Oxidative stress of CeO2 nanoparticles via p38-Nrf-2 signaling pathway in human bronchial epithelial cell, Beas-2B
Oxidative stress of CeO2 nanoparticles via p38-Nrf-2 signaling pathway in human bronchial epithelial cell, Beas-2B
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DOI：
10.1016/j.toxlet.2009.01.028
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发表时间：
2009-06-01
影响因子：
3.5
通讯作者：
Choi, Jinhee
中科院分区：
文献类型：
--
作者：
Eom, Hyun-Jeong;Choi, Jinhee
为了了解氧化应激纳米颗粒诱导氧化应激的分子机制，利用人支气管上皮细胞BEAS-2B进行了体外毒性实验，重点研究氧化应激反应信号转导通路和转录因子在CeO2纳米颗粒毒性中的作用。细胞外信号调节激酶(ERK)、p38和c-jun氨基末端激酶(JNK)信号通路以及核因子-kappaB(NF-kappaB)和核因子-E2相关因子-2(NRF-2)是CeO2纳米颗粒暴露所致氧化应激的上游事件。这些结果表明，CeO2纳米颗粒可能通过氧化应激发挥其毒性作用，因为它们导致细胞内ROS浓度显著增加，从而通过p38-NRF-2信号通路强烈诱导血红素加氧酶-1(HO-1)。进一步研究CeO2纳米颗粒诱导p38-NRF-2信号通路的机制有助于更好地理解CeO2纳米颗粒诱导的氧化应激；通过浓度-反应和时程实验对其他信号通路的研究也是合理的。(C)2009年，爱思唯尔爱尔兰有限公司出版。
To understand the molecular mechanism of previously observed cerium oxide (CeO2) nanoparticles-induced oxidative stress, an in vitro toxicity assay was conducted using human bronchial epithelial cell, Beas-2B, focusing on the involvement of the oxidative stress responding signal transduction pathway and transcription factors in the toxicity of CeO2 nanoparticles. Extracellular signal-regulating kinase (ERK), p38 and c-Jun N-terminal kinase (JNK) signaling pathways, along with nuclear factor-kappaB (NF-kappa B) and nuclear factor-E2-related factor-2 (Nrf-2), were investigated as the upstream events of oxidative stress from exposure to CeO2 nanoparticles. The overall results suggest that CeO2 nanoparticles may exert their toxicity through oxidative stress, as they cause significant increases in the cellular reactive oxygen species (ROS) concentrations, subsequently leading to the strong induction of heme oxygenase-1 (HO-1) via the p38-Nrf-2 signaling pathway. Further studies on the mechanism by which CeO2 nanoparticles induce the p38-Nrf-2 signaling pathway are warranted for a better understanding of the CeO2 nano particles-induced oxidative stress; studies with other signaling pathways, with concentration-response and time course experiments would also be justified. (C) 2009 Published by Elsevier Ireland Ltd.