Role of mitochondria in neuronal cell death induced by oxidative stress; neuroprotection by Coenzyme Q10

被引:145
作者
Somayajulu, M
McCarthy, S
Hung, M
Sikorska, M
Borowy-Borowski, H
Pandey, S
机构
[1] Univ Windsor, Dept Biochem & Chem, Windsor, ON N9B 3P4, Canada
[2] CNR, Ottawa, ON, Canada
基金
加拿大自然科学与工程研究理事会; 加拿大创新基金会;
关键词
apoptosis; ROS; oxidative stress; neurodegeneration; Coenzyme Q10;
D O I
10.1016/j.nbd.2004.10.021
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Neuronal cells depend on mitochondrial oxidative phosphorylation for most of their energy needs and therefore are at a particular risk for oxidative stress. Mitochondria play an important role in energy production and oxidative stress-induced apoptosis. In the present study, we have demonstrated that external oxidative stress induces mitochondrial dysfunction leading to increased ROS generation and ultimately apoptotic cell death in neuronal cells. Furthermore, we have investigated the role of Coenzyme Q(10) as a neuroprotective agent. Coenzyme Q(10) is a component of the mitochondrial respiratory chain and a potent anti-oxidant. Our results indicate that total cellular ROS generation was inhibited by Coenzyme Q(10). Further, pre-treatment with Coenzyme Q(10) maintained mitochondrial membrane potential during oxidative stress and reduced the amount of mitochondrial ROS generation. Our study suggests that water-soluble Coenzyme Q(10) acts by stabilizing the mitochondrial membrane when neuronal cells are subjected to oxidative stress. Therefore, Coenzyme Q(10) has the potential to be used as a therapeutic intervention for neurodegenerative diseases. (c) 2004 Elsevier Inc. All rights reserved.
引用
收藏
页码:618 / 627
页数:10
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