Premium
Acute TiO 2 exposure does not alter endothelial function in isolated rat lung
Author(s) -
Westphal Joslyn,
Naik Jay
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.lb115
Subject(s) - ionomycin , vasodilation , endothelial dysfunction , chemistry , reactive oxygen species , pharmacology , endothelium , lung , endothelial stem cell , medicine , biochemistry , in vitro
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 nanomaterials may increase their toxicity. Studies have shown that short‐term (24 hr) exposure to nanomaterials, including titanium dioxide (TiO 2 ), is associated with increased reactive oxygen species (ROS) production. An increase in ROS production within the vasculature could potentially elicit a decrease in NO bioavailability. 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. To this end, experiments were performed using isolated, saline perfused Wistar rat lung. The pulmonary vasculature was exposed to TiO 2 (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 TiO 2 treated lungs. These results suggest that acute TiO 2 exposure does not alter endothelial‐dependent vasodilation in the rat pulmonary vasculature.