p38 MAPK Activation, DNA Damage, Cell Cycle Arrest and Apoptosis As Mechanisms of Toxicity of Silver Nanoparticles in Jurkat T Cells
p38 MAPK Activation, DNA Damage, Cell Cycle Arrest and Apoptosis As Mechanisms of Toxicity of Silver Nanoparticles in Jurkat T Cells
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DOI：
10.1021/es1020668
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发表时间：
2010-11-01
影响因子：
11.4
通讯作者：
Choi, Jinhee
中科院分区：
文献类型：
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作者：
Eom, Hyun-Jeong;Choi, Jinhee
为了确定银纳米颗粒（AgNPs）对人类健康的潜在有害影响，使用氧化应激相关终点对人Jurkat T细胞进行全面毒性测定。还研究了Ag离子的作用，并与AgNP的作用进行了比较，因为预期Ag离子将从AgNP中释放，这可能是其毒性的原因。细胞活力测试表明，与Ag离子相比，暴露于AgNP时Jurkat T细胞的敏感性较高;然而，AgNP和Ag离子在初始暴露期间诱导相似水平的细胞活性氧; 24小时后，与Ag离子相比，暴露于AgNP时它们增加，这表明氧化应激可能是观察到的AgNP细胞毒性的间接原因。AgNPs暴露通过核因子E2相关因子2和核因子κ B信号通路激活p38丝裂原活化蛋白激酶，随后诱导DNA损伤、细胞周期停滞和凋亡。银纳米颗粒对Jurkat T细胞的选择性毒性表明，在广泛使用银纳米颗粒之前，应使用各种不同的细胞类型和生物系统进行严格的毒性评估。
To identify potential harmful effects of silver nanoparticles (AgNPs) on human health, a comprehensive toxicity assay was conducted on human Jurkat T cells, using oxidative stress-related endpoint. The effect of Ag ions was also investigated and compared with that of AgNPs, as it is anticipated that Ag ions will be released from AgNPs, which may be responsible for their toxicity. Cell viability tests indicated high sensitivity of Jurkat T cells when exposed to AgNPs compared to Ag ions; however, both AgNPs and Ag ions induce similar levels of cellular reactive oxygen species during the initial exposure period and; after 24 h, they were increased on exposure to AgNPs compared to Ag ions, which suggest that oxidative stress may be an indirect cause of the observed cytotoxicity of AgNPs. AgNPs exposure activates p38 mitogen-activated protein kinase through nuclear factor-E2-related factor-2 and nuclear factor-kappaB signaling pathways, subsequently inducing DNA damage, cell cycle arrest and apoptosis. Selective toxicity of AgNPs on Jurkat T cells suggests that rigorous toxicity evaluation should be conducted using various different cell types and biological systems prior to the widespread use of AgNPs.