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 （reactiv...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.展开更多
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)+4 种基金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)
文摘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.
