Determination by UPLC / MSMS of Coenzyme Q 10 ( CoQ 10 ) in Plasma of Healthy Volunteers before and after Oral Intake of Food Supplements Containing CoQ 10 (original) (raw)
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Biochimica et Biophysica Acta (BBA) - Bioenergetics, 2005
Coenzyme Q (Q) is an obligatory component of both respiratory chain and uncoupling proteins. Also, Q acts as an antioxidant in cellular membranes. Several neurodegenerative diseases are associated with modifications of Q 10 levels. For these reasons, therapies based on Q supplementation in the diet are currently studied in order to mitigate the symptoms of these diseases. However, the incorporation of exogenous Q also affects aging process in nematodes probably affecting reactive oxygen species (ROS) production. The aim of the present work is to clarify if supplementation with both Q 10 and Q 6 isoforms affects mitochondrial Q 10 content, respiratory chain activity and ROS levels in human cells. Cells incorporated exogenously added Q 10 and Q 6 isoforms into mitochondria that produced changes in mitochondrial activity depending on the side chain length. Supplementation with Q 10 , but not with Q 6 , increased mitochondrial Q-dependent activities. However, Q 6 affected the mitochondrial membrane potential, ROS production, and increased the protein levels of both catalase and Mnsuperoxide dismutase (Mn-SOD). Also, Q 6 induced a transient decrease in endogenous mitochondrial Q 10 levels by increasing its catabolism. These results show that human cells supplemented with Q 6 undergo a mitochondrial impairment, which is not observed with Q 10 supplementation. D
Free Radical Biology and Medicine, 2002
Coenzyme Q (CoQ 10) is a component of the mitochondrial electron transport chain and also a constituent of various cellular membranes. It acts as an important in vivo antioxidant, but is also a primary source of O 2 Ϫ• /H 2 O 2 generation in cells. CoQ has been widely advocated to be a beneficial dietary adjuvant. However, it remains controversial whether oral administration of CoQ can significantly enhance its tissue levels and/or can modulate the level of oxidative stress in vivo. The objective of this study was to determine the effect of dietary CoQ supplementation on its content in various tissues and their mitochondria, and the resultant effect on the in vivo level of oxidative stress. Rats were administered CoQ 10 (150 mg/kg/d) in their diets for 4 and 13 weeks; thereafter, the amounts of CoQ 10 and CoQ 9 were determined by HPLC in the plasma, homogenates of the liver, kidney, heart, skeletal muscle, brain, and mitochondria of these tissues. Administration of CoQ 10 increased plasma and mitochondria levels of CoQ 10 as well as its predominant homologue CoQ 9. Generally, the magnitude of the increases was greater after 13 weeks than 4 weeks. The level of antioxidative defense enzymes in liver and skeletal muscle homogenates and the rate of hydrogen peroxide generation in heart, brain, and skeletal muscle mitochondria were not affected by CoQ supplementation. However, a reductive shift in plasma aminothiol status and a decrease in skeletal muscle mitochondrial protein carbonyls were apparent after 13 weeks of supplementation. Thus, CoQ supplementation resulted in an elevation of CoQ homologues in tissues and their mitochondria, a selective decrease in protein oxidative damage, and an increase in antioxidative potential in the rat.
Ubiquinol-10 is an effective lipid-soluble antioxidant at physiological concentrations
Proceedings of the National Academy of Sciences, 1990
It is well known that ubiquinone-10 (coenzyme Q10, ubiquinone 50) acts as an electron carrier of the respiratory chain in mitochondria. In this paper we show that ubiquinol-10, the reduced form of ubiquinone-10, also efficiently scavenges free radicals generated chemically within liposomal membranes. Ubiquinol-10 is about as effective in preventing peroxidative damage to lipids as alpha-tocopherol, which is considered the best lipid-soluble antioxidant in humans. The number of radicals scavenged by each molecule of ubiquinol-10 is 1.1 under our experimental conditions. In contrast to alpha-tocopherol, ubiquinol-10 is not recycled by ascorbate. However, it is known that ubiquinol-10 can be recycled by electron transport carriers present in various biomembranes and possibly by some enzymes. We also show that ubiquinol-10 spares alpha-tocopherol when both antioxidants are present in the same liposomal membranes and that ubiquinol-10, like alpha-tocopherol, does not interact with reduce...
Bioenergetic and Antioxidant Properties of Coenzyme Q 10 : Recent Developments
Molecular Biotechnology, 2007
For a number of years, coenzyme Q (CoQ10 in humans) was known for its key role in mitochondrial bioenergetics; later studies demonstrated its presence in other subcellular fractions and in plasma, and extensively investigated its antioxidant role. These two functions constitute the basis on which research supporting the clinical use of CoQ10 is founded. Also at the inner mitochondrial membrane level, coenzyme Q is recognized as an obligatory co-factor for the function of uncoupling proteins and a modulator of the transition pore. Furthermore, recent data reveal that CoQ10 affects expression of genes involved in human cell signalling, metabolism, and transport and some of the effects of exogenously administered CoQ10 may be due to this property. Coenzyme Q is the only lipid soluble antioxidant synthesized endogenously. In its reduced form, CoQH2, ubiquinol, inhibits protein and DNA oxidation but it is the effect on lipid peroxidation that has been most deeply studied. Ubiquinol inhibits the peroxidation of cell membrane lipids and also that of lipoprotein lipids present in the circulation. Dietary supplementation with CoQ10 results in increased levels of ubiquinol-10 within circulating lipoproteins and increased resistance of human low-density lipoproteins to the initiation of lipid peroxidation. Moreover, CoQ10 has a direct anti-atherogenic effect, which has been demonstrated in apolipoprotein E-deficient mice fed with a high-fat diet. In this model, supplementation with CoQ10 at pharmacological doses was capable of decreasing the absolute concentration of lipid hydroperoxides in atherosclerotic lesions and of minimizing the size of atherosclerotic lesions in the whole aorta. Whether these protective effects are only due to the antioxidant properties of coenzyme Q remains to be established; recent data point out that CoQ10 could have a direct effect on endothelial function. In patients with stable moderate CHF, oral CoQ10 supplementation was shown to ameliorate cardiac contractility and endothelial dysfunction. Recent data from our laboratory showed a strong correlation between endothelium bound extra cellular SOD (ecSOD) and flow-dependent endothelial-mediated dilation, a functional parameter commonly used as a biomarker of vascular function. The study also highlighted that supplementation with CoQ10 that significantly affects endothelium-bound ecSOD activity. Furthermore, we showed a significant correlation between increase in endothelial bound ecSOD activity and improvement in FMD after CoQ10 supplementation. The effect was more pronounced in patients with low basal values of ecSOD. Finally, we summarize the findings, also from our laboratory, on the implications of CoQ10 in seminal fluid integrity and sperm cell motility.
Coenzyme Q10: multiple benefits in one ingredient
Oilseeds and fats, crops and lipids, 2011
Coenzyme Q (CoQ) also known as ubiquinone, is a lipid molecule widely distributed in nature. In mitochondria, like in other cellular compartments, it is present both in its oxidised state (ubiquinone) and in its reduced one (ubiquinol). The first homolog to be discovered about 50 years ago, in beef mitochondria, was coenzyme Q 10 (Crane et al., 1957). In fact, CoQ is made of benzoquinone moiety and an isoprenoid side chain the length of which is 10 units both in man and many mammals; therefore we talk about CoQ 10 and reduced CoQ 10 (ubiquinol-10). Other living organisms possess different species of CoQ, for instance Saccharomyces cerevisiae produces CoQ 6 , other microorganisms CoQ 7 , and many mammals CoQ 9. Each organism possesses a dominant homolog of CoQ, and minor amounts of other homologs. Most of CoQ 10 available as a
Characterization of cellular uptake and distribution of coenzyme Q10 and vitamin E in PC12 cells☆
The Journal of Nutritional Biochemistry, 2009
Coenzyme Q (CoQ) is a well-known electron transporter in the mitochondrial respiratory chain. Furthermore, ubiquinol (UQH 2 )a reduced form of ubiquinone (UQ)has been shown to act as a radical-scavenging antioxidant. Some studies have reported the beneficial effect of CoQ addition to cultured cells; however, the cellular uptake and distribution of CoQ have not been elucidated. In the present study, we used rat pheochromocytoma PC12 cells to investigate and compare the cellular uptake and distribution of CoQ 10 and α-tocopherol (αT). UQ 10 or UQ 10 H 2 treatment resulted in an increase in the cellular content of both CoQ 10 in a time-and concentration-dependent manner. A subcellular fractionation study revealed that the added UQ 10 as well as UQ 10 H 2 mainly localized in the mitochondrial fraction, which is similar to the localization of endogenous CoQ but different from that of αT. The cellular distribution of αT directly corresponded to the lipid distribution, while the CoQ distribution did not show any relationship with the lipid distribution, particularly in the mitochondrial and microsomal fractions. These results indicate that the cellular distribution of CoQ is completely different from that of αT; moreover, a certain system which accumulates CoQ preferentially in mitochondria may be suggested.