董良佳¹,
杨峰¹,
王京真^1,2,,,
刘文华^1,,
1. 汕头大学海洋生物研究所 广东省海洋生物技术重点实验室, 汕头 515063;
2. 钦州学院海洋学院广西北部湾海洋生物多样性养护重点实验室, 钦州 535011

作者简介: 董良佳(1991-),女,硕士研究生,研究方向为环境毒理学,E-mail:13ljdong@stu.edu.cn.

通讯作者: 王京真,whliu@stu.edu.cn ; 刘文华,wangjingzhen-1@163.com

基金项目: 国家自然科学基金项目（41306180）；国家自然科学基金项目（41176155）；教育部高等学校博士点科研基金项目（20134402110005）；海洋公益性行业科研专项经费项目（201405007）


中图分类号: X171.5

Tris (1,3-dichloro-2-propyl) PhosphateInduces NRK-52E Cells Fibrosisin vitro

Dong Liangjia¹,
Yang Feng¹,
Wang Jingzhen^1,2,,,
Liu Wenhua^1,,
1. Shantou University Marine Biology Institute, Guangdong Province Marine Biotechnology Key Laboratory, Shantou 515063, China;
2. Guangxi Key Laboratory of Beibu Gulf Marine Biodiversity Conservation, Qinzhou University, Qinzhou, China

Corresponding authors: Wang Jingzhen,whliu@stu.edu.cn ; Liu Wenhua,wangjingzhen-1@163.com

CLC number: X171.5

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摘要:自2004年禁止使用五溴联苯醚混合物阻燃剂以来,有机磷阻燃剂(organophosphorus flame retardants,OPFR)作为替代品开始被广泛生产和使用,因而成为当今阻燃剂研究的热点。目前,有机磷阻燃剂在水体环境及生物体中已有较高的检出率,而其对生物体及生态环境的潜在毒性效应还知之甚少。本研究利用磷酸三(2,3-二氯丙基)酯(tri (2,3-dichloropropyl) phosphate,TDCPP)对大鼠肾小管上皮细胞(NRK-52E)的毒性暴露实验,探讨TDCPP潜在的肾脏毒性。结果表明:一定剂量的TDCPP对NRK-52E的细胞活性有抑制作用,能诱导细胞内活性氧自由基(reactive oxide species,ROS)生成量增加,并触发上皮-间充质转换(epithelial-mesenchymal transition,EMT)及胞外基质沉积因子如波形蛋白(vimentin)、转化生长因子-β1(transforming growth factor-β1,TGF-β1)、胞外基质成分纤连蛋白-1(fibronectin-1,FN-1)等基因mRNA表达的显著上调以及上皮细胞钙粘蛋白(E-cadherin)等基因mRNA表达的显著下调。上述研究结果表明,TDCPP可促进NRK-52E细胞发生上皮间充质转化及纤维化。本研究为进一步综合评估TDCPP的生物和环境毒理效应提供了基础实验数据。
关键词: 磷酸三(2,3-二氯丙基)酯/
大鼠肾小管上皮细胞/
毒理效应/
有机磷阻燃剂/
上皮-间充质转换

Abstract:Since the prohibition of the commercialized pentabromodiphenyl ether compound fire retardants in 2004, organic phosphorus flame retardants (OPFRs) have been produced and applied comprehensively as the substitute. Recently, the detectable rate of OPFRs in water environment and organisms is quite high, but studies about the potential adverse effect of OPFRs on organisms and thus ecosystems are scarce. The aim of the present study was to examine the possible toxic effect of tris (1,3-dichloro-2-propyl) phosphate (TDCPP) as a model OPFR substance. NRK-52E cells were exposed to TDCPP, cell viability and extracellular matrix gene expression levels were measured. The results showed that the viability of NRK-52E cells was significantly inhibited by TDCPP in both a dose-dependent and time-dependent manner. TDCPP augmented the reactive oxygen species production inNRK-52E cells. The expression of vimentin, transforming growth factor-β1 (TGF-β1) andfibronectin-1 was significantly up-regulated, while E-cadherin was significantly down-regulated by TDCPP. In conclusion, TDCPP may have the ability to promote epithelial-mesenchymal transition and fibrosis in NRK-52E cells. The result forms the foundation for future comprehensive evaluation of TDCPP toxic effects on the environment.
Key words:tris (1,3-dichloro-2-propyl) phosphate/
NRK-52E cells/
toxicological effect/
OPFR/
epithelial-mesenchymal transition.