Affiliations: Department of Biochemistry and Molecular Pathology,
Osaka City University Medical School, Osaka, Japan
Note: [] Address for correspondence: Isuke Imada, Department of
Biochemistry and Molecular Pathology, Osaka City University Medical School,
1-4-3 Asahimachi, Abeno, Osaka 545-8585, Japan. E-mail:
imada@med.osaka-cu.ac.jp
Abstract: Effect of CoQ compounds (Qs) on reactive oxygen (ROS) generation by
mitochondrial complex I was studied using rat liver mitochondria and
chemiluminescence probe L012. Kinetic analysis revealed that short chain Qs,
such as Q_{2} and idebenone enhanced ROS generation by
mitochondrial NADH oxidase system by a succinate-inhibitable mechanism. Lipid
peroxidation in mitochondrial membranes induced by NADH and iron was inhibited
by short chain Qs. The inhibitory activity was enhanced by co-oxidation of
succinate as determined by chemiluminescence method and by electron spin
resonance spectroscopy. These results suggested that the reduced form of short
chain Qs inhibited mitochondrial ROS generation and lipid peroxidation.
Keywords: Coenzyme Q, idebenone, complex I, reactive oxygen species, lipid peroxidation, oxidative stress
Journal: BioFactors, vol. 32, no. 1-4, pp. 41-48, 2008
