The role of ubiquinol as an antioxidant is much more controversial than its role in ATP synthesis (Beyer, 1992). In liposomes, ubiquinol has antioxidant ability similar to that of alpha-tocopherol but, unlike alpha-tocopherol, is not recycled by vitamin C (ascorbate) (Frei et al., 199O; Shi et al., 1999). There is, however, evidence suggesting that the semiquinone form of CoQ1O may be a pro-oxidant and generate superoxide radicals (Beyer, 1992). In vitro data suggest, however, that CoQ1O can conserve vitamin E in rat liver microsomes and mitochondrial membranes and thereby increase the resistance of these membranes to oxidative damage (Hiramatsu et al., 1991).
Dietary supplementation with CoQ1O is known to increase the level of ubiquinol in LDL and to increase the resistance of LDL to the initiation of lipid peroxidation (Mohr et al., 1992). As detailed above, the ability of dietary antioxidants to prevent the formation of oxLDL may be an important factor in preventing the very early stages of atherosclerosis, i.e. foam cell formation (Giugliano, 2OOO). In a very well-designed clinical study, Kaikkonen et al. (2OOO) compared the antioxidant effectiveness of CoQ1O and RRR-alpha-tocopherol (the natural form of vitamin E) in mildly hypercholesterolemic subjects using a randomized placebo-controlled experimental design. In this study, only vitamin E supplementation increased the resistance of LDL to oxidation. In subjects taking both vitamin E and CoQ1O supplements there was no enhanced effect of vitamin E to increase the resistance of LDL to oxidation. This result is somewhat surprising since in vitro experiments suggest that ubiquinol can regenerate alpha-tocopherol from the alpha-tocopheroxyl radical (an oxidized form of vitamin E) and thereby enhance the antioxidative effectiveness of vitamin E (Cabrini et al., 1991).
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