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Coenzyme Q10 (CoQ10) is the primary lipid-phase antioxidant synthesized endogenously in humans. It has a key role in mitochondrial ATP generation and is essential for immune, neurologic, and muscle function. Clinical trials have shown the efficacy of CoQ10 supplementation in the treatment of hypertension, edema, migraine, and statin-induced muscle pain. Limited epidemiologic data and clinical data support its protective role in cancer incidence and progression as well. Using stored pre-diagnostic plasma samples obtained from a nested case-control study of prostate cancer within the Multiethnic Cohort (MEC) Study, we have measured reduced CoQ10 (ubiquinol), and oxidized CoQ10 (ubiquinone) in 819 men (273 cases and 546 age and ethnicity-matched controls). Significant inverse associations between plasma ubiquinone level and prostate cancer risk were observed in men (50% reduction in risk) with levels in the 200-400 ng/ml range, but not in men with higher levels (Table 1). A similar pattern (not reaching significance) was observed for all-cause mortality with the lowest OR for men with plasma ubiquinone in the 200-400 ng/ml range . Based on these observations, we hypothesize that non-optimal plasma ubiquinone levels may serve as markers of increased risk. Low levels may be indicative of reduced CoQ10 synthesis, whereas higher levels may reflect increased oxidation and cell turnover resulting from inflammatory conditions. Ubiqiunone was also found to be strongly associated with plasma α-tocopherol level (Spearmanr = 0.5383; p < 0.0001), whereas ubiquinol was positively associated with plasma γ-tocopherol levels (Spearmanr = 0.4045; p < 0.0001). These relationships have important ramifications for studies exploring the association of plasma lipid antioxidants and cancer. Understanding the mechanisms by which these factors interact, and the physiological meaning of their plasma levels will be important for future epidemiologic studies.


99th AACR Annual Meeting-- Apr 12-16, 2008; San Diego, CA