Quantum dots enhance Cu^(2+)-induced hepatic L02 cells toxicity

作     者：Yuxia Zhao,Kuangfei Lin,Wei Zhang,Lili Liu State Environmental Protection Key Laboratory of Environmental Risk Assessment and Control on Chemical Process,Shanghai 200237,China 

作者机构：State Environmental Protection Key Laboratory of Environmental Risk Assessment and Control on Chemical Process Shanghai 200237 China. E-mail: maryzyx@*** 

出 版 物：《Journal of Environmental Sciences》 (环境科学学报（英文版）)

年 卷 期：2010年第22卷第12期

页      面：1987-1992页

核心收录：

学科分类：0830[工学-环境科学与工程（可授工学、理学、农学学位）] 07[理学] 0713[理学-生态学] 

基　　金：supported by the National Natural Science Foundation of China(No. 40871223,40901148,20677015) the National High-Tech Research and Development Program(863) of China (No. 2007AA06Z331) the Fundamental Research Funds for the Central Universities(No. WB0911011,WB0914041) the National Environmental Protection Public Welfare Science and Technology Research Program of China(No. 200909089) the Shang-hai Educational Development Foundation "ChenguangProject"(No. 2007CG39) the Shanghai Natural Science Fund(No. 09ZR1407700) the State Key Lab of Urban Water Resource and Environment,Harbin Institute of Technology(No. ES200902) 

主　　题：quantum dots hepatic L02 cell reactive oxygen species glutathione S-transferase 

摘      要：As a new class of xenogenous nanoparticle, quantum dots （QDs） possess the potential to co-exist with Cu^2＋ in human liver. The combined toxicity is thus concerned. Considering QDs and Cu^2＋ are known ROS （reactive oxygen species） inducer, we investigated the combined oxidative stress and corresponding protective strategy using human hepatic L02 cells. The results demonstrated that the presence of a small amount of MPA-CdTe QDs （2 μg/mL） in a Cu^2＋ solution （2.5-20 μg/mL） resulted in a higher toxicity with up to 8-fold cell viability decrease, which was accompanied by cell morphology changes. The combined toxicity was then confirmed as ROS associated oxidative stress with up to 300% and 35% increase of the intracellular ROS level and glutathione S-transferase （GST） activity, respectively. N-acetylcysteine （NAC） can also provide almost complete protection against the induced toxicity. Therefore, the ROS associated oxidant injury might be responsible for the QDs-Cu^2＋/Cu^2＋ induced toxicity and could be balanced through cytoprotective antioxidant enzyme GST.