Cerium oxide nanoparticle-induced pulmonary inflammation and alveolar macrophage functional change in rats
Cerium oxide nanoparticle-induced pulmonary inflammation and alveolar macrophage functional change in rats
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DOI：
10.3109/17435390.2010.519835
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发表时间：
2011-09-01
期刊：
影响因子：
5
通讯作者：
Ma, Joseph K.
中科院分区：
文献类型：
--
作者：
Ma, Jane Y.;Zhao, Hongwen;Ma, Joseph K.
使用铈化合物作为柴油燃料催化剂导致在排气中排放氧化铈纳米颗粒（CeO 2）。这项研究描述了CeO 2暴露对肺毒性的潜在影响。雄性Sprague道利大鼠通过单次气管内滴注暴露于0.15、0.5、1、3.5或7 mg/kg体重的CeO 2。暴露后1天，CeO 2显着减少NO的产生，但增加IL-12的产生，肺泡巨噬细胞（AM）在响应离体脂多糖（LPS）的挑战，并引起AM凋亡，通过激活半胱天冬酶9和3。CeO 2暴露后1天肺细胞中细胞因子信号传导抑制因子-1显著增加，28天肺细胞中骨桥蛋白酶-1升高，而肺组织中骨桥蛋白在两个时间点均显著升高。CeO 2诱导炎症、细胞毒性、空气/血液屏障损伤和磷脂质病伴AM增大。因此，CeO 2诱导肺部炎症和损伤，可能导致纤维化。
The use of cerium compounds as diesel fuel catalyst results in the emission of cerium oxide nanoparticles (CeO2) in the exhaust. This study characterized the potential effects of CeO2 exposure on lung toxicity. Male Sprague Dawley rats were exposed to CeO2 by a single intratracheal instillation at 0.15, 0.5, 1, 3.5 or 7 mg/kg body weight. At 1 day after exposure, CeO2 significantly reduced NO production, but increased IL-12 production, by alveolar macrophages (AM) in response to ex vivo lipopolysacchride (LPS) challenge, and caused AM apoptosis, through activation of caspases 9 and 3. CeO2 exposure markedly increased suppressor of cytokine signaling-1 at 1-day and elevated arginase-1 at 28-day post exposure in lung cells, while osteopontin was significantly elevated in lung tissue at both time points. CeO2 induced inflammation, cytotoxicity, air/blood barrier damage, and phospholipidosis with enlarged AM. Thus, CeO2 induced lung inflammation and injury in lungs which may lead to fibrosis.