Oxidative damage of lung and its protective mechanism in mice caused by long-term exposure to titanium dioxide nanoparticles
Oxidative damage of lung and its protective mechanism in mice caused by long-term exposure to titanium dioxide nanoparticles
复制标题
长期接触纳米二氧化钛对小鼠肺的氧化损伤及其保护机制
DOI：
10.1002/jbm.a.34190
复制
发表时间：
2012-10-01
影响因子：
4.9
通讯作者：
Hong, Fashui
中科院分区：
文献类型：
--
作者：
Sun, Qingqing;Tan, Danlin;Hong, Fashui
Exposure to titanium dioxide nanoparticles (TiO2 NPs) elicits an adverse response such as oxidative damage. The molecular targets of TiO2 NPs remain largely unidentified. In the present study, the function and signal pathway of nuclear factor erythroid 2 related factor 2 (Nrf2) in protection against TiO2 NPs-induced oxidative stress in the mouse lung were investigated. Mice were exposed to 10 mg/kg body weight by an intratracheal administration for 1590 days. With increasing exposed terms, TiO2 NPs were significantly accumulated and increased the reactive oxygen species (ROS) production in lung, which resulted in severe pulmonary edema, inflammatory response and pneumonocyte apoptosis for 90 days. Furthermore, TiO2 NPs exposure could greatly induce expression of Nrf2, heme oxygenase 1 (HO-1), and glutamate-cysteine ligase catalytic subunit (GCLC) from 15-day to 75-day exposure, whereas 90-day exposure caused significant decreases of three factors expression levels in lung. Our findings imply that the induction of Nrf2 expression is an adaptive intracellular response to TiO2 NPs-induced oxidative stress in the mouse lung, and that Nrf2 is protective against TiO2 NPs-induced pulmonary damages during certain exposure terms. (c) 2012 Wiley Periodicals, Inc. J Biomed Mater Res Part A 100A:2554-2562, 2012.
