Research Advances on Pathways of Nickel-Induced Apoptosis

被引：75
作者：
Guo, Hongrui [1 ]
Chen, Lian [1 ]
Cui, Hengmin [1 ,2 ]
Peng, Xi [1 ,2 ]
Fang, Jing [1 ,2 ]
Zuo, Zhicai [1 ,2 ]
Deng, Junliang [1 ,2 ]
Wang, Xun [1 ,2 ]
Wu, Bangyuan [1 ]
机构：
[1] Sichuan Agr Univ, Key Lab Anim Dis & Environm Hazards Sichuan Prov, Yaan 625014, Peoples R China
[2] Sichuan Agr Univ Yaan, Coll Vet Med, Yaan 625014, Peoples R China
来源：
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES | 2016年 / 17卷 / 01期
关键词：
Ni; apoptosis; molecular mechanism; mitochondria; endoplasmic reticulum; MESSENGER-RNA EXPRESSION; INDUCED OXIDATIVE STRESS; PROTEIN CROSS-LINKS; CELL-CYCLE ARREST; ER-STRESS; DIETARY NICKEL; BCL-2; FAMILY; ENDOPLASMIC-RETICULUM; CASPASE ACTIVATION; SIGNALING PATHWAY;
D O I：
10.3390/ijms17010010
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
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.
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页数：18
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