Methylmercury chloride induces alveolar type II epithelial cell damage through an oxidative stress-related mitochondrial cell death pathway

doi:10.1016/j.toxlet.2010.02.003

中山醫學大學機構典藏 CSMUIR > 健康管理學院 > 職業安全衛生學系暨碩士班 > 博碩士論文 > Item 310902500/20395

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题名:	Methylmercury chloride induces alveolar type II epithelial cell damage through an oxidative stress-related mitochondrial cell death pathway
作者:	Lu, Tien Hui Chen, Chun Hung Lee, Ming Jye Ho, Tsung Jung Leung, Yuk Man Hung, Dong Zong Yen, Cheng Chien He, Tsung Ying Chen, Ya Wen
贡献者:	職業安全衛生學系
关键词:	Methylmercury;Alveolar type II epithelial cell;Oxidative stress;Cell death;Surfactant proteins (SPs);mRNA
日期:	2010-05
上传时间:	2019-10-24T02:51:36Z (UTC)
出版者:	Toxicology Letters
ISSN:	0378-4274
摘要:	Mercury, one of the widespread pollutants in the world, induces oxidative stress and dysfunction in many cell types. Alveolar type II epithelial cells are known to be vulnerable to oxidative stress. Alveolar type II epithelial cells produce and secrete surfactants to maintain morphological organization, biophysical functions, biochemical composition, and immunity in lung tissues. However, the precise action and mechanism of mercury on alveolar type II epithelial cell damage remains unclear. In this study, we investigate the effect and possible mechanism of methylmercury chloride (MeHgCl) on the human lung invasive carcinoma cell line (Cl1-0) and mouse lung tissue. Cl1-0 cells were exposed to MeHgCl (2.5–10 μM) for 24–72 h. The results showed a decrease in cell viability and an increase in malondialdehyde (MDA) level and ROS production at 72 h after MeHgCl exposure in a dose-dependent manner. Caspase-3 activity, sub-G1 contents and annexin-V binding were dramatically enhanced in Cl1-0 cells treated with MeHgCl. MeHgCl could also activate Bax, release cytochrome c, and cleave poly(ADP-Ribose) polymerase (PARP), and decrease surfactant proteins mRNA levels. Moreover, in vivo study showed that mercury contents of blood and lung tissues were significantly increased after MeHgCl treatment in mice. The MDA levels in plasma and lung tissues were also dramatically raised after MeHgCl treatment. Lung tissue sections of MeHgCl-treated mice showed pathological fibrosis as compared with vehicle control. The mRNA levels of proteins in apoptotic signaling, including p53, mdm-2, Bax, Bad, and caspase-3 were increased in mice after exposure to MeHgCl. In addition, the mRNA levels of surfactant proteins (SPs), namely, SP-A, SP-B, SP-C, and SP-D (alveolar epithelial cell functional markers) were significantly decreased. These results suggest that MeHgCl activates an oxidative stress-induced mitochondrial cell death in alveolar epithelial cells.
URI:	https://ir.csmu.edu.tw:8080/ir/handle/310902500/20395
關聯:	Toxicology Letters, Vol. 194, Issue 3, 70-78
显示于类别:	[職業安全衛生學系暨碩士班] 博碩士論文

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