Chronic exposure to trichloroethene causes early onset of SLE-like disease in female MRL +/+ mice

被引:39
作者
Cai, Ping [1 ]
Koenig, Rolf [2 ]
Boor, Paul J. [1 ]
Kondraganti, Shakuntala [3 ]
Kaphalia, Bhupendra S. [1 ]
Khan, M. Firoze [1 ]
Ansari, G. A. S. [1 ,3 ]
机构
[1] Univ Texas Galveston, Med Branch, Dept Pathol, Galveston, TX 77555 USA
[2] Univ Texas Galveston, Med Branch, Dept Microbiol & Immunol, Galveston, TX 77555 USA
[3] Univ Texas Galveston, Med Branch, Dept Biochem & Mol Biol, Galveston, TX 77555 USA
关键词
trichloroethene (TCE); MRL plus / plus mice; cytokines; immunotoxicity; autoimmunity; hepatitis;
D O I
10.1016/j.taap.2007.11.031
中图分类号
R9 [药学];
学科分类号
1007 ;
摘要
Trichloroethene (TCE) exacerbates the development of autoimmune responses in autoimmune-prone MRL +/+ mice. Although TCE-mediated autoimmune responses are associated with an increase in serum immunoglobulins and autoantibodies, the underlying mechanism of autoimmunity is not known. To determine the progression of TCE-mediated immunotoxicity, female MRL +/+ mice were chronically exposed to TCE through the drinking water (0.5 mg/ml of TCE) for various periods of time. Serum concentrations of antinuclear antibodies increased after 36 and 48 weeks of TCE exposure. Histopathological analyses showed lymphocyte infiltration in the livers of MRL +/+ mice exposed to TCE for 36 or 48 weeks. Lymphocyte infiltration was also apparent in the pancreas, lungs, and kidneys of mice exposed to TCE for 48 weeks. Immunoglobulin deposits in kidney glomeruli were found after 48 weeks of exposure to TCE. Our results suggest that chronic exposure to TCE promotes inflammation in the liver, pancreas, lungs, and kidneys, which may lead to SLE-like disease in MRL +/+ mice. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:68 / 75
页数:8
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