Pulmonary exposure to particles from diesel exhaust, urban dust or single-walled carbon nanotubes and oxidatively damaged DNA and vascular function in apoE-/- mice

• Published in: Nanotoxicology 2014-02, Vol.8 (1), p.61-71
• Main Authors: Vesterdal, Lise K, Jantzen, Kim, Sheykhzade, Majid, Roursgaard, Martin, Folkmann, Janne K, Loft, Steffen, Møller, Peter
• Format: Article
• Language: English
• Subjects: Animals; Aorta - drug effects; Aorta - pathology; Apolipoproteins E - genetics; comet assay; DNA Damage - drug effects; Female; Gene Expression - drug effects; Lung - drug effects; Lung - pathology; Mice; Mice, Transgenic; nanoparticles; Nanotubes, Carbon - chemistry; Nanotubes, Carbon - toxicity; nitric oxide; oxidative stress; Oxidative Stress - drug effects; Reactive Oxygen Species - analysis; Reactive Oxygen Species - metabolism; Vasodilation - drug effects; vasomotor dysfunction; Vehicle Emissions - toxicity
• ISSN: 1743-5390; 1743-5404
• DOI: 10.3109/17435390.2012.750385

Abstract This study compared the oxidative stress level and vasomotor dysfunction after exposure to urban dust, diesel exhaust particles (DEP) or single-walled carbon nanotubes (SWCNT). DEP and SWCNT increased the production of reactive oxygen species (ROS) in cultured endothelial cells and acellullarly, whereas the exposure to urban dust did not generate ROS. The apoE-/- mice, which were exposed twice to 0.5 mg/kg of the particles by intratracheal (i.t.) instillation, had unaltered acetylcholine-elicited vasorelaxation in aorta segments. There was unaltered pulmonary expression level of Vcam-1, Icam-1, Hmox-1 and Ogg1. The levels of oxidatively damaged DNA were unchanged in lung tissue. The exposure to SWCNT significantly increased the expression of Ccl-2 in the lung tissue of the mice. The exposure to DEP and SWCNT was associated with elevated ROS production in cultured cells, whereas i.t. instillation of the same particles had no effect on biomarkers of pulmonary oxidative stress and dilatory dysfunction in the aorta.