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

Neurobiol Dis. 2005 Apr;18(3):618-27. doi: 10.1016/j.nbd.2004.10.021.

Abstract

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 Q10 as a neuroprotective agent. Coenzyme Q10 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 Q10. Further, pre-treatment with Coenzyme Q10 maintained mitochondrial membrane potential during oxidative stress and reduced the amount of mitochondrial ROS generation. Our study suggests that water-soluble Coenzyme Q10 acts by stabilizing the mitochondrial membrane when neuronal cells are subjected to oxidative stress. Therefore, Coenzyme Q10 has the potential to be used as a therapeutic intervention for neurodegenerative diseases.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Cell Death / drug effects
  • Cell Death / physiology
  • Cell Line, Tumor
  • Coenzymes
  • Humans
  • Mitochondria / drug effects*
  • Mitochondria / physiology
  • Neurons / drug effects*
  • Neurons / physiology
  • Neuroprotective Agents / pharmacology*
  • Oxidative Stress / drug effects*
  • Oxidative Stress / physiology
  • Ubiquinone / analogs & derivatives*
  • Ubiquinone / pharmacology*

Substances

  • Coenzymes
  • Neuroprotective Agents
  • Ubiquinone
  • coenzyme Q10