Possible role of complement activation in renal impairment in trichloroethylene-sensitized guinea pigs

被引：21
作者：
Yu, Jun-Feng [1 ,2 ]
Leng, Jing [2 ]
Shen, Tong [1 ]
Zhou, Cheng-Fan [1 ,2 ]
Xu, Hui [2 ]
Jiang, Tao [2 ]
Xu, Shu-Hai [2 ]
Zhu, Qi-Xing [1 ,2 ]
机构：
[1] Anhui Med Univ, Inst Dermatol, Hefei 230032, Anhui, Peoples R China
[2] Anhui Med Univ, Dept Occupat Hlth & Environm Hlth, Sch Publ Hlth, Hefei 230032, Anhui, Peoples R China
来源：
TOXICOLOGY | 2012年 / 302卷 / 2-3期
基金：
中国国家自然科学基金;
关键词：
Trichloroethylene; Renal injury; Urine protein; Urease; Complement; 3; MAC; EXPOSURE; CELLS; S-(1,2-DICHLOROVINYL)-L-CYSTEINE; DYSFUNCTION; EXPRESSION; TOXICITY; STRESS; MICE;
D O I：
10.1016/j.tox.2012.06.008
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
Recent studies have revealed that trichloroethylene (ICE) can induce occupational medicamentosa-like dermatitis (OMLD) with multi-system injuries, including liver, kidney and skin injuries, which can subsequently cause multiple organ failure later. But the mechanism of immune dysfunction leading to organ injury was rarely clarified. The present study was initiated to analyze the influence of trichloroethylene on renal injury and study the relevant mechanism in guinea pigs. Guinea pig maximization test (GPMT) was carried out. Inflammation on the guinea pigs' skin was scored. Kidney function, urine protein and ultra-structural change of kidney were determined by biochemical detection and electron microscope. Deposition of complement 3 and membrane attack complex (MAC, C5b-9) were determined by immunohistochemistry. Erythema and edema of skin impairment were observed in TCE sensitized groups, and sensitization rate was 63.16%. Through electron microscope, tubular epithelial cell mitochondrial swelling, vacuolar degeneration and atrophy of microvillus were observed in TCE sensitized groups. The parameters of urease and urinary protein elevated markedly, and a high degree of C3 and MAC deposition was found in the renal tubular epithelial cells in TCE sensitized groups. By demonstrating that TCE and its metabolites can cause the deposition of C3 and MAC in renal epithelial cells, we found that activated complement system may be the mechanism of the acceleration and the development of TCE-induced kidney disease. (C) 2012 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码：172 / 178
页数：7
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