. However, there is evidence that the size-dependent properties of nanoparticles may increase their toxicity. Studies have shown that short-term (24 hr) exposure to nanomaterials, including titanium dioxide (TiO2), is associated with increased reactive oxygen species (ROS) production. Previous work has suggested that this increase in ROS production may involve cellular internalization. However, we hypothesized that nanomaterials interact with the endothelial cell surface resulting in an impaired endothelial-dependent vasodilation. Experiments were performed using the isolated saline-perfused rat lung. The pulmonary vasculature was exposed to TiO2 (0.05% V/V or 0.1% V/V) for 1 hr. Endothelial function was assessed using graded doses of an endothelial-dependent vasodilator (ionomycin; 0.03 - 1.0 µM), administered luminally. Ionomycin induced a dose-dependent vasodilation. There were no statistically significant differences in the vasodilatory response to ionomycin between vehicle and TiO2 treated lungs. These results suggest that acute TiO2 exposure does not alter endothelial-dependent vasodilation in the rat pulmonary vasculature.