Study on the relationship between cadmium chloride-induced adrenocortical cell of guinea pig apoptosis and stress-activated protein kinase activity

被引:1
作者
Zhao Min [1 ]
Yang Xingfen [1 ]
Wei Qing [2 ]
Lu Ciyong [2 ]
Chen Tiejiang [2 ]
机构
[1] Ctr Dis Control & Prevent Guangdong Prov, Guangzhou 510300, Guangdong, Peoples R China
[2] Sun Yat Sen Univ, Sch Publ Hlth, Guangzhou 510080, Guangdong, Peoples R China
关键词
cadmium chloride; apoptosis; stress-activated protein kinase; adrenocortical cell; guinea pig;
D O I
10.1016/j.etp.2008.04.008
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Heavy metals are important environmental pollutants that affect many cellular functions. The signaling pathways that lead to apoptosis of adrenocortical cells following exposure to cadmium chloride (CdCl(2)) have not yet been fully clarified. We developed a primary culture of guinea pig adrenocortical cells and treated it with various concentrations of CdCl(2) for different time periods. The apoptosis induced by CdCl(2) was detected by fluorescein isothiocyanate-labeled annexin V and propidium iodide staining using a flow cytometer. Stress-activated protein kinase (SAPK) activities were measured by immunoprecipitation and chemiluminescence assay. After 2h of treatment, the apoptotic cell rate increased in a dose-dependent manner. The difference between the high-dose group and the control group was significant (P < 0.01). The apoptosis was also found to increase in a time-dependent manner in cells treated with 50 mu mol/L CdCl(2)). Among the various treatment period groups, the difference between more than 1 h-treated groups and the control group was significant (P < 0.01). The SAPK activity increased with an increase in CdCl(2) dose after 5 min of exposure. However, after 15 min of exposure to CdCl(2), the SAPK activity decreased with an increase in exposure time. Our findings suggest that the SAPK signaling pathway might play an important role in CdCl(2)-induced apoptosis of adrenocortical cells. (C) 2008 Elsevier GmbH. All rights reserved.
引用
收藏
页码:459 / 468
页数:10
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