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

查看全文 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

出　　处：《Journal of Environmental Sciences》索引2010年第22卷第12期,共6页

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) 摘　　要：As a new class of xenogenous nanoparticle,quantum dots (QDs) possess the potential to co-exist with Cu2+ in human liver.The combined toxicity is thus concerned.Considering QDs and Cu2+ 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 Cu2+ 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-Cu2+/Cu2+ induced toxicity and could be balanced through cytoprotective antioxidant enzyme GST. 关键词：细胞毒性量子点高铜诱导肝脏细胞形态变化氧化应激活性氧

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

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