Research Advances on Pathways of Nickel-Induced Apoptosis.
Research Advances on Pathways of Nickel-Induced Apoptosis.
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DOI：
10.3390/ijms17010010
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发表时间：
2015-12-23
影响因子：
5.6
通讯作者：
Wu B
中科院分区：
文献类型：
--
作者：
Guo H;Chen L;Cui H;Peng X;Fang J;Zuo Z;Deng J;Wang X;Wu B
高浓度的镍（Ni）对人类和动物有害。镍靶向许多器官并产生多种毒性作用。细胞凋亡在镍诱导的肾、肝、神经和免疫系统毒性中是重要的。活性氧、线粒体、内质网、Fas和c-Myc介导的凋亡途径参与镍诱导的细胞凋亡。然而，镍引起细胞凋亡的确切机制仍不清楚。了解镍诱导细胞凋亡的机制有助于设计预防镍毒性的措施。
High concentrations of nickel (Ni) are harmful to humans and animals. Ni targets a number of organs and produces multiple toxic effects. Apoptosis is important in Ni-induced toxicity of the kidneys, liver, nerves, and immune system. Apoptotic pathways mediated by reactive oxygen species (ROS), mitochondria, endoplasmic reticulum (ER), Fas, and c-Myc participate in Ni-induced cell apoptosis. However, the exact mechanism of apoptosis caused by Ni is still unclear. Understanding the mechanism of Ni-induced apoptosis may help in designing measures to prevent Ni toxicity.