Whole-body aerosol exposure of cadmium chloride (CdCI2) and tetrabromobisphenol A (TBBPA) induced hepatic changes in CD-1 male mice

被引:24
作者
Chen, Yuanhong [1 ]
Hu, Yabing [1 ]
Liu, Shuyun [1 ]
Zheng, Huiying [1 ]
Wu, Xiaojuan [1 ]
Huang, Zhengyu [1 ]
Li, Hao [1 ]
Peng, Baoqi [1 ]
Long, Jinlie [1 ]
Pan, Bishu [2 ]
Huang, Changjiang [1 ]
Dong, Qiaoxiang [1 ]
机构
[1] Wenzhou Med Univ, Inst Environm Safety & Human Hlth, Wenzhou 325035, Peoples R China
[2] Taizhou Ctr Dis Control & Prevent, Taizhou 318000, Peoples R China
基金
中国国家自然科学基金;
关键词
Tetrabromobisphenol A; Cadmium; Hepatic toxicity; Inhalation toxicity; Oxidative stress marker; BROMINATED FLAME RETARDANTS; SOUTHEAST CHINA; HEAVY-METALS; RATS; GLUTATHIONE; BIOMARKERS; DUST; SITE; HEXABROMOCYCLODODECANE; XENOBIOTICS;
D O I
10.1016/j.jhazmat.2016.06.054
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Cadmium (Cd) and tetrabromobisphenol A (TBBPA) are two prevalent contaminants in e-waste recycling facilities. However, the potential adversely health effect of co-exposure to these two types of pollutants in an occupational setting is unknown. In this study, we investigated co-exposure of these two pollutants on hepatic toxicity in CD-1 male mice through a whole-body aerosol inhalation route. Specifically, mice were exposed to solvent control (5% DMSO), Cd (8 mu g/m(3)), TBBPA (16 mu g/m(3)) and Cd/TBBPA mixture for 8h/day and 6 days a week for 60 days. Hepatic changes include increased organ weight, focal necrosis, and elevated levels of liver enzymes in serum. These changes were most severe in mice exposed to TBBPA, followed by Cd/TBBPA mixture and Cd. These chemicals also led to suppressed antioxidant defensive mechanisms and increased oxidative stress. Further, these chemicals induced gene expression of apoptosis-related genes, activated genes encoding for phase I detoxification enzymes and inhibited genes encoding for phase II detoxification enzymes. These findings indicate that the hepatic damages induced by subchronic aerosol exposure of Cd and TBBPA may result from the oxidative damages caused by excessive ROS production when these chemicals were metabolized in the liver. (C) 2016 Elsevier B.V. All rights reserved.
引用
收藏
页码:109 / 116
页数:8
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