کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
2570496 | 1128588 | 2009 | 10 صفحه PDF | دانلود رایگان |

Respiratory exposure of mice to carbon nanotubes induces pulmonary toxicity and adverse cardiovascular effects associated with atherosclerosis. We hypothesize that the direct contact of carbon nanotubes with endothelial cells will result in dose-dependent effects related to altered cell function and cytotoxicity which may play a role in potential adverse pulmonary and cardiovascular outcomes. To test this hypothesis, we examined the effects of purified single- and multi-walled carbon nanotubes (SWCNT and MWCNT) on human aortic endothelial cells by evaluating actin filament integrity and VE-cadherin distribution by fluorescence microscopy, membrane permeability by measuring the lactate dehydrogenase (LDH) release, proliferation/viability by WST-1 assay, and overall functionality by tubule formation assay. Marked actin filament and VE-cadherin disruption, cytotoxicity, and reduced tubule formation occurred consistently at 24 h post-exposure to the highest concentrations [50–150 μg/106 cells (1.5–4.5 μg/ml)] for both SWCNT and MWCNT tested in our studies. These effects were not observed with carbon black exposure and carbon nanotube exposure in lower concentrations [1–10 μg/106 cells (0.04–0.4 μg/ml)] or in any tested concentrations at 3 h post-exposure. Overall, the results indicate that SWCNT and MWCNT exposure induce direct effects on endothelial cells in a dose-dependent manner.
Journal: Toxicology and Applied Pharmacology - Volume 236, Issue 3, 1 May 2009, Pages 319–328