Abstract
Coenzyme Q10 (CoQ10) is the predominant form of ubiquinone in man. CoQ10 functions as an electron carrier in the mitochondrial respiratory chain as well as serving as an important intracellular antioxidant. Lowered blood and tissue concentrations of CoQ10 have been reported in a number of diseases, although whether this deficiency is the cause or an effect of the disease remains largely unresolved. Some studies have reported lowered plasma CoQ10 concentrations after statin drug treatment of hypercholesterolaemic patients. However, a deficiency in CoQ10 status has yet to be demonstrated in patients experiencing the rare myotoxic side-effects of these drugs.
Most clinical investigations assessing the therapeutic potential of CoQ10 have focused on cardiovascular disease, specifically congestive heart failure. Although a number of studies have reported clinical improvement in congestive heart failure patients after CoQ10 supplementation to standard therapy, concerns about the design of these studies coupled to the small number of patients involved have limited their acceptance.
Assessment of CoQ10 status is generally based on plasma measurements. As plasma concentrations are influenced by a number of physiological factors and may not represent cellular concentrations, platelets, lymphocytes and fibroblasts may provide suitable alternatives for these measurements.