Quantum dots enhance Cu2+ -induced hepatic L02 cells toxicity.
Quantum dots enhance Cu2+ -induced hepatic L02 cells toxicity.
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DOI：
10.1016/s1001-0742(09)60350-8
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发表时间：
2010-12
影响因子：
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通讯作者：
Yuxia Zhao;Kuangfei Lin;Wei Zhang;Lili Liu
中科院分区：
文献类型：
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作者：
Yuxia Zhao;Kuangfei Lin;Wei Zhang;Lili Liu
作为一类新型异源纳米颗粒，量子点（QD）具有与人类肝脏中的 Cu2+ 共存的潜力。因此，需要考虑联合毒性。考虑到QDs和Cu2+是已知的ROS（活性氧）诱导剂，我们利用人肝L02细胞研究了联合氧化应激和相应的保护策略。结果表明，Cu2+溶液（2.5-20 μg/mL）中存在少量 MPA-CdTe QD（2 μg/mL）会导致较高的毒性，细胞活力下降高达 8 倍，并伴有细胞形态变化。然后，综合毒性被证实为 ROS 相关的氧化应激，细胞内 ROS 水平和谷胱甘肽 S-转移酶 (GST) 活性分别增加了 300% 和 35%。 N-乙酰半胱氨酸（NAC）还可以提供几乎完全的保护，防止诱导毒性。因此，ROS 相关的氧化损伤可能是 QDs-Cu2+/Cu2+ 诱导的毒性的原因，并且可以通过细胞保护性抗氧化酶 GST 来平衡。
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.