UBIQUINONE SUPPLEMENTATION DURING LOVASTATIN TREATMENT - EFFECT ON LDL OXIDATION EX-VIVO

A randomized, double-masked, placebo-controlled cross-over trial was c arried out to evaluate whether ubiquinone supplementation (180 mg dail y) corrects impaired defence against initiation of oxidation of low de nsity lipoprotein (LDL) related to effective (60 mg daily) lovastatin treatment. Nineteen men with coronary heart disease and hypercholester olemia received lovastatin with or without ubiquinone during 6-week pe riods after wash-out. The depletion times for LDL ubiquinol and reduce d alpha-tocophherol were determined during oxidation induced by 2,2-az o-bis(2,4-dimethylvaleronitrile) (AMVN). Copper-mediated oxidation of LDL isolated by rapid density-gradient ultracentrifugation was used to measure the lag time to the propagation phase of conjugated diene for mation. Compared to mere lovastatin therapy ubiquinone supplementation lead to a 4.4-fold concentration of LDL ubiquinol (P < 0.0001), In sp ite of the 49% lengthening in depletion time (P < 0.0001) of LDL ubiqu inol, the lag time in copper-mediated oxidation increased only by 5% ( P = 0.02). Ubiquinone loading had no statistically significant effect on LDL alpha-tocopherol redox kinetics daring high radical flux. ex vi vo. The faster depletion of LDL ubiquinol and shortened lag time in co njugated diene formation during high-dose lovastatin therapy may, at l east partially, be restored with ubiquinone supplementation. However, the observed improvement in LDL antioxidative capacity was scarce, and the clinical relevance of ubiquinone supplementation during statin th erapy remains open.