Effect of mitochondrial dysfunction and oxidative stress on endogenous levels of coenzyme Q(10) in human cells |
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Authors: | Yen Hsiu-Chuan Chen Feng-Yuan Chen Shih-Wei Huang Yu-Hsiang Chen Yun-Ru Chen Chih-Wei |
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Institution: | Department and Graduate Institute of Medical Biotechnology and Laboratory Science, Chang Gung University, Kwei-Shan, Tao-Yuan 333, Taiwan, Republic of China. yen@mail.cgu.edu.tw |
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Abstract: | 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-p-trifluoromethoxyphenylhydrazone (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. |
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Keywords: | Antimycin A Coenzyme Q10 COQ genes Cyanide‐p‐trifluoromethoxyphenylhydrazone (FCCP) Hydrogen peroxide |
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