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.

引用

页数：18

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