title: Coenzyme Q improves LDL resistance to ex vivo oxidation but does not enhance endothelial function in hypercholesterolemic young adults.
abstract: 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 (CoQ(10)) 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 CoQ(10) (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 CoQ(10) 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. CoQ(10) treatment increased plasma CoQ(10) levels from 1.1 +/-0.5 to 5.0+/-2.8 micromol/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, CoQ(10) supplementation significantly increased the time for CoQ(10)H(2) 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 micromol/l (p =.04). We conclude that dietary supplementation with CoQ(10) decreases ex-vivo LDL oxidizability but has no significant effect on arterial endothelial function in patients with moderate hypercholesterolemia.
authors.affiliation: Department of Cardiology, Royal Prince Alfred Hospital, Sydney, Australia.
authors.forename: O T
authors.initials: OT
authors.lastname: Raitakari
authors.forename: R J
authors.initials: RJ
authors.lastname: McCredie
authors.forename: P
authors.initials: P
authors.lastname: Witting
authors.forename: K A
authors.initials: KA
authors.lastname: Griffiths
authors.forename: J
authors.initials: J
authors.lastname: Letters
authors.forename: D
authors.initials: D
authors.lastname: Sullivan
authors.forename: R
authors.initials: R
authors.lastname: Stocker
authors.forename: D S
authors.initials: DS
authors.lastname: Celermajer
mesh_terms: D000293:Adolescent; D000328:Adult; D008078:Cholesterol, LDL / Q000097:blood; D018592:Cross-Over Studies; D004108:Dilatation, Pathologic / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism; D004311:Double-Blind Method; D004730:Endothelium, Vascular / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology*; D005260:Female; D006801:Humans; D006937:Hypercholesterolemia / Q000000981:diagnostic imaging / Q000188:drug therapy / Q000201:enzymology / Q000378:metabolism*; D015227:Lipid Peroxidation / Q000187:drug effects*; D008077:Lipoproteins, LDL / Q000097:blood / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D014451:Ubiquinone / Q000097:blood / Q000627:therapeutic use*; D014463:Ultrasonography
chemical_list: D008078:Cholesterol, LDL; D008077:Lipoproteins, LDL; D014451:Ubiquinone