Coenzyme Q improves LDL resistance to ex vivo oxidation but does not enhance endothelial function in hypercholesterolemic young adults

Oxidative modification of low-density lipoprotein (LDL) may cause arterial endothelial dysfunction in hyperlipidemic subjects. Antioxidants can protect LDL from oxidation and therefore improve endothelial function. Dietary supplementation with coenzyme Q (CoQ10) raises its level within LDL, which may subsequently become more resistant to oxidation. Therefore, the aim of this study was to assess whether oral supplementation of CoQ10 (50 mg three times daily) is effective in reducing ex vivo LDL oxidizability and in improving vascular endothelial function. Twelve nonsmoking healthy adults with hypercholesterolemia (age 34 ± 10 years, nine women and three men, total cholesterol 7.4 ± 1.1 mmol/l) and endothelial dysfunction (below population mean) at baseline were randomized to receive CoQ10 or matching placebo in a double-blind crossover study (active/placebo phase 4 weeks, washout 4 weeks). Flow-mediated (FMD, endothelium-dependent) and nitrate-mediated (NMD, smooth muscle-dependent) arterial dilatation were measured by high-resolution ultrasound. CoQ10 treatment increased plasma CoQ10 levels from 1.1 ± 0.5 to 5.0 ± 2.8 μmol/l (p = .009) but had no significant effect on FMD (4.3 ± 2.4 to 5.1 ± 3.6 %, p = .99), NMD (21.6 ± 6.1 to 20.7 ± 7.8 %, p = .38) or serum LDL-cholesterol levels (p = .51). Four subjects were selected randomly for detailed analysis of LDL oxidizability using aqueous peroxyl radicals as the oxidant. In this subgroup, CoQ10 supplementation significantly increased the time for CoQ10H2 depletion upon oxidant exposure of LDL by 41 ± 19 min (p = .04) and decreased the extent of lipid hydroperoxide accumulation after 2 hours by 50 ± 37 μmol/l (p = .04). We conclude that dietary supplementation with CoQ10 decreases ex-vivo LDL oxidizability but has no significant effect on arterial endothelial function in patients with moderate hypercholesterolemia.