Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

被引:31
|
作者
Cheng, Hong [1 ]
Yang, Bobo [2 ]
Ke, Tao [2 ]
Li, Shaojun [3 ]
Yang, Xiaobo [1 ,4 ]
Aschner, Michael [2 ]
Chen, Pan [2 ]
机构
[1] Guangxi Med Univ, Sch Publ Hlth, Dept Occupat Hlth & Environm Hlth, Nanning 530021, Peoples R China
[2] Albert Einstein Coll Med, Dept Mol Pharmacol, Bronx, NY 10461 USA
[3] Guangxi Med Univ, Sch Publ Hlth, Dept Toxicol, Nanning 530021, Peoples R China
[4] Guangxi Univ Sci & Technol, Sch Med, Dept Publ Hlth, Liuzhou 545006, Peoples R China
基金
中国国家自然科学基金;
关键词
mitochondrial dysfunction; neurological disorders; metals; neurotoxicity; AMYOTROPHIC-LATERAL-SCLEROSIS; INDUCED CHOLINERGIC DYSFUNCTIONS; ALUMINUM-INDUCED NEUROTOXICITY; ENDOPLASMIC-RETICULUM STRESS; PERMEABILITY TRANSITION PORE; INDUCED OXIDATIVE STRESS; INDUCED CALCIUM SIGNALS; LEVEL ARSENIC EXPOSURE; INDUCED NEURONAL DEATH; APOPTOTIC CELL-DEATH;
D O I
10.3390/toxics9060142
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Metals are actively involved in multiple catalytic physiological activities. However, metal overload may result in neurotoxicity as it increases formation of reactive oxygen species (ROS) and elevates oxidative stress in the nervous system. Mitochondria are a key target of metal-induced toxicity, given their role in energy production. As the brain consumes a large amount of energy, mitochondrial dysfunction and the subsequent decrease in levels of ATP may significantly disrupt brain function, resulting in neuronal cell death and ensuing neurological disorders. Here, we address contemporary studies on metal-induced mitochondrial dysfunction and its impact on the nervous system.
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页数:26
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