Iron oxide nanoparticles induced dysfunction and cytotoxicity in human endothelial cells

ENVR 254

Mo-Tao Zhu, fengwy@mail.ihep.ac.cn and Weiyue Feng, fengwy@mail.ihep.ac.cn. Laboratory for Bio-Environmental Effects of Nanomaterials and Nanosafety, Institute of High Energy Physics, Chinese Academy of Sciences, 19 B, Yu Quan Road, Shi Jing Shan, Beijing, 100049, China
Recent epidemiologic researches indicate that exposure to ultrafine (nanoparticles) seems to be an important and independent risk factor for several cardiovascular diseases. However, the exact mechanisms of the relationship remain largely unknown. Endothelial dysfunction was hypothesized to be an attractive mechanism involved in the induction of these cardiovascular diseases. To investigate this hypothesis, some widely used iron nanomaterials, including ferric oxide (Fe2O3) and ferroso-ferric oxide (Fe3O4) were incubated with human aortic endothelial cells (HAECs) and human umbilical venous endothelial cells (HUVECs). Our results indicate that Fe3O4 nanoparticles are more obvious to provoke an inflammatory response and cytotoxicity than Fe2O3 ones; the disturbance of endothelial functions was more serious by Fe3O4 nanoparticles' treatment than by Fe2O3 as well. Uptake and internalization of both Fe2O3 and Fe3O4 into HAECs and HUVECs could be observed. These results demonstrate that dysfunction of endothelial cells correlates with iron valence state and particle composition.