Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Morgantown, WV 26505, USA.
Nanotoxicology. 2012 Nov;6(7):736-45. doi: 10.3109/17435390.2011.611915. Epub 2011 Aug 30.
The inhalation of engineered nanoparticles stimulates the development of atherosclerosis and impairs vascular function. However, the cardiac effects of inhaled engineered nanoparticles are unknown. Here, we investigate the effects of ultrafine titanium dioxide (UFTiO(2)) on the heart, and we define the possible mechanisms underlying the measured effects. Pulmonary exposure of rats to UFTiO(2) increased the phosphorylation levels of p38 mitogen-activated protein kinase and cardiac troponin I, but not Akt, in the heart and substance P synthesis in nodose ganglia. Circulatory levels of pro-inflammatory cytokines, and blood cell counts and differentials were not significantly changed after pulmonary exposure. Separately, the incubation of cardiac myocytes isolated from naïve adult rat hearts in vitro with UFTiO(2) did not alter the phosphorylation status of the same cardiac proteins. In conclusion, the inhalation of UFTiO(2) enhanced the phosphorylation levels of cardiac proteins. Such responses are likely independent of systemic inflammation, but may involve a lung-neuron-regulated pathway.
吸入工程纳米颗粒会刺激动脉粥样硬化的发展并损害血管功能。然而，吸入的工程纳米颗粒对心脏的影响尚不清楚。在这里，我们研究了超细微二氧化钛 (UFTiO(2)) 对心脏的影响，并确定了所测量的影响的可能机制。大鼠肺部暴露于 UFTiO(2) 会增加心脏中 p38 丝裂原活化蛋白激酶和肌钙蛋白 I 的磷酸化水平，但不会增加 Akt 的磷酸化水平，同时也会增加结状神经节中 P 物质的合成。肺部暴露后，促炎细胞因子的循环水平、血细胞计数和分类没有明显变化。此外，将来自成年大鼠心脏的心肌细胞在体外与 UFTiO(2) 一起孵育不会改变相同的心脏蛋白的磷酸化状态。总之，吸入 UFTiO(2) 会增强心脏蛋白的磷酸化水平。这种反应可能独立于全身炎症，但可能涉及肺-神经元调节途径。
