Effect of mitochondrial dysfunction and oxidative stress on endogenous levels of coenzyme Q10 in human cells

✍ Scribed by Hsiu-Chuan Yen; Feng-Yuan Chen; Shih-Wei Chen; Yu-Hsiang Huang; Yun-Ru Chen; Chih-Wei Chen

• Publisher: John Wiley and Sons
• Year: 2011
• Tongue: English
• Weight: 322 KB
• Volume: 25
• Category: Article
• ISSN: 1095-6670
• DOI: 10.1002/jbt.20387

✦ Synopsis

Little is known about the regulation of endogenous CoQ 10 levels in response to mitochondrial dysfunction or oxidative stress although exogenous CoQ 10 has been extensively used in humans. In this study, we first demonstrated that acute treatment of antimycin A, an inhibitor of mitochondrial complex III, and the absence of mitochondrial DNA suppressed CoQ 10 levels in human 143B cells. Because these two conditions also enhanced formation of reactive oxygen species (ROS), we further investigated whether oxidative stress or mitochondrial dysfunction primarily contributed to the decrease of CoQ 10 levels. Results showed that H 2 O 2 augmented CoQ 10 levels, but carbonyl cyanide-ptrifluoromethoxyphenylhydrazone (FCCP), a chemical uncoupler, decreased CoQ 10 levels in 143B cells. However, H 2 O 2 and FCCP both increased mRNA levels of multiple COQ genes for biosynthesis of CoQ 10 . Our findings suggest that ROS induced CoQ 10 biosynthesis, whereas mitochondrial energy deficiency caused secondary suppression of CoQ 10 levels possibly due to impaired import of COQ proteins into mitochondria.