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The roles of coenzyme-Q10 and vitamin E on peroxidation of human low density subfractions

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... The pioneer studies in the 1960s highlighted its key role in mitochondrial bioenergetics; later studies demonstrated the antioxidant role of ubiquinol, its reduced form, in protecting biomolecules from oxidation by reactive oxygen species (ROS). In particular, inhibition of lipid peroxidation has been addressed [12] showing that increased levels of ubiquinol within circulating lipoproteins result in increased resistance of LDL to peroxidation [13,14]. Moreover, CoQ 10 has a direct antiatherogenic effect, which has been demonstrated in apolipoprotein E-deficient mice fed with a high-fat diet [15]. ...
... This study, aimed at evaluating the use of EV olive oil as food matrix for vehiculating lipophilic antioxidants and the [13]. In fact, with our low (20 mg) dosage the average increase over baseline was 73 and 170% for the 40 mg dosage. ...
... Regarding the formulations with CoQ 10 , although a positive trend toward a dose-dependent benefit was evincible, only the high dose of CoQ 10 produced a significantly lower peroxidisability . These data are in agreement with previous reports [13,14] related to similar plasma concentrations, reached following oral administration of 100 mg/day CoQ 10 in soft gel capsules for 1 month. Intriguingly, our data highlight the contribution of CoQ 10 to the potentially antiatherogenic properties of this functional food formulation, even if associated with a lower daily intake. ...
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Olive oil consumption is associated with protective cardiovascular properties, including some beneficial modifications in lipoprotein profile and composition. Coenzyme Q(10) (CoQ(10)) exerts a protective effect on plasma lipoproteins. Aim of the study was to investigate whether extra virgin (EV) olive oil enriched with CoQ(10) affects CoQ(10) levels and oxidative status in plasma and in isolated lipoproteins. Twelve subjects were administered 20 mL olive oil per day for 2 weeks, followed by 2 weeks of olive oil enriched with 20 mg and 2 more weeks with 40 mg of CoQ(10). Plasma and isolated lipoproteins were collected in each phase of the study and subsequently analyzed to assess lipid profile, CoQ10 levels, ORAC assay, resistance of lipoproteins to peroxidation and paroxonase 1 activity. Plasma CoQ(10) levels significantly increased with the 20 mg (+73%) and 40 mg dose (+170%), while the percentage of oxidized CoQ(10) decreased. A significant inverse correlation was found in plasma between percentage of oxidized CoQ(10) and total antioxidant capacity. A lower susceptibility of LDL to peroxidation was also found. Finally, a positive correlation was observed between concentration of CoQ(10) in HDL and paraoxonase-1 activity. EV olive oil enriched with both doses of CoQ(10) significantly affects its bioavailability and plasma redox status. These changes are associated with a decreased susceptibility of plasma lipoproteins to peroxidation associated with a chain-breaking antioxidant activity of the formulation.
... A few years later, Kontush found that, when oxidizing LDL in vitro, the susceptibility to oxidation was inversely correlated with the Q 10 /polyunsaturated fatty acids (PUFA) ratio [12]. Studies carried out in our laboratory [13] have shown that the heavier LDL subfraction, which is the one most susceptible to peroxidation, has a lower content of CoQ 10 compared to the lighter subfractions. After a daily administration of 100 mg of CoQ 10 for 4 weeks, with a single dose, subjects showed a mean plasma level of 1.5 mg/mL, comparable to the concentration measured in our study. ...
... Furthermore , in a previous work, we showed that supplementation of healthy volunteers with CoQ 10 leads to an increase of CoQ 10 itself and of vit. E, particularly in LDL3, the heavy, atherogenic subfraction of LDL [13]. No significant variations were found in the profile of plasma fatty acids. ...
... The closest relationship was undoubtedly between CoQ 10 increase and TEAC enhancement in plasma (Fig. 1). The plasma levels of antioxidants reached in our study are comparable to those found to improve the resistance to peroxidation of LDL in previous studies: Peroxidation of these lipoproteins is known to be involved in the pathogenesis of atherosclerosis [13, 29]. Plasma CoQ 10 levels equal to those found in our study have been shown to significantly implement the CoQ 10 content on the stratum corneum [30]. ...
Article
Twenty healthy subjects integrated their diet with two types of products sequentially: In the first phase (first 14 days), the volunteers were given the following food items not supplemented with vitamin E (vit. E) or Coenzyme Q10 (CoQ10): breakfast, 250 mL skimmed milk; mid-morning snack, 330 mL fruit juice; mid-afternoon snack, low-fat yogurt 125 g; after dinner, low-fat dessert 110 g. In the second phase, from day 14 to day 35, the same items were added with vit. E and CoQ10 (a total daily supplementation of 19.4 mg CoQ10 and 13.7 mg vit.E). After taking the supplemented products for 2 weeks, plasma CoQ10 reached 1.30 µg/mL, nearly twice the initial values. These levels further increased after 3 weeks of supplementation. Vit. E levels significantly (p <0.001) increased only after 3 weeks of supplementation, reaching 7.9 ± 2.8 µg/mL, 39% more than the initial value. The total plasma fatty acid pattern did not change substantially throughout the study. The increase of the total antioxidant capacity of plasma was significant (p <0.001) for days 28 and 35, with values close to 0.24 ± 0.09 mM Trolox (a nearly 60% increase).
... CoQ10 and vitamin E can have synergic effects and CoQ deficiency may decrease the beneficial effect of vitamin B6 [56]. Littarru and coworkers [57] demonstrated a deficiency of CoQ in cardiac muscle and possibly in the arterial smooth muscle which are important in the pathogenesis of left ventricular hypertrophy (LVH) and atherosclerosis respectively [58][59][60][61][62]. LVH and atherosclerosis are risk factors of acute myocardial infarction (AMI) and sudden cardiac death (SCD). ...
... Littarru and coworkers [57] demonstrated a deficiency of CoQ in cardiac muscle and possibly in the arterial smooth muscle which are important in the pathogenesis of left ventricular hypertrophy (LVH) and atherosclerosis respectively [58][59][60][61][62]. LVH and atherosclerosis are risk factors of acute myocardial infarction (AMI) and sudden cardiac death (SCD). It is now widely accepted that unstable atheroma and subsequent plaque rupture is a major cause of myocardial infarction and stroke [52][53][54][55][56][57][58][59][60][61][62][63][64][65]. Clinical trials with statins [49,66,67] showed only minor effects on the size of existing lesions but major reduction in clinical events, despite the fact that these agents decrease CoQ as a side effect of drugs. ...
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Background: Several cardiovascular, neurological and other diseases are associated with coenzyme Q10(CoQ) deficiency. The objective is to evaluate possible benefits of ubiquinone supplementation in cardiovascular diseases and degenerative diseases of the brain. Methods: An internet search in PubMed, Vitasearch, In Circulation. Net, till 2008, discussions with colleagues, own experiences. Results: Ubiquinone (Coenzyme Q10) deficiency has been observed in several cardiovascular and neurological diseases. CoQ10 has strong influence on lipid metabolism, oxidation of blood lipids, vascular inflammation and on the cell mem-branes of cardiac and arterial cells and neurons. These pathogenetic mechanisms seem to be important in patients with neurological and cardiac disease as well as in brain-heart connection. Its supplementation has several beneficial effects in-cluding the stabilisation of atherosclerotic plaque and decreasing the size of myoacardial infarction and the protection of neurons. Antioxidant properties of CoQ10 are responsible for the prevention of many drug side effects. Several studies have suggested the beneficial effect of CoQ10 in neuro-cardiovascular diseases, that will require further confirmation. Adverse effects such as nausea and vomiting may be reduced by using highly bio-available brands, that reduce the oral dosage of COQ. Conclusions: CoQ10 is still in the investigational stages and the list of possible indications related to brain and heart dis-eases and their linkage, appears to be quite extensive. There is still the need for a number of large, double blind multicen-ter, randomized, controlled clinical trials, in order to confirm the possible beneficial effects of CoQ10 supplementation in different neurocardiological conditions.
... coli) uses coenzyme Q 8 (CoQ 8 ), and Schizosaccharomyces pombe and humans use coenzyme Q 10 (CoQ 10 ; Ernster and Dallner 1995; Grunler et al. 1994; Okada et al. 1998; Suzuki et al. 1997). CoQ is an electron transporter in the respiratory chains of prokaryotes and eukaryotes and functions as an effective intracellular antioxidant (Alleva et al. 1995; Kontush et al. 1995). CoQ also accepts electrons from sources outside the respiratory chain, such as the electrons generated during the formation of protein disulfide bonds in E. coli (Bader et al. 1999). ...
... Over the last 20 years, CoQ 10 has been widely and successfully used as an orally administered prophylactic and therapy for a variety of diseases, including heart disease. CoQ 10 deficiencies can be reversed by supplementation, and its administration has no known toxicity or side effects (Alleva et al. 1995). Appl Microbiol Biotechnol (2007) 74:974–980 DOI 10.1007/s00253-006-0744-4 S.-J. ...
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This report describes the optimization of culture conditions for coenzyme Q10 (CoQ10) production by Agrobacterium tumefaciens KCCM 10413, an identified high-CoQ10-producing strain (Kim et al., Korean patent. 10-0458818, 2002b). Among the conditions tested, the pH and the dissolved oxygen (DO) levels were the key factors affecting CoQ10 production. When the pH and DO levels were controlled at 7.0 and 0–10%, respectively, a dry cell weight (DCW) of 48.4 g l−1 and a CoQ10 production of 320 mg l−1 were obtained after 96 h of batch culture, corresponding to a specific CoQ10 content of 6.61 mg g-DCW−1. In a fed-batch culture of sucrose, the DCW, specific CoQ10 content, and CoQ10 production increased to 53.6 g l−1, 8.54 mg g-DCW−1, and 458 mg l−1, respectively. CoQ10 production was scaled up from a laboratory scale (5-l fermentor) to a pilot scale (300 l) and a plant scale (5,000 l) using the impeller tip velocity (V tip) as a scale-up parameter. CoQ10 production at the laboratory scale was similar to those at the pilot and plant scales. This is the first report of pilot- and plant-scale productions of CoQ10 in A. tumefaciens.
... CoQ10 and vitamin E can have synergic effects and CoQ deficiency may decrease the beneficial effect of vitamin B6 [56]. Littarru and coworkers [57] demonstrated a deficiency of CoQ in cardiac muscle and possibly in the arterial smooth muscle which are important in the pathogenesis of left ventricular hypertrophy (LVH) and atherosclerosis respectively [58][59][60][61][62]. LVH and atherosclerosis are risk factors of acute myocardial infarction (AMI) and sudden cardiac death (SCD). ...
... Littarru and coworkers [57] demonstrated a deficiency of CoQ in cardiac muscle and possibly in the arterial smooth muscle which are important in the pathogenesis of left ventricular hypertrophy (LVH) and atherosclerosis respectively [58][59][60][61][62]. LVH and atherosclerosis are risk factors of acute myocardial infarction (AMI) and sudden cardiac death (SCD). It is now widely accepted that unstable atheroma and subsequent plaque rupture is a major cause of myocardial infarction and stroke [52][53][54][55][56][57][58][59][60][61][62][63][64][65]. Clinical trials with statins [49,66,67] showed only minor effects on the size of existing lesions but major reduction in clinical events, despite the fact that these agents decrease CoQ as a side effect of drugs. ...
Chapter
Full-text available
CoQ10 (CoQ10) deficiency has been reported in apparently healthy subjects as well as in patients with congestive heart failure, angina pectoris, coronary artery disease, cardiomyopathy, hypertension, mitral valve prolapse, diabetes mellitus and after coronary revascularization. Since CoQ10 bolsters the synthesis of ATP and inhibits free radical damage, its administration may be useful in cellular energy production as well as preventing cellular damage during ischaemia-reperfusion injury. Clinical benefits of CoQ10 are mainly due to its ability to improve energy production, antioxidant activity, and membrane stabilizing properties. Several small scale studies indicate that CoQ10 could be useful in patients with congestive heart failure, angina pectoris, cardiomyopathy, coronary artery disease, acute myocardial infarction, diabetes, and in the preservation of myocardium. It may also decrease plasma lipoproteins, insulin and angiotensin converting enzyme. CoQ10 is normally present in the low density lipoprotein cholesterol fraction and inhibits its oxidation, indicating that it can inhibit atherosclerosis. CoQ10 also regenerates vitamin E. These actions of CoQ10 indicate that it can inhibit the development of atherosclerosis and prevent the instability and disruption of plaques. The adverse effects of CoQ10 are minor gastrointestinal discomfort and elevation in SGOT and LDH.
... The heaviest fraction of LDL, namely LDL3, is also the most peroxidizable, and epidemiological studies have demonstrated that the abundance of this subfraction is correlated with the incidence of ischemic heart disease. In 1995, we demonstrated that LDL3 also have a lower content of CoQ 10 compared to LDL1 and LDL2; moreover, administration of CoQ 10 to normal volunteers increased the CoQ 10 content, particularly in the LDL3 subfraction, and decreased their peroxidizability [11]. ...
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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.
... Studies in humans have shown that oxidative stress, as assessed by plasma and urinary F 2 -isoprostanes, is reduced by supplementation with n-3 fatty acids [14][15][16]. Another potential modifier of oxidative stress is coenzyme Q10 (CoQ) an intracellular antioxidant that protects membrane phospholipids, mitochondrial membrane protein, low-density lipoprotein and lymphocyte DNA from free radical-induced oxidative damage [17][18][19]. As oxidative stress is regarded as a major contributor to risk of CVD in patients with CKD [20], the implementation of interventions using n-3 fatty acids and/or CoQ are therefore considered possible modifiers of oxidative stress that might inhibit telomere shortening and have the potential to modify CVD risk. ...
Article
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DNA telomere shortening associates with the age-related increase cardiovascular disease (CVD) risk. Reducing oxidative stress, could modify telomere erosion during cell replication, and CVD risk in patients with chronic kidney disease (CKD). The effect of n-3 fatty acids and coenzyme Q10 (CoQ) on telomere length was studied in a double-blind placebo-controlled trial in CKD. Eighty-five CKD patients were randomized to: n-3 fatty acids (4 g); CoQ (200 mg); both supplements; or control (4 g olive oil), daily for 8 weeks. Telomere length was measured in neutrophils and peripheral blood mononuclear cells (PBMC) at baseline and 8 weeks, with and without correction for cell counts. Main and interactive effects of n-3 fatty acids and CoQ on telomere length were assessed adjusting for baseline values. F₂-isoprostanes were measured as markers of oxidative stress. There was no effect of n-3 fatty acids or CoQ on neutrophil or PBMC telomere length. However, telomere length corrected for neutrophil count was increased after n-3 fatty acids (p = 0.015). Post-intervention plasma F₂-isoprostanes were negative predictors of post-intervention telomere length corrected for neutrophil count (p = 0.025).The effect of n-3 fatty acids to increased telomere length corrected for neutrophil count may relate to reduced oxidative stress and increased clearance of neutrophils with shorter telomeres from the circulation. This may be a novel mechanism of modifying CVD risk in CKD patients.
... An increase in energy expenditure caused by exercise training and possible metabolic alterations might be the major cause behind the improvements in the triglycerides profiles and a better aerobic capacity with enhanced utilization of lipids. Additionally, Alleva et al. (1995) reported that coenzyme Q10 is an intracellular antioxidant that protects the membrane phospholipids and mitochondrial membrane protein. Moreover, Q10 supplementation significantly affected the protein levels of NFκB, IκB, Nrf2 and HO-1 in exercise group when compared with the sedentary-untreated groups. ...
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This study reports the effects of Q10, coenzyme Q10 or ubiquinone, a component of the electron transport chain in mitochondria, on nuclear factor kappa-light-chain-enhancer of activated B cells (NF kappa B), inhibitors of kappa B (I kappa B), nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and hemeoxygenase 1 (HO-1) in rats after chronic exercise training for 6 weeks. 8-week old male Wistar rats were assigned randomly to one of four treatments planned in a 2 x 2 factorial arrangement of two condition (sedentary vs. exercise training), and two coenzyme Q10 levels (0 and 300 mg/kg per day for 6 weeks). The expression levels of the target proteins were determined in the heart, liver and muscle, and biochemical parameters including creatinine, urea, glucose and lipid profile were investigated in plasma. When compared with sedentary group, significant decreases in heart, liver and muscle NF kappa B levels by 45%, 26% and 44% were observed in Q10 supplemented rats after exercise training, respectively, while the inhibitory protein I kappa B increased by 179%, 111% and 127% in heart, liver and muscle tissues. Q10 supplementation caused an increase in Nrf2 (167%, 165% and 90%) and HO-1 (107%, 156% and 114%) after exercise training in heart, liver and muscle tissues (p < 0.05). No significant change was observed in any of the parameters associated with protein, carbohydrate and lipid metabolism, except that exercise caused a decrease in plasma triglyceride, which was further decreased by Q10. In conclusion, these results suggest that Q10 modulates the expression of NF kappa B, I kappa B, Nrf2 and HO-1 in exercise training, indicating an anti-inflammatory effect of Q10 and emphasizes its role in antioxidant defense.
... We have demonstrated that CoQ was capable of inducing a recovery of the levels of DHT up to control values, and also with further increases. CoQ has been proved to be a potent antioxidant in vitro [74] and in vivo studies [75]. It has been proposed as a potential treatment for mitochondrial diseases [74,76] and for vascular diseases [77] in type 2 diabetes patients [78]. ...
Article
There is a growing awareness that oxidative stress may play a role in periodontal disease. The aim of this investigation was to evaluate potential oxidant/antioxidant interactions of nicotine with antioxidants (Coenzyme Q10 (CoQ), Pycnogenol and phytoestrogens in a cell culture model. Duplicate incubations of human periosteal fibroblasts and osteoblasts were performed with 14C-testosterone as substrate, in the presence or absence of CoQ (20 microg/ml), Pycnogenol (150 microg/ml), and phytoestrogens (10 and 40 microg/ml), alone and in combination with nicotine (250 microg/ml). At the end of a 24-h incubation period, the medium was solvent extracted and testosterone metabolites were separated by thin-layer chromatography and quantified using a radioisotope scanner. The incubations of osteoblasts and periosteal fibroblasts with CoQ, Pycnogenol or phytoestrogens stimulated the synthesis of the physiologically active androgen DHT, while the yields of DHT were significantly reduced in response to nicotine compared to control values (p<0.001 for phytoestrogens). The combination of nicotine with CoQ, Pycnogenol or phytoestrogens increased the yields of DHT compared with incubation with nicotine alone in both cell types. This investigation suggests that the catabolic effects of nicotine could be reversed by the addition of antioxidants such as CoQ or Pycnogenol and phytoestrogens.
... This protective role of CoQ 10 is independent of the effect of exogenous antioxidants, such as Vitamin E, and it can both prevent the formation of free lipid radicals and eliminate them either directly or by regenerating Vitamin E (Pobezhimova & Voinikov, 2000). In the last decade the antioxidant role of CoQ 10 in plasma lipoproteins has been deeply investigated (Alleva et al., 1995; Thomas, Witting & Stocker, 1999 ). Furthermore , dihydroorotate dehydrogenase, the fourth enzyme of pyrimidine synthesis, needs CoQ 10 for activity. ...
Article
Coenzyme Q10 is an essential cofactor in the electron transport chain and serves as an important antioxidant in both mitochondria and lipid membranes. CoQ10 is also an obligatory cofactor for the function of uncoupling proteins. Furthermore, dietary supplementation affecting CoQ10 levels has been shown in a number of organisms to cause multiple phenotypic effects. However, the molecular mechanisms to explain pleiotrophic effects of CoQ10 are not clear yet and it is likely that CoQ10 targets the expression of multiple genes. We therefore utilized gene expression profiling based on human oligonucleotide sequences to examine the expression in the human intestinal cell line CaCo-2 in relation to CoQ10 treatment. CoQ10 caused an increased expression of 694 genes at threshold-factor of 2.0 or more. Only one gene was down-regulated 1.5-2-fold. Real-time RT-PCR confirmed the differential expression for seven selected target genes. The identified genes encode proteins involved in cell signalling (n = 79), intermediary metabolism (n = 58), transport (n = 47), transcription control (n = 32), disease mutation (n = 24), phosphorylation (n = 19), embryonal development (n = 13) and binding (n = 9). In conclusion, these findings indicate a prominent role of CoQ10 as a potent gene regulator. The presently identified comprehensive list of genes regulated by CoQ10 may be used for further studies to identify the molecular mechanism of CoQ10 on gene expression.
... These observations suggest that Atorvastatin, by altering lipoprotein composition, affects stages or factors of the peroxidation cascade that are not modulated by -tocopherol. For instance, copper-induced peroxidation is determined by the content in hydroperoxide, cholesterol [42], PUFA [43,44], the linoleic to oleic ratio [45] and by the antioxidant composition [46,47] . Of particular interest are observations showing a decrease in coenzyme Q10 levels after statins [48] and that increased lipid peroxidation in myocardial ischemia patients treated with pravastatin was reversed by ubiquinone supplementation [49]. ...
Article
To investigate the impact of Vitamin E on lipids and peroxidation during statin treatment. T1DM patients with high cholesterol received Atorvastatin 20mg with either placebo (group AP, n = 11) or d-alpha-tocopherol 750 IU (group AE, n = 11) daily. They were monitored for blood biochemistry, low-density lipoprotein (LDL) subfractions and lipid peroxidation at inclusion and after 3 and 6 months. Serum cholesterol and triglycerides decreased to the same extent (29 and 21% respectively) in both groups. Serum tocopherol decreased by 18% in AP and increased by 50% in AE (P < 0.0001, between-group comparison by repeated measures ANOVA) but relative to lipids it increased by 15% in AP and by 100% in AE. Copper-induced production of thiobarbituric reactive substances in the LDL + VLDL fraction increased by 18% in AP and did not change in AE (P = 0.02). The lagtime for the production of fluorescent products was prolonged by 13 min only in group AE (P = 0.028). Plasma malondialdehyde decreased by 35% in both groups (P = 0.002) but not when adjusted for lipids. In T1DM Vitamin E supplements do not affect the lowering of lipids and plasma malondialdehyde achieved by Atorvastatin. They reverse the increase of in vitro peroxidation caused by Atorvastatin but do not achieve the decreases observed in patients not receiving lipid-lowering drugs. These results indicate that the antioxidant effect of Vitamin E is attenuated when given in conjunction with this statin.
... In one in vitro experiment [46] vitamin E supplementation alone resulted in an LDL which was more prone to oxidation as compared to the combination of CoQ and vitamin E which increased the resistance to oxidation. In 1997, another study documented a doubling of CoQ10 content in LDL particles after supplementing CoQ10 at 100 mg/day [47] which decreases the peroxidation of LDL cholesterol [48]. HMG-Co A reductase has been reported to be a major regulator of biosynthesis of CoQ10, therefore statins which lower cholesterol by inhibiting this coenzyme, also lower the synthesis of CoQ10 [49, 50] . ...
Article
In a randomized, double-blind, controlled trial, the effects of oral treatment with coenzyme Q10 (CoQ10, 120 mg/day), a bioenergetic and antioxidant cytoprotective agent, were compared for 1 year, on the risk factors of atherosclerosis, in 73 (CoQ, group A) and 71 (B vitamin group B) patients after acute myocardial infarction (AMI). After 1 year, total cardiac events (24.6 vs. 45.0%, p < 0.02) including non-fatal infarction (13.7 vs. 25.3%, p < 0.05) and cardiac deaths were significantly lower in the intervention group compared to control group. The extent of cardiac disease, elevation in cardiac enzymes, left ventricular enlargement, previous coronary artery disease and elapsed time from symptom onset to infarction at entry to study showed no significant differences between the two groups. Plasma level of vitamin E (32.4 +/- 4.3 vs. 22.1 +/- 3.6 umol/L) and high density lipoprotein cholesterol (1.26 +/- 0.43 vs. 1.12 +/- 0.32 mmol/L) showed significant (p < 0.05) increase whereas thiobarbituric acid reactive substances, malondialdehyde (1.9 + 0.31 vs. 3.1 + 0.32 pmol/L) and diene conjugates showed significant reduction respectively in the CoQ group compared to control group. Approximately half of the patients in each group (n = 36 vs. 31) were receiving lovastatin (10 mg/day) and both groups had a significant reduction in total and low density lipoprotein cholesterol compared to baseline levels. It is possible that treatment with CoQ10 in patients with recent MI may be beneficial in patients with high risk of atherothrombosis, despite optimal lipid lowering therapy during a follow-up of 1 year. Adverse effect of treatments showed that fatigue (40.8 vs. 6.8%, p < 0.01) was more common in the control group than CoQ group.
... Therefore Q 10 also has a role as a lipid soluble antioxidant. Several studies have described reduced LDL oxidation in vitro and in vivo after Q 10 supplementation (Alleva et al, 1995; Kaikkonen et al, 1997). A sparing effect on vitamin E as well as a direct anti-oxidative effect has been reported (Stocker et al, 1996). ...
Article
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The literature concerning the importance of coenzyme Q10 in health and disease has been reviewed. Usual dietary intake together with normal in vivo synthesis seems to fulfil the demands for Q10 in healthy individuals. The importance of Q10 supplementation for general health has not been investigated in controlled experiments. The literature allows no firm conclusions about the significance of Q10 in physical activity. In different cardiovascular diseases, including cardiomyopathy, relatively low levels of Q10 in myocardial tissue have been reported. Positive clinical and haemodynamic effects of oral Q10 supplementation have been observed in double-blind trials, especially in chronic heart failure. These effects should be further examined. No important adverse effects have been reported from experiments using daily supplements of up to 200 mg Q10 for 6-12 months and 100 mg daily for up to 6 y.
... One possibility proposed by some authors [23] is that the physical chemical organization of the remnants of lipolyzed triglyceride-rich lipoproteins could increase the sensitivity of macrophages to the cytotoxic effects of FFA, and, synergistically, of other lipid components localized at the surface of remnants. The increased FFA concentration in late postprandial E4/3 VLDL particles could influence the susceptibility of these lipoprotein to oxidation [34], even though it has been demonstrated that, unlike LDL, a prior modification (either oxidation or acylation) of the remnants of triglyceride-rich lipoproteins is not a necessary prerequisite for their atherogenicity [35]. While lipid and apolipoprotein composition of E4/3 was quite similar to that of E3/3 VLDL in the fasting state, we found some interesting differences between the two apo E phenotypes as regards the chemical composition of 8 h postprandial VLDL particles. ...
Article
It has been demonstrated that normolipidemic young men with apolipoprotein E4/3 phenotype have a prolonged postprandial clearance of triglyceride-rich lipoproteins following a high-fat diet. In the present study, we isolated fasting and postprandial (3 and 8 h) lipoprotein fraction from normolipidemic young men with E3/3 and E4/3 phenotypes and examined the in vitro cytotoxicity of these lipoproteins towards J774 macrophages. 8 h E4/3 very low density lipoprotein (VLDL) were significantly more cytotoxic than either 8 h E3/3 VLDL or fasting and 3 h E4/3 VLDL (lactate dehydrogenase (LDH) released: 161 +/- 21, 107 +/- 9, 88 +/- 16 and 101 +/- 12 I.U./l, respectively). Fasting E4/3 intermediate density lipoprotein (IDL) were also significantly more cytotoxic than either fasting E3/3 IDL or 3 h and 8 h E4/3 IDL (LDH released: 105 +/- 23, 60 +/- 9, 37 +/- 5 and 53 +/- 16 I.U./l, respectively), whereas either fasting or postprandial low density lipoprotein (LDL) and high density lipoprotein (HDL) samples did not show any difference in cytotoxicity between the two groups studied. 8 h E4/3 VLDL samples incubated with J774 macrophages had a lower esterified cholesterol (40 +/- 3 versus 52 +/- 3 micrograms), and higher triglyceride (783 +/- 133 versus 418 +/- 64 micrograms) and free fatty acid (FFA) (2.0 +/- 0.4 versus 0.9 +/- 0.1 microgram) content than fasting E4/3 VLDL. The increased macrophage cytotoxicity of late postprandial triglyceride-rich lipoproteins seems to be related to the FFA content of E4/3 VLDL.
... Tissues with high-energy requirements, such as the heart, kidney, liver, and skeletal muscle cells, need a larger amount of coenzyme Q10 to synthesize adenosine triphosphate. Coenzyme Q10 is recognized as an intracellular antioxidant that protects membrane phospholipids, mitochondrial membrane protein, and low-density lipoprotein against free radical-induced oxidative damage [3,4]. Coenzyme Q10 can be synthesized in the tissue from farnesyl diphosphate and tyrosine and can be obtained from the diet in an oxidized form of which 75% to 95% is then converted into a reduced form in the body; however, the total absorption of coenzyme Q10 is thought to be less than 10% [5,6]. ...
... Coenzyme Q10 (also called ubiquinone) is a lipid-soluble benzoquinone with 10 isoprenyl units in the side chain and is a key component of the mitochondrial respiratory chain for adenosine triphosphate synthesis [1,2]. Coenzyme Q10 is recognized as an intracellular antioxidant that protects membrane phospholipids, mitochondrial membrane protein, and low-density lipoprotein from free radical-induced oxidative damage [3,4]. Coenzyme Q10 can be synthesized in tissue from farnesyl diphosphate and tyrosine and can be obtained from the consumption of meat, poultry, fish, vegetables and fruits; however, total absorption of coenzyme Q10 from food is thought to be lower than 10% [5,6]. ...
Article
The purpose of this study was to investigate the effect of coenzyme Q10 supplementation on oxidative stress and antioxidant enzyme activity in patients with coronary artery disease (CAD). This was an intervention study. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery or receiving percutaneous transluminal coronary angioplasty (n = 51) were randomly assigned to the placebo group (n = 14) or one of the two coenzyme Q10-supplemented groups (60 mg/d, n = 19 [Q10-60 group]; 150 mg/d, n = 18 [Q10-150 group]). Intervention was administered for 12 wk. Patients' blood samples were analyzed every 4 wk for plasma coenzyme Q10 concentrations, malondialdehyde (MDA), and antioxidant enzyme (catalase [CAT], superoxide dismutase [SOD], glutathione peroxidase) activity. Forty-three subjects with CAD completed intervention study. Plasma coenzyme Q10 concentration increased significantly after coenzyme the Q10-150 intervention (P < 0.01). The MDA levels were significantly lower than baseline in the Q10-150 group at week 4 (P = 0.03). The Q10-150 group had significantly lower MDA levels than the placebo group at week 8 (P = 0.03). With respect to antioxidant enzyme activity, subjects in the Q10-150 group had significantly higher CAT (P = 0.03) and SOD (P = 0.03) activity than the placebo group at week 12. The plasma coenzyme Q10 concentration was significantly correlated with MDA levels (r = -0.35, P = 0.02) and CAT (r = 0.43, P = 0.01) and SOD activity (r = 0.39, P = 0.01). The ratio of plasma coenzyme Q10 to total cholesterol was significantly correlated with SOD activity (r = 0.39, P = 0.02). The ratio of plasma coenzyme Q10 to low-density lipoprotein was significantly correlated with CAT (r = 0.35, P = 0.04) and SOD (r = 0.45, P = 0.01) activity. However, there was no relation between coenzyme Q10 concentration and glutathione peroxidase activity. Coenzyme Q10 supplements at a dose of 150 mg can decrease oxidative stress and increase antioxidant enzyme activity in patients with CAD. A higher dose of coenzyme Q10 supplements (>150 mg/d) might promote rapid and sustainable antioxidation in patients with CAD.
... The ubiquinone formed in this process is reduced back to ubiquinol in the electron transport chain by metabolic supply of NADH or NADPH [371,372]. Ubiquinol has also been reported to protect LDL from oxidation [373]. Myocardial tissues of CVD patients are reported to be deficient in CoQ10374375376. ...
Article
The pathology of cardiovascular disease (CVD) is complex; multiple biological pathways have been implicated, including, but not limited to, inflammation and oxidative stress. Biomarkers of inflammation and oxidative stress may serve to help identify patients at risk for CVD, to monitor the efficacy of treatments, and to develop new pharmacological tools. However, due to the complexities of CVD pathogenesis there is no single biomarker available to estimate absolute risk of future cardiovascular events. Furthermore, not all biomarkers are equal; the functions of many biomarkers overlap, some offer better prognostic information than others, and some are better suited to identify/predict the pathogenesis of particular cardiovascular events. The identification of the most appropriate set of biomarkers can provide a detailed picture of the specific nature of the cardiovascular event. The following review provides an overview of existing and emerging inflammatory biomarkers, pro-inflammatory cytokines, anti-inflammatory cytokines, chemokines, oxidative stress biomarkers, and antioxidant biomarkers. The functions of each biomarker are discussed, and prognostic data are provided where available.
... Ubiquinone or coenzyme Q (CoQ) is a lipid-soluble molecule of the electron transport chain located in the mitochondrial inner membrane of human cells as well as the cytoplasmic membrane of bacteria. This coenzyme is essential in energy generation and some other processes including formation of disulfide bonds in proteins, regulation of gene expression and detoxification of reactive oxygen species (ROS) (Groneberg et al., 2005; Søballe and Poole, 2000; Alleva et al., 1995; Ernster et al., 1995; Kontush et al., 1995). CoQ is generally composed of a benzene ring and an isoprenoid side chain comprised of isoprene units (isopentenyl diphosphate, IPP) (Fig. 1). ...
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CoQ 10 and lycopene are isoprenoid compounds with nutraceutical and pharmaceutical benefits. In this study, the effect of concomitant lycopene biosynthesis on CoQ 10 accumulation in transformed Escherichia coli DH5α was studied. A lycopene production pathway including geranylgeranyl diphosphate synthase (crtE), phytoene synthase (crtB), and phytoene desaturase (crtI) from Erwinia herbicola was constructed in two CoQ 10-producing E. coli strains. E. coli Ba and E. coli Br containing dds orthologs encoding for decaprenyl diphosphate synthase (Dds), respectively from Agrobacterium tumefaciens and Rhodobacter sphaeroides were transformed by the lycopene pathway resulting in E. coli Ba-lyc and E. coli Br-lyc. The lycopene pathway in E. coli Br-lyc interestingly resulted in a significant increase in CoQ 10 production from 564 ± 28 to 989 ± 22 μg /g DCW. To confirm that the improvement of CoQ 10 production in E. coli Br-lyc was due to lycopene biosynthesis and not just geranylger-anyl diphosphate formation in the lycopene pathway, crtE was only introduced into E. coli Ba and E. coli Br strains. Surprisingly, crtE expression had adverse effects on CoQ 10 production in both strains. The results shed light on the Dds-catalyzed reaction as a bottleneck controlled by precursors; and the efficiency of a parallel lycopene pathway to streamline the flow of metabolites.
... Coenzyme Q10 (also called ubiquinone) is a lipid-soluble benzoquinone with 10 isoprenyl units in the side chain and is a key component of the mitochondrial respiratory chain for adenosine triphosphate (ATP) synthesis [1, 2] . Coenzyme Q10 is an intracellular antioxidant that protects the membrane phospholipids, mitochondrial membrane protein, and low-density lipoprotein-cholesterol (LDL-C) from free radical-induced oxidative damage [3, 4]. Many studies567 have indicated a relationship between low plasma coenzyme Q10 concentration and coronary artery disease (CAD), which may contribute to the higher susceptibility of some individuals to CAD, especially in Asian Indian and Chinese pop- ulation [8]. ...
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A higher oxidative stress may contribute to the pathogenesis of coronary artery disease (CAD). The purpose of this study was to investigate the relationship between coenzyme Q10 concentration and lipid peroxidation, antioxidant enzymes activities and the risk of CAD. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery were assigned to the case group (n = 51). The control group (n = 102) comprised healthy individuals with normal blood biochemical values. The plasma coenzyme Q10, malondialdehyde (MDA) and antioxidant enzymes activities (catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx)) were measured. Subjects with CAD had significant lower plasma coenzyme Q10, CAT and GPx activities and higher MDA and SOD levels compared to those of the control group. The plasma coenzyme Q10 was positively correlated with CAT and GPx activities and negatively correlated with MDA and SOD. However, the correlations were not significant after adjusting for the potential confounders of CAD with the exception of SOD. A higher level of plasma coenzyme Q10 (≥ 0.52 μmol/L) was significantly associated with reducing the risk of CAD. Our results support the potential cardioprotective impact of coenzyme Q10.
... Higher levels of oxidative stress and inflammation play a role in the development of CAD [10,11]. Coenzyme Q10 is an intracellular antioxidant that protects the membrane phospholipids, mitochondrial membrane protein, and LDL- C from free radical-induced oxidative damage [12,13] . Recently , we have demonstrated that coenzyme Q10 had a cardio-protective impact on CAD. ...
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High oxidative stress and chronic inflammation can contribute to the pathogenesis of coronary artery disease (CAD). Coenzyme Q10 is an endogenous lipid-soluble antioxidant. Statins therapy can reduce the biosynthesis of coenzyme Q10. The purpose of this study was to investigate the effects of a coenzyme Q10 supplement (300 mg/d; 150 mg/b.i.d) on antioxidation and anti-inflammation in patients who have CAD during statins therapy. Patients who were identified by cardiac catheterization as having at least 50% stenosis of one major coronary artery and who were treated with statins for at least one month were enrolled in this study. The subjects (n = 51) were randomly assigned to the placebo (n = 24) and coenzyme Q10 groups (Q10-300 group, n = 27). The intervention was administered for 12 weeks. The concentrations of coenzyme Q10, vitamin E, antioxidant enzymes activities (superoxide dismutase, catalase, and glutathione peroxidase), and inflammatory markers [C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-alpha), and interleukin-6 (IL-6)] were measured in the 42 subjects (placebo, n = 19; Q10-300, n = 23) who completed the study. The levels of the plasma coenzyme Q10 (P < 0.001) and antioxidant enzymes activities (P < 0.05) were significantly higher after coenzyme Q10 supplementation. The levels of inflammatory markers (TNF-alpha, P = 0.039) were significantly lower after coenzyme Q10 supplementation. The subjects in the Q10-300 group had significantly higher vitamin E (P = 0.043) and the antioxidant enzymes activities (P < 0.05) than the placebo group at week 12. The level of plasma coenzyme Q10 was significantly positively correlated with vitamin E (P = 0.008) and antioxidant enzymes activities (P < 0.05) and was negatively correlated with TNF-alpha (P = 0.034) and IL-6 (P = 0.027) after coenzyme Q10 supplementation. Coenzyme Q10 supplementation at 300 mg/d significantly enhances antioxidant enzymes activities and lowers inflammation in patients who have CAD during statins therapy.Trial registration: Clinical Trials.gov Identifier: NCT01424761.
... Coenzyme Q10 is a key component of the mitochondrial respiratory chain and is required for adenosine triphosphate (ATP) synthesis [16, 17]. Coenzyme Q10 is an intracellular antioxidant that protects low-density lipoprotein cholesterol (LDL-C) from free radical-induced oxidative damage [18, 19] . It has demonstrated potential cardioprotective properties and reduces the risk of coronary artery disease [20]; however, few studies have examined the concentration of coenzyme Q10 in patients with MS. ...
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The purpose of this study was to investigate the levels of coenzyme Q10 and vitamin E and the antioxidant status in subjects with metabolic syndrome (MS). Subjects with MS (n = 72) were included according to the criteria for MS. The non-MS group (n = 105) was comprised of healthy individuals with normal blood biochemical values. The plasma coenzyme Q10, vitamin E concentrations, lipid profiles, and antioxidant enzymes levels (catalase, superoxide dismutase, and glutathione peroxidase) were measured. The subjects with MS had significantly higher concentrations of plasma coenzyme Q10 and vitamin E than those in the non-MS group, but these differences were not significant after being normalized for triglyceride level. The levels of antioxidant enzymes were significantly lower in the MS group than in the non-MS group. The subjects with the higher antioxidant enzymes activities had significant reductions in the risk of MS (P < 0.01) after being adjusted for coenzyme Q10 and vitamin E. In conclusion, the subjects with MS might be under higher oxidative stress resulting in low levels of antioxidant enzyme activities. A higher level of antioxidant enzymes activities was significantly associated with a reduction in the risk of MS independent of the levels of coenzyme Q10 and vitamin E.
... An increase in energy expenditure caused by exercise training and possible metabolic alterations might be the major cause behind the improvements in the triglycerides profiles and a better aerobic capacity with enhanced utilization of lipids. Additionally, Alleva et al. (1995) reported that coenzyme Q10 is an intracellular antioxidant that protects the membrane phospholipids and mitochondrial membrane protein. Moreover, Q10 supplementation significantly affected the protein levels of NFκB, IκB, Nrf2 and HO-1 in exercise group when compared with the sedentary-untreated groups. ...
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This study reports the effects of Q10, coenzyme Q10 or ubiquinone, a component of the electron transport chain in mitochondria, on nuclear factor kappa-light-chain-enhancer of activated B cells (NFκB), inhibitors of kappa B (IκB), nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and hemeoxygenase 1 (HO-1) in rats after chronic exercise training for 6 weeks. 8-week old male Wistar rats were assigned randomly to one of four treatments planned in a 2 x 2 factorial arrangement of two condition (sedentary vs. exercise training), and two coenzyme Q10 levels (0 and 300 mg/kg per day for 6 weeks). The expression levels of the target proteins were determined in the heart, liver and muscle, and biochemical parameters including creatinine, urea, glucose and lipid profile were investigated in plasma. When compared with sedentary group, significant decreases in heart, liver and muscle NFκB levels by 45%, 26% and 44% were observed in Q10 supplemented rats after exercise training, respectively, while the inhibitory protein IκB increased by 179%, 111% and 127% in heart, liver and muscle tissues. Q10 supplementation caused an increase in Nrf2 (167%, 165% and 90%) and HO-1 (107%, 156% and 114%) after exercise training in heart, liver and muscle tissues (p < 0.05). No significant change was observed in any of the parameters associated with protein, carbohydrate and lipid metabolism, except that exercise caused a decrease in plasma triglyceride, which was further decreased by Q10. In conclusion, these results suggest that Q10 modulates the expression of NFκB, IκB, Nrf2 and HO-1 in exercise training, indicating an anti-inflammatory effect of Q10 and emphasizes its role in antioxidant defense.
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Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Oxida-tive stress appears to play a pivotal role in atherosclerosis. Coenzyme Q10 (CoQ10), one of the most important antioxidants, is synthesized de novo by every cell in the body. Its biosynthesis decreases with age and its deficit in tissues is associated with degenerative changes of aging, thus implicating a possible therapeutic role of CoQ10 in human diseases. There is evidence to support the therapeutic value of CoQ10 as an adjunct to standard medical therapy in congestive heart failure. However, much further research is required, especially in the use of state-of-the-art techniques to assess functional outcomes in patients with congestive heart failure.
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Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Oxidative stress appears to play a pivotal role in atherosclerosis. Coenzyme Q10 (CoQ10), one of the most important antioxidants, is synthesized de novo by every cell in the body. Its biosynthesis decreases with age and its deficit in tissues is associated with degenerative changes of aging, thus implicating a possible therapeutic role of CoQl0 in human diseases. There is evidence to support the therapeutic value of CoQ10 as an adjunct to standard medical therapy in congestive heart failure. However, much further research is required, especially in the use of state-of-the-art techniques to assess functional outcomes in patients with congestive heart failure.
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INTRODUÇÃO: os músculoesqueléticos são tecidos dinâmicos que podem alterar suas características fenotípicas proporcionando melhor adaptação funcional com estímulos variados. A L-tiroxina é um hormônio produzido pela glândula tireoide e tem sido utilizada como modelo experimental para estimulação de estresse oxidativo no músculo esquelético. A coenzima Q10 é uma provitamina lipossolúvel sintetizada endogenamente e naturalmente encontrada em alimentos como carne vermelha, peixes, cereais, brócolis e espinafre. Apresenta propriedade antioxidante e tem potencial no tratamento de doenças degenerativas e neuromusculares. OBJETIVO: avaliar o efeito protetor da coenzima Q10 no músculo sóleo de ratos frente aos danos oxidativos provocados pela L-tiroxina. MÉTODOS: os ratos foram distribuídos em quatro grupos de seis animais cada: Grupo 1 controle; Grupo 2 coenzima Q10; Grupo 3 L-tiroxina e Grupo 4 coenzima Q10 e L-tiroxina. Após a eutanásia, o sangue dos animais foi colhido e foi analisada a atividade sérica das enzimas creatina quinase CK e aspartato aminotransferase AST. No homogenato do músculo sóleo foram avaliados fatores relacionados ao estresse oxidativo. RESULTADOS: a coenzima Q10 protegeu o músculo sóleo dos danos provocados pela L-tiroxina e favoreceu a manutenção da atividade das enzimas antioxidantes glutationa redutase e glutationa peroxidase, da concentração de glutationa reduzida e oxidada, além de evitar a lipoperoxidação. CONCLUSÃO: os resultados indicam que a coenzima Q10 protege o músculo sóleo de ratos dos danos oxidativos provocados pela L-tiroxina.
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Although the functional ingredient has been evaluated by the Korea Food and Drug Administration (KFDA) based on scientific evidence, the levels of scientific evidence and consistency of the results might vary according to emerging data. Therefore, periodic re-evaluation may be needed for some functional ingredients. In this study, we re-evaluated scientific evidence for the antioxidant activity of coenzyme Q10 as a functional ingredient in health functional food. Literature searches were conducted using the Medline and Cochrane, KISS, and IBIDS databases for the years 1955-2010 with the search term of coenzyme Q10 in combination with antioxidant. The search was limited to human studies published in Korean, English, and Japanese. Using the KFDA's evidence based evaluation system for scientific evaluation of health claims, 33 human studies were identified and reviewed in order to evaluate the strength of the evidence supporting a relation between coenzyme Q10 and antioxidant activity. Among 33 studies, significant effects for antioxidant activities were reported in 22 studies and their daily intake amount was 60 to 300 mg. Based on this systematic review, we concluded that there was possible evidence to support a relation between coenzyme Q10 intake and antioxidant activities. However, because inconsistent results have recently been reported, future studies should be monitored.
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Ubiquinone is an essential component of the electron transfer system in both prokaryotes and eukaryotes and is synthesized from chorismate and polyprenyl diphosphate by eight steps.p-Hydroxybenzoate (PHB) polyprenyl diphosphate transferase catalyzes the condensation of PHB and polyprenyl diphosphate in ubiquinone biosynthesis. We isolated the gene (designated ppt1) encoding PHB polyprenyl diphosphate transferase from Schizosaccharomyces pombe and constructed a strain with a disrupted ppt1 gene. This strain could not grow on minimal medium supplemented with glucose. Expression ofCOQ2 from Saccharomyces cerevisiae in the defective S. pombe strain restored growth and enabled the cells to produce ubiquinone-10, indicating that COQ2 andppt1 are functional homologs. Theppt1-deficient strain required supplementation with antioxidants, such as cysteine, glutathione, and α-tocopherol, to grow on minimal medium. This suggests that ubiquinone can act as an antioxidant, a premise supported by our observation that theppt1-deficient strain is sensitive to H2O2 and Cu2+. Interestingly, we also found that the ppt1-deficient strain produced a significant amount of H2S, which suggests that oxidation of sulfide by ubiquinone may be an important pathway for sulfur metabolism in S. pombe. Ppt1-green fluorescent protein fusion proteins localized to the mitochondria, indicating that ubiquinone biosynthesis occurs in the mitochondria in S. pombe. Thus, analysis of the phenotypes of S. pombe strains deficient in ubiquinone production clearly demonstrates that ubiquinone has multiple functions in the cell apart from being an integral component of the electron transfer system.
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Treatment of coenzyme Q with ozone yielded a degradation product having unmodified ring that retained its spectral characteristics and a truncated side-chain that made it water-soluble. This derivative, but not the intact lipid-quinone, showed relaxation of phenylephrine-contracted rat arterial rings. This effect offers an explanation for the known hypotensive action of exogenous coenzyme Q regardless of its side-chain length.
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Coenzyme Q10 (CoQ10) is an important mitochondrial electron transfer component and has been postulated to function as a powerful antioxidant protecting LDL from oxidative damage. It could thus reduce the risk of cardiovascular disease. Thus far, beneficial effects of supplementation with CoQ10 have been reported. To study the relation between unsupplemented concentrations of plasma CoQ10 and coronary atherosclerosis, we performed a case-control study among 71 male cases with angiographically documented severe coronary atherosclerosis and 69 healthy male controls free from symptomatic cardiovascular disease and without atherosclerotic plaques in the carotid artery. Plasma CoQ10 concentrations (mean +/- SE) were 0.86+/-0.04 vs. 0.83+/-0.04 micromol/l for cases and controls, respectively. The CoQ10/LDL-cholesterol ratio (micromol/ mmol) was slightly lower in cases than in controls (0.22+/-0.01 vs. 0.26+/-0.03). Differences in CoQ10 concentrations and CoQ10/LDL-cholesterol ratio did not reach significance. The odds ratios (95% confidence interval) for the risk of coronary atherosclerosis calculated per micromol/l increase of CoQ10 was 1.12 (0.28-4.43) after adjustment for age, smoking habits, total cholesterol and diastolic blood pressure. We conclude that an unsupplemented plasma CoQ10 concentration is not related to risk of coronary atherosclerosis.
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Treatment of coenzyme Q with ozone, permanganate, and ferrous sulfate in presence of ascorbate or hydrogen peroxide yielded water-soluble degradation products, possibly having truncated side-chain and modified ring.These derivatives, but not the intact lipid-quinone, showed relaxation of phenylephrine-contracted rat arterial rings. Representative samples of these also decreased blood pressure when injected into the femoral vein in the rat.These effects offer an explanation for the hypotensive action of exogenous coenzyme Q regardless of its side-chain length.
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To determine the concentration of coenzyme Q10 (CoQ10) in the human retina. Eye tissues were lyophilized and exhaustively extracted with heptane. The extracts were analyzed for CoQ10 by high-performance liquid chromatography (HPLC). The average concentration of CoQ10 in the retina was 42+/-11 nanomoles/g dry retina for donors younger than 30 years of age and 24+/-13 nanomoles/g dry retina for donors older than 80 years of age. The average concentrations of CoQ10 in the choroid was 27+/-16 nanomoles/g dry choroid for donors younger than 30 age and 18+/-11 nanomoles/g dry choroid for donors older than 80. CoQ10 levels in the retina can decline by approximately 40% with age. This decline may have two consequences: a decrease in antioxidant ability and a decrease in the rate of ATP synthesis in the retina and, as such, this decline may be linked to the progression of macular degeneration.
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Schistosoma mansoni (S. mansoni) eggs trapped in the host liver elicit a chain of oxidative processes that may be, at least in part, responsible for the pathology and progression of fibrosis associated with schistosomal hepatitis. This study was designed to assess the protective effect of the antioxidant coenzyme-Q10 (Co-Q10) against experimental S. mansoni-induced oxidative stress in the liver, and its potential role as an adjuvant to praziquantel (PZQ) therapy. The oxidative stress and overall liver function were improved under Co-Q10 therapy as evidenced by significant reduction in oxidative stress markers and preservation of antioxidant factors. Liver fibrosis was also reduced with a positive impact on liver function. Moreover, addition of Co-Q10 to PZQ therapy caused: significant reduction of liver egg load, significant improvement of the redox status, and lastly decreased liver fibrosis.
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Coenzyme Q 10 (CoQ 10 ) is an isoprenoid component used widely in nutraceutical industries. Farnesyl diphosphate synthase (FPPS) is a responsible enzyme for biosynthesis of farnesyl diphosphate (FPP), a key precursor for CoQs production. This research involved investigating the effect of FPPS over-expression on CoQs production in engineered CoQ 10 -producing Escherichia coli (E. coli). Two CoQ 10 -producing strains, as referred to E. coli Ba and E. coli Br, were transformed by the encoding gene for FPPS (ispA) under the control of either the trc or P BAD promoters. Over-expression of ispA under the control of P BAD promoter led to a relative increase in CoQ 10 production only in recombinant E. coli Br although induction by arabinose resulted in partial reduction of CoQ 10 production in both recombinant E. coli Ba and E. coli Br strains. Over-expression of ispA under the control of stronger trc promoter, however, led to a severe decrease in CoQ 10 production in both recombinant E. coli Ba and E. coli Br strains, as reflected by reductions from 629±40 to 30±13 and 564±28 to 80±14 μg/g Dried Cell Weight (DCW), respectively. The results showed high level of FPP reduces endogenous CoQ 8 production as well and that CoQs are produced in a complimentary manner, as the increase in production of one decreases the production of the other. The reduction in CoQ 10 production can be a result of Dds inhibition by high FPP concentration. Therefore, more effort is needed to verify the role of intermediate metabolite concentration and to optimize production of CoQ 10 .
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Paraquat is highly toxic compound for humans and animals. It has been used widely in agriculture as herbicide. The present study was designed to investigate the potential protective effect of Coenzyme Q10 against the hepatotoxicity of paraquat in male rats. The experiment was carried out using 24 male albino rats. Four groups of animals were used in this study: control, Coenzyme Q10 (10 mg/kg), paraquat-treated (9 mg/kg b.w), paraquat along with Coenzyme Q10 for 4 weeks. Light microscopic observations revealed that the hepatic tissue of control and Coenzyme Q10 groups showed normal hepatocytes structure. Histopathological observations of paraquat treated group showed severe damage in liver tissue such as hepatocytes degeneration and necrosis, congestion of blood vessels and hemorrhage. Biochemical studies indicated that serum Alanine aminotransferase (ALT), Aspartate aminotransferase (AST) and Alkaline Phosphatase (ALP) levels were elevated in paraquat treated group. Administration of paraquat significantly increased hepatic malondialdehyde (MDA) levels. Superoxide dismutase (SOD) activity and Glutathione (GSH) content in the liver of the paraquat administered rats were significantly decreased as compared with control group. Paraquat treated rats showed negative immunoreactivity to Alfa Fetoprotein (AFP) in the cytoplasm of the liver cells. Coenzyme Q10 administration attenuated the damages induced by paraquat in the liver of rats. The results of the present study indicated that Coenzyme Q10 has protective effect against liver damage induced by paraquat.
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