期刊
NEUROBIOLOGY OF DISEASE
卷 18, 期 3, 页码 618-627出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2004.10.021
关键词
apoptosis; ROS; oxidative stress; neurodegeneration; Coenzyme Q10
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.
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