Molecular mechanism of kidney injury of mice caused by exposure to titanium dioxide nanoparticles
Molecular mechanism of kidney injury of mice caused by exposure to titanium dioxide nanoparticles
复制标题
纳米二氧化钛致小鼠肾损伤的分子机制
DOI：
10.1016/j.jhazmat.2011.08.055
复制
发表时间：
2011-11-15
影响因子：
13.6
通讯作者：
Hong, Fashui
中科院分区：
文献类型：
--
作者：
Gui, Suxing;Zhang, Zengli;Hong, Fashui
大量研究表明，纳米二氧化钛(TiO2NPs)可致小鼠肾脏损伤。然而，纳米二氧化钛致肾脏损伤的分子机制尚不清楚。本研究探讨了纳米二氧化钛灌胃致小鼠肾脏损伤的机制。结果表明，纳米二氧化钛在肾脏中蓄积，导致肾脏炎症、细胞坏死和功能障碍。纳米二氧化钛可激活核因子-kappaB，促进肿瘤坏死因子-α、巨噬细胞移动抑制因子、白介素2、白介素4、白介素6、白介素8、白介素10、白介素18、白介素1β、交叉反应蛋白、转化生长因子-β、干扰素-γ和细胞色素P1A1的表达，抑制热休克蛋白70的表达。提示纳米二氧化钛致小鼠肾脏损伤可能与炎性细胞因子表达改变，减少纳米二氧化钛的解毒作用有关。皇冠版权所有(C)2011由爱思唯尔出版。保留所有权利。
Numerous studies have demonstrated that damage of kidney of mice can be caused by exposure to titanium dioxide nanoparticles (TiO2 NPs). However, the molecular mechanism of TiO2 NPs-induced nephric injury remains unclear. In this study, the mechanism of nephric injury in mice induced by an intragastric administration of TiO2 NPs was investigated. The results showed that TiO2 NPs were accumulated in the kidney, resulting in nephric inflammation, cell necrosis and dysfunction. Nucleic factor-kappa B was activated by TiO2 NPs exposure, promoting the expression levels of tumor necrosis factor-alpha, macrophage migration inhibitory factor, interleukin-2, interleukin-4, interleukin-6, interleukin-8, interleukin-10, interleukin-18, interleukin-1 beta, cross-reaction protein, transforming growth factor-beta, interferon-gamma and CYP1A1, while heat shock protein 70 expression was inhibited. These findings implied that TiO2 NPs-induced nephric injury of mice might be associated with alteration of inflammatory cytokine expression and reduction of detoxification of TiO2 NPs. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.