Ubiquinol-10 protects human low density lipoprotein more efficiently against lipid peroxidation than does alpha-tocopherol.

Abstract

The temporal disappearance of natural antioxidants associated with human low density lipoprotein (LDL) in relation to the appearance of various classes of lipid hydroperoxides was investigated under three types of oxidizing conditions. Freshly isolated LDL from plasma of healthy subjects was free of detectable amounts of lipid hydroperoxides as measured by HPLC postcolumn chemiluminescence detection. Exposure of such LDL to a mild, constant flux of aqueous peroxyl radicals led to rapid and complete oxidation of ubiquinol-10, followed by slower partial depletion of lycopene, 13-carotene, and a-tocopherol. After an initial lag period of complete inhibition of detectable lipid peroxidation, formation of hydroperoxides of cholesterol esters, triglycerides, and phospholipids was observed. The onset of detectable lipid peroxidation corresponded closely with the completion of ubiquinol-10 consumption. However, small amounts of ascorbate, present as a contaminant in the LDL preparation, rather than ubiquinol-10 itself were responsible for the initial lag period. Thus, complete consumption of ubiquinol-10 was preceded by that of ascorbate, and exposure of ascorbate-free LDL to aqueous peroxyl radicals resulted in immediate formation of detectable amounts of lipid hydroperoxides. The rate of radical-mediated formation of lipid hydroperoxides in ascorbate-free LDL was low as long as ubiquinol-10 was present, but increased rapidly after its consumption, even though more than 80% and 95% of endogenous carotenoids and a-tocopherol, respectively, were still present. Qualitatively similar results were obtained when peroxyl radicals were generated within LDL or when the lipoprotein was exposed to oxidants produced by activated human polymorphonuclear leukocytes. LDL oxidation was reduced significantly by supplementing the lipoprotein preparation with physiological amounts ofeither ascorbate or ubiquinol-10. Our data show that ubiquinol-10 is much more efficient in inhibiting LDL oxidation than either lycopene, ,B-carotene, or a-tocopherol.

Modifications of plasma proteome in long-lived rats fed on a coenzyme Q10-supplemented diet

“…It has been proposed that the aging-related decrease of serum albumin in the rat may be partially responsible for decreased serum thiol levels and a shifted redox serum balance towards oxidation during aging (Chlebovská and Chlebovský, 1999). In addition to its antioxidant role inhibiting lipid peroxidation and regenerating α-tocopherol in serum lipoproteins (Stocker et al, 1991;Mohr et al, 1992), dietary CoQ 10 supplementation might further enhance antioxidant capacity of blood plasma by increasing albumin levels.…”

Coenzyme Q10 improves endothelial dysfunction of the brachial artery in Type II diabetes mellitus

“…In contrast to forearm microcirculatory blood flow responses to acetylcholine, post-ischaemic FMD of the brachial artery has been shown to be a surrogate for the coronary circulation and to predict coronary events in patients with angina [35,36]. The beneficial properties of CoQ could relate not only to its antioxidant effect [15,16], but also to improvements in glycaemic control [18] and blood pressure [14]. Coenzyme Q 10 is a powerful antioxidant that might decrease superoxide generation from endothelial cells [13,14].…”

“…CoQ is a more powerful antioxidant than vitamin E, inhibiting its pro-oxidant activity [15,16]. Its deficiency can occur in diabetes in relation to impaired mitochondrial substrate metabolism [17] and increased oxidative stress [6].…”

Autoxidation of Ubiquinol-6 Is Independent of Superoxide Dismutase

“…Much in Vitro evidence supports the idea that reduced coenzyme Q (QH 2 ) acts as an effective antioxidant in membrane systems by scavenging lipid peroxyl radicals (Mellors & Tappel, 1966;Stocker et al, 1991;Frei et al, 1990;Ernster & Forsmark-Andree, 1993;. QH 2 performs this function through the redox transitions of the benzoquinone ring.…”