Copper oxide nanoparticles induce oxidative stress and cytotoxicity in airway epithelial cells.

Copper oxide nanoparticles induce oxidative stress and cytotoxicity in airway epithelial cells.
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DOI:
10.1016/j.tiv.2009.08.005
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发表时间:
2009-10
影响因子:
3.2
通讯作者:
Cormier, Stephania A.
Cormier, Stephania A.
中科院分区:
医学3区
文献类型:
--
作者:
Fahmy, Baher;Cormier, Stephania A.

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金属氧化物纳米颗粒经常被用作工业催化剂,在工厂周围的地点已经清楚地证明了这些颗粒水平的升高。到目前为止,关于金属氧化物纳米颗粒的毒性数据有限。为了了解这些空气污染物对呼吸系统的影响,将呼吸道上皮细胞(HEP-2)暴露于越来越多的二氧化硅(SiO_2)、氧化铁(Fe2O)和氧化铜(CuO)纳米颗粒中,这些纳米颗粒是工厂周围环境空气中发现的主要金属氧化物。CuO对Hep-2细胞的毒性作用最强,且呈剂量依赖关系,而高剂量(400µg/cm2)的SiO_2和Fe_2O_3对Hep-2细胞无毒性作用。虽然所有的金属氧化物纳米颗粒都能在Hep-2细胞中产生ROS,但CuO更能压倒抗氧化防御系统(如过氧化氢酶和谷胱甘肽还原酶)。暴露于CuO的Hep-2细胞的8-异前列腺素水平和GSSG/总谷胱甘肽的比值显著增加,提示CuO产生的ROS诱导了Hep-2细胞的氧化应激。CuO与抗氧化剂白藜芦醇共同处理细胞后,细胞存活率增加,提示氧化应激可能是CuO细胞毒性作用的原因。这些研究表明,金属氧化物的细胞毒性效应存在高度的变异性,这种变异性不是由于过渡金属的溶解性造成的,而且这种变异性似乎涉及到持续的氧化应激,可能是由于氧化还原循环。
Metal oxide nanoparticles are often used as industrial catalysts and elevated levels of these particles have been clearly demonstrated at sites surrounding factories. To date, limited toxicity data on metal oxide nanoparticles are available. To understand the impact of these airborne pollutants on the respiratory system, airway epithelial (HEp-2) cells were exposed to increasing doses of silicon oxide (SiO2), ferric oxide (Fe2O3) and copper oxide (CuO) nanoparticles, the leading metal oxides found in ambient air surrounding factories. CuO induced the greatest amount of cytotoxicity in a dose dependent manner; while even high doses (400 µg/cm2) of SiO2 and Fe2O3 were non-toxic to HEp-2 cells. Although all metal oxide nanoparticles were able to generate ROS in HEp-2 cells, CuO was better able to overwhelm antioxidant defenses (e.g. catalase and glutathione reductase). A significant increase in the level of 8-isoprostanes and in the ratio of GSSG to total glutathione in cells exposed to CuO suggested that ROS generated by CuO induced oxidative stress in HEp-2 cells. Co-treatment of cells with CuO and the antioxidant resveratrol increased cell viability suggesting that oxidative stress may be the cause of the cytotoxic effect of CuO. These studies demonstrated that there is a high degree of variability in the cytotoxic effects of metal oxides, that this variability is not due to the solubility of the transition metal, and that this variability appears to involve sustained oxidative stress possibly due to redox cycling.
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