Mechanisms of Metal-Induced Mitochondrial Dysfunction in Neurological Disorders

Toxics

Pan Chen¹  Michael Aschner¹  Bobo Yang¹  Tao Ke¹  Xiaobo Yang²  Hong Cheng²  Shaojun Li³ 

[1] Department of Molecular Pharmacology, Albert Einstein College of Medicine, Bronx, NY 10461, USA;Department of Occupational Health and Environmental Health, School of Public Health, Guangxi Medical University, Nanning 530021, China;Department of Toxicology, School of Public Health, Guangxi Medical University, Nanning 530021, China;

关键词: mitochondrial dysfunction;    neurological disorders;    metals;    neurotoxicity;   

DOI  :  10.3390/toxics9060142

来源: DOAJ

【 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.

【 授权许可】

Unknown