Coenzyme Q10 (CoQ10)
Effect of precursors and modulators of coenzyme Q biosynthesis on the heart mitochondria function in aged rats
Kumchenko EB, Petukhov DN, Donchenko GV, Mkhitarian LS, Timoshchuk SV,
Strutinskaia NA, Vavilova GL, Sagach VF.
Biomed Khim. 2010 Mar-Apr;56(2):244-56.
Our research demonstrate that ageing leads to changes in activity of electron-transporting enzyme complexes in myocardial mitochondria of old rats and to increased sensitivity of mitochondrial permeability transition pore to inductors of its opening–Ca2+ and phenylarsine oxide. We also observed activation of lipid and protein free-radical peroxidation processes. Administration of a complex of biologically active substances that included precursors and modulators of coenzyme Q biosynthesis (alpha-tocopherol acetate, 4-hydroxybenzoic acid, and methionine) we observed the increase in coenzyme Q content, correction of functional activity of mitochondrial electron-transport chain enzyme complexes, the decrease in intensivity of lipid and protein free-radical peroxidation in the heart and the decrease in sensitivity of mitochondrial permeability transition pore to inductors of its opening. This complex may be used to treat mitochondrial dysfunction under numerous pathologies of cardiovascular system, as well as in ageing. PMID: 21341512
Exogenous CoQ10 supplementation prevents plasma ubiquinone reduction induced by HMG-CoA reductase inhibitors
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A. M. Bargossi, G. Grossi, P. L. Fiorella, A. Gaddi, R. Di Giulio and M. Battino
Mol Aspects Med. 1994;15 Suppl:s187-93
The biosynthetic pathway of the CoQ polyisoprenoid side chain, starting from acetyl-CoA and proceeding through mevalonate and isopentenylpyrophosphate, is the same as that of cholesterol. We performed this study to evaluate whether vastatins (hypocholesterolemic drugs that inhibit HMG-CoA reductase) modify blood levels of ubiquinone. Thirty-four unrelated outpatients with hypercholesterolemia (IIa phenotype) were treated with 20 mg of simvastatin for a 6-month period (group S) or with 20 mg of simvastatin plus 100 mg CoQ10 (group US). The following parameters were evaluated at time 0, 45, 90, 135 and 180 days: total plasma cholesterol (TC), HDL-cholesterol, LDL-cholesterol (LDL-C), triglycerides (TG), apo A1, apo B and CoQ10 in plasma and platelets. In the S group, there was a marked decrease in TC and LDL-C (from 290.3 mg/dl to 228.7 mg/dl for TC and from 228.7 mg/dl to 167.6 mg/dl for LDL-C) and in plasma CoQ10 levels from 1.08 mg/dl to 0.80 mg/dl. In contrast, in the US group we observed a significant increase of CoQ10 in plasma (from 1.20 to 1.48 mg/dl) while the hypocholesterolemic effect was similar to that observed in the S group. Platelet CoQ10 also decreased in the S group (from 104 to 90 ng/mg) and increased in the US group (from 95 to 145 ng/mg). This study demonstrates that simvastatin lowers both LDL-C and apo B plasma levels together with the plasma and platelet levels of CoQ10, and that CoQ10 therapy prevents both plasma and platelet CoQ10 decrease, without affecting the cholesterol lowering effect of simvastatin. PMID: 7752830
Oxidative stress and antioxidant defense in plasma after repeated bouts of supramaximal exercise: the effect of coenzyme Q10.
Gül I, Gökbel H, Belv Iranli M, Okudan N, Büyükbas S, Bas Arali K.
J Sports Med Phys Fitness. 2011 Jun;51(2):305-12
The purpose was to determine the changes of oxidative stress and antioxidant markers in plasma after repeated bouts of supramaximal exercise and the effects of coenzyme Q10 supplementation on these changes.This randomized, double blind, crossover study was composed of two 8-week periods of supplementation with either 100 mg.day-1 CoQ10 or placebo. Fifteen healthy and sedentary men participated in the study. Five Wingate tests with 2 min rest between tests were performed. Blood samples were collected at rest, immediately after, 15 and 60 min after the fifth Wingate test for oxidative stress (malondialdehyde, nitric oxide, xanthine oxidase and adenosine deaminase) and antioxidant (superoxide dismutase, glutathione peroxidase and uric acid) markers. At baseline exercise session, malondialdehyde increased 15 and 60 min after the exercise compared to the rest and immediately after the exercise. Malondialdehyde at rest, immediately after and 60 min after the exercise decreased with coenzyme Q10 supplementation when compared to baseline. At baseline exercise session, uric acid increased 15 and 60 min after the exercise when compared to the rest. In conclusion, lipid peroxidation and antioxidant defense increase after repeated short-term supramaximal exercise. Coenzyme Q10 supplementation partially prevents the increase in lipid peroxidation after repeated short-term supramaximal exercise. PMID: 21681167
A randomized trial of coenzyme Q10 in mitochondrial disorders.
Glover EI, Martin J, Maher A, Thornhill RE, Moran GR, Tarnopolsky MA.
Muscle Nerve. 2010 Nov;42(5):739-48.
Case reports and open-label studies suggest that coenzyme Q(10) (CoQ(10)) treatment may have beneficial effects in mitochondrial disease patients; however, controlled trials are warranted to clinically prove its effectiveness. Thirty patients with mitochondrial cytopathy received 1200 mg/day CoQ(10) for 60 days in a randomized, double-blind, cross-over trial. Blood lactate, urinary markers of oxidative stress, body composition, activities of daily living, quality of life, forearm handgrip strength and oxygen desaturation, cycle exercise cardiorespiratory variables, and brain metabolites were measured. CoQ(10) treatment attenuated the rise in lactate after cycle ergometry, increased (∽1.93 ml) VO(2)/kg lean mass after 5 minutes of cycling (P < 0.005), and decreased gray matter choline-containing compounds (P < 0.05). Sixty days of moderate- to high-dose CoQ(10) treatment had minor effects on cycle exercise aerobic capacity and post-exercise lactate but did not affect other clinically relevant variables such as strength or resting lactate. PMID: 20886510
Antifatigue effect of coenzyme Q10 in mice.
Fu X, Ji R, Dam J.
J Med Food. 2010 Feb;13(1):211-5.
The aim of this study was to investigate whether coenzyme Q10 (CoQ10) has an antifatigue effect in mice. ICR male mice were orally given CoQ10 in the form of Bio-Quinone (Pharma Nord, Vejle, Denmark) at doses of 0, 1.5, 15, or 45 mg/kg/day for 4 weeks. Mice were made to perform swimming exercise with loads attached to their tails, corresponding to approximately 5% of their body weights, and the total swimming time until exhaustion was measured. Furthermore, the post-exercise concentration of serum urea nitrogen (SUN), pre-/post-exercise and post-rest concentration of lactic acid (LA), and pre-exercise hepatic glycogen were determined. Mice treated with CoQ10 showed a significantly prolonged exhaustive swim time (15 mg/kg/day; P < .05), increased liver glycogen contents (15 and 45 mg/kg/day; P < .01 and P < .05, respectively), and decreased SUN levels (1.5, 15, and 45 mg/kg/day; P < .01) compared to control animals. The LA level was not significantly changed. These results suggest that CoQ10 improves swimming endurance and has an antifatigue effect. PMID: 20136457
Clinical aspects of coenzyme Q10: an update.
Littarru GP, Tiano L.
Nutrition. 2010 Mar;26(3):250-4.
The fundamental role of coenzyme Q(10) (CoQ(10)) in mitochondrial bioenergetics and its well-acknowledged antioxidant properties constitute the basis for its clinical applications, although some of its effects may be related to a gene induction mechanism. Cardiovascular disease is still the main field of study and the latest findings confirm a role of CoQ(10) in improving endothelial function. The possible relation between CoQ(10) deficiency and statin side effects is highly debated, particularly the key issue of whether CoQ(10) supplementation counteracts statin myalgias. Furthermore, in cardiac patients, plasma CoQ(10) was found to be an independent predictor of mortality. Studies on CoQ(10) and physical exercise have confirmed its effect in improving subjective fatigue sensation and physical performance and in opposing exercise-related damage. In the field of mitochondrial myopathies, primary CoQ(10) deficiencies have been identified, involving different genes of the CoQ(10) biosynthetic pathway; some of these conditions were found to be highly responsive to CoQ(10) administration. The initial observations of CoQ(10) effects in Parkinson’s and Huntington’s diseases have been extended to Friedreich’s ataxia, where CoQ(10) and other quinones have been tested. CoQ(10) is presently being used in a large phase III trial in Parkinson’s disease. CoQ(10) has been found to improve sperm count and motility on asthenozoospermia. Moreover, for the first time CoQ(10) was found to decrease the incidence of preeclampsia in pregnancy. The ability of CoQ(10) to mitigate headache symptoms in adults was also verified in pediatric and adolescent populations. PMID: 19932599
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Role of coenzyme Q10 (CoQ10) in cardiac disease, hypertension and Meniere-like syndrome.
Kumar A, Kaur H, Devi P, Mohan V.
Pharmacol Ther. 2009 Dec;124(3):259-68
Coenzyme Q10 (ubiquinone) is a mitochondrial coenzyme which is essential for the production of ATP. Being at the core of cellular energy processes it assumes importance in cells with high energy requirements like the cardiac cells which are extremely sensitive to CoQ10 deficiency produced by cardiac diseases. CoQ10 has thus a potential role for prevention and treatment of heart ailments by improving cellular bioenergetics. In addition it has an antioxidant, a free radical scavenging and a vasodilator effect which may be helpful in these conditions. It inhibits LDL oxidation and thus the progression of atherosclerosis. It decreases proinflammatory cytokines and decreases blood viscosity which is helpful in patients of heart failure and coronary artery disease. It also improves ischemia and reperfusion injury of coronary revascularisation. Significant improvement has been observed in clinical and hemodynamic parameters and in exercise tolerance in patients given adjunctive CoQ10 in doses from 60 to 200 mg daily in the various trials conducted in patients of heart failure, hypertension, ischemic heart disease and other cardiac illnesses. Recently it has been found to be an independent predictor of mortality in congestive heart failure. It has also been found to be helpful in vertigo and Meniere-like syndrome by improving the immune system. Further research is going on to establish firmly its role in the therapy of cardiovascular diseases. PMID: 19638284
Influence of CoQ10 on autonomic nervous activity and energy metabolism during exercise in healthy subjects.
Zheng A, Moritani T.
J Nutr Sci Vitaminol (Tokyo). 2008 Aug;54(4):286-90.
CoQ10 has come to be widely used as a dietary supplement, and daily intake of it has increased in recent years. CoQ10 is produced in all living organisms and is an essential coenzyme for energy synthesis in the mitochondria and an important scavenger of reactive oxygen species. This is a randomized, double-blind, placebo-controlled experiment to examine the acute effects of a single dose of CoQ10 on the autonomic nervous system (ANS) by using power spectral analysis of HRV and energy metabolism at rest and during low intensity exercise in healthy subjects. Eleven nonsmoking healthy male students (age: 26+/-1 y) volunteered to participate in this experiment. CM5 lead ECG and gas exchange parameters were recorded 5 min before, and 30 min and 60 min after the oral administration of CoQ10 or a placebo. Following this, the subjects exercised using a stationary cycle ergometer for 10 min at 60 rpm with an intensity of 30% of heart rate reserve. During the exercise, the ECG and gas exchange parameters were recorded continuously. There were no significant differences in heart rate between the CoQ10 and placebo trials at rest or during exercise. With regard to the integrated values of the spectrum, there were no significant differences in the HF power representing parasympathetic activity or LF power representing both sympathetic and parasympathetic nervous activities between the trials at any timepoint. However, during the exercise, HF power and LF power in the CoQ10 trial showed a tendency to increase compared with the placebo trial (p<0.1). Total power representing the over-all ANS activity was significantly increased in the CoQ10 trial during exercise, which implied that autonomic nervous activity was augmented by CoQ10 (p<0.05). CoQ10 also induced enhanced lipid oxidation as shown by the significantly lower respiratory gas exchange ratio (R) and increased fat oxidation during exercise. The results shed some light upon the relationship between the autonomic nervous activity and energy metabolism. These results suggested that CoQ10 may increase fat oxidation with augmented autonomic nervous activity during low intensity exercise. PMID: 18797149
Randomised double-blind, placebo-controlled trial of coenzyme Q, therapy in class II and III systolic heart failure.
Keogh A, Fenton S, Leslie C, Aboyoun C, Macdonald P, Zhao YC, Bailey M, Rosenfeldt F.
Heart Lung Circ. 2003;12(3):135-41
Coenzyme Q10 (CoQ10) supplementation has been reported to improve symptoms of heart failure and quality of life, and to reduce hospitalisation. Most prior trials have been open-label and in some, only 50% of patients took angiotensin converting enzyme inhibitors (ACEI). To determine the effects of CoQ10 in patients with a New York Heart Association (NYHA) Class II or III heart failure due to ischaemic or dilated cardiomyopathy who have been treated with ACEI but not beta-blockers. Methods: Thirty-nine patients in NYHA Class II or III heart failure were randomised in ad ouble-blind, placebo-controlled study with 150 mg/day of oral CoQ10 or placebo. Thirty-five patients completed the trial. After 3 months of therapy, the NYHA class in the CoQ10 group (n = 17) showed a significant improvement of 0.5 class compared with the placebo (n = 18) (P = 0.01). Specific Activities Scale class showed a significant (P = 0.004) improvement in the CoQ10 group, but no change in the placebo group. The C-min walk-test distance showed a significant (P = 0.047) increase in the CoQ10 group with no change in the placebo group (between-group difference P = 0.29). For the Naughton exercise test times the difference in increase in exercise time approached significance in favour of the CoQ10 group (P = 0.056). There was a correlation between the increase in exercise time and the increase in serum CoQ10 level (P = 0.024). There was a threefold increase in the CoQ10 level in the treated group (0.7 +/- 0.4 to 2.1+/- 0.3 microg/mL), but no change in the placebo group. This pilot study accords with published data suggesting that CoQ10 therapy improves cardiac functional status in patients with moderately severe dilated cardiomyopathy receiving maximal non beta-blocker therapy. Future multicentre studies with larger numbers are indicated. PMID: 18705154
Antifatigue effects of coenzyme Q10 during physical fatigue.
Mizuno K, Tanaka M, Nozaki S, Mizuma H, Ataka S, Tahara T, Sugino T, Shirai T, Kajimoto Y, Kuratsune H, Kajimoto O, Watanabe Y.
Nutrition. 2008 Apr;24(4):293-9
This study examined the effects of coenzyme Q10 administration on physical fatigue. In a double-blinded, placebo-controlled, three crossover design, 17 healthy volunteers were randomized to oral coenzyme Q10 (100 or 300 mg/d) or placebo administration for 8 d. As a fatigue-inducing physical task, subjects performed workload trials on a bicycle ergometer at fixed workloads twice for 2 h and then rested for 4 h. During the physical tasks, subjects performed non-workload trials with maximum velocity for 10 s at 30 min (30-min trial) after the start of physical tasks and 30 min before the end of the tasks (210-min trial). The change in maximum velocity from the 30- to the 210-min trial in the 300-mg coenzyme Q10-administered group was higher than that in the placebo group. In addition, subjective fatigue sensation measured on a visual analog scale in the 300-mg coenzyme Q10-administered group after the fatigue-inducing physical task and recovery period was alleviated when compared with that in the placebo group. Oral administration of coenzyme Q10 improved subjective fatigue sensation and physical performance during fatigue-inducing workload trials and might prevent unfavorable conditions as a result of physical fatigue. PMID: 18272335
Effect of Coenzyme Q10 supplementation on exercise-induced muscular injury of rats.
Kon M, Kimura F, Akimoto T, Tanabe K, Murase Y, Ikemune S, Kono I.
Exerc Immunol Rev. 2007;13:76-88.
We aimed to examine the effect of Coenzyme Q10 (CoQ10) supplementation on the exhaustive exercise-induced injury and oxidative stress in skeletal muscle and liver. Rats were divided into four groups: rest group [control (Con)-Rest; n = 6)], exercise group (Con-Ex; n = 6), rest group with CoQ10 supplement (CoQ10-Rest; n = 6), and exercise group with CoQ10 supplement (CoQ10-Ex; n = 6). The exercise groups were run on a treadmill until exhaustion. The CoQ10 supplemented groups received an oral administration of CoQ10 (300 mg kg(-1), 4 weeks). After 4 weeks, total CoQ concentration, creatine kinase (CK), glutamic-oxaloacetic transaminase (GOT), malondialdehyde (MDA), scavenging activity against reactive oxygen species [ROS; superoxide anions (O2*-) and hydroxyl radicals (HO*)] were measured. Total CoQ concentration in plasma, slow-twitch muscles (soleus and gastronemius deep portion), and liver were significantly increased by CoQ10 supplementation. Plasma CK was significantly higher in Con-Ex compared with Con-Rest, whereas there was no difference between CoQ10-Rest and CoQ10-Ex. There were no significant differences in muscle MDA in each group. Plasma GOT and liver MDA in exercise groups were significantly higher than that of rest groups, but not significantly different between CoQ10 supplemented groups and control groups. CoQ10 supplementation was not able to favorably influence ROS scavenging activity in skeletal muscle and liver. These data indicated that CoQ10 supplementation increased total CoQ concentration in the slow-twitch muscles, and was useful for reducing exhaustive exercise-induced muscular injury by enhancing stabilization of muscle cell membrane. PMID: 18198662
Effects of coenzyme Q10 supplementation on liver mitochondrial function and aerobic capacity in adolescent athletes.
Liao P, Zhang Y, Liao Y, Zheng NJ, Zhang X.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2007 Nov;23(4):491-4.
To investigate the effects of CoQlo supplementation on liver mitochondrial function and aerobic capacity in adolescent athletes. Based on a single blinded study design, 18 male adolescent swimming athletes were randomized into two groups, supplement CoQ10 100 mg/d (Q group), or placebo (P group) for 28 days respectively. (1) After supplementation, the plasma CoQ10 concentration in Q group was significantly elevated and significantly higher compared to P group. (2) After supplementation, the rest plasma MDA level in Q group remained unchanged and was significantly lower compared to P group. (3) The plasma CoQ10 concentration of the 18 athletes was significantly decreased during the first constant endurance exercise. (4) The baseline plasma CoQ10 of the 18 subjects showed significantly positive correlation with VO2max measured in the first incremental exercise. (5) No significant difference of increased level of AKBR between Q group and P group. (6) No significant difference of increase level of VO2max, individual lactate threshold and exercise economy between Q and P group. Although there is an increased demand for plasma CoQ10 during endurance exercise and CoQ10 supplement can depress lipid peroxidation, there is no effect of CoQ10 supplementation on liver mitochondrial function and aerobic capacity in adolescent athletes. PMID: 21180141