Original Contribution EFFECTS OF COENZYME Q10 ADMINISTRATION ON ITS TISSUE CONCENTRATIONS, MITOCHONDRIAL OXIDANT GENERATION, AND OXIDATIVE STRESS IN THE RAT

Coenzyme Q (CoQ10) is a component of the mitochondrial electron transport chain and also a constituent of various cellular membranes. It acts as an important in vivo antioxidant, but is also a primary source of O2 /H2O2 generation in cells. CoQ has been widely advocated to be a beneficial dietary adjuvant. However, it remains controversial whether oral administration of CoQ can significantly enhance its tissue levels and/or can modulate the level of oxidative stress in vivo. The objective of this study was to determine the effect of dietary CoQ supplementation on its content in various tissues and their mitochondria, and the resultant effect on the in vivo level of oxidative stress. Rats were administered CoQ10 (150 mg/kg/d) in their diets for 4 and 13 weeks; thereafter, the amounts of CoQ10 and CoQ9 were determined by HPLC in the plasma, homogenates of the liver, kidney, heart, skeletal muscle, brain, and mitochondria of these tissues. Administration of CoQ10 increased plasma and mitochondria levels of CoQ10 as well as its predominant homologue CoQ9. Generally, the magnitude of the increases was greater after 13 weeks than 4 weeks. The level of antioxidative defense enzymes in liver and skeletal muscle homogenates and the rate of hydrogen peroxide generation in heart, brain, and skeletal muscle mitochondria were not affected by CoQ supplementation. However, a reductive shift in plasma aminothiol status and a decrease in skeletal muscle mitochondrial protein carbonyls were apparent after 13 weeks of supplementation. Thus, CoQ supplementation resulted in an elevation of CoQ homologues in tissues and their mitochondria, a selective decrease in protein oxidative damage, and an increase in antioxidative potential in the rat. © 2002 Elsevier Science Inc. Keywords—Coenzyme Q, Antioxidants, Dietary intake, Mitochondria, Protein carbonyls, Free radicals, Oxidative