Coenzyme Q -
Festenstein was the first to isolate a small amount of CoQ 10 from the lining of a horse's gut at Liverpool , England. In subsequent studies the compound was briefly called substance SA , it was deemed to be quinone , and it was noted that it could be found from many tissues of a number of animals.
In , Frederick L. Crane and colleagues at the University of Wisconsin—Madison Enzyme Institute isolated the same compound from mitochondrial membranes of beef heart and noted that it transported electrons within mitochondria. They called it Q for short as it was a quinone.
In , its full chemical structure was reported by D. Wolf and colleagues working under Karl Folkers at Merck in Rahway. Green and colleagues belonging to the Wisconsin research group suggested that ubiquinone should be called either mitoquinone or coenzyme Q due to its participation to the mitochondrial electron transport chain.
In , A. Mellors and A. Tappel at the University of California were the first to show that reduced CoQ 6 was an effective antioxidant in cells. In s Peter D. Mitchell enlarged upon the understanding of mitochondrial function via his theory of electrochemical gradient , which involves CoQ 10 , and in late s studies of Lars Ernster enlargened upon the importance of CoQ 10 as an antioxidant.
The s witnessed a steep rise in the number of clinical trials involving CoQ Detailed reviews on occurrence of CoQ 10 and dietary intake were published in Despite the scientific community's great interest in this compound, however, a very limited number of studies have been performed to determine the contents of CoQ 10 in dietary components.
The first reports on this aspect were published in , but the sensitivity and selectivity of the analytical methods at that time did not allow reliable analyses, especially for products with low concentrations. Dairy products are much poorer sources of CoQ 10 than animal tissues.
Among vegetables, parsley and perilla are the richest CoQ 10 sources, but significant differences in their CoQ 10 levels may be found in the literature. Broccoli , grapes , and cauliflower are modest sources of CoQ Most fruit and berries represent a poor to very poor source of CoQ 10 , with the exception of avocados , which have a relatively high CoQ 10 content.
In the developed world, the estimated daily intake of CoQ 10 has been determined at 3—6 mg per day, derived primarily from meat. Contents move to sidebar hide. Article Talk. Read Edit View history. Tools Tools.
What links here Related changes Upload file Special pages Permanent link Page information Cite this page Get shortened URL Download QR code Wikidata item. Download as PDF Printable version. In other projects. Wikimedia Commons.
Chemical compound. This article is missing information about biological function weight too low compared to dietary , need a section with links to Q cycle and Complex III at minimum. Please expand the article to include this information. Further details may exist on the talk page.
September CAS Number. Interactive image. CHEBI Y. ChEMBL Y. PubChem CID. EJ27X76M46 Y. CompTox Dashboard EPA. Chemical formula. Solubility in water. ATC code. Related quinones. Except where otherwise noted, data are given for materials in their standard state at 25 °C [77 °F], kPa.
Y verify what is Y N? Infobox references. Biochimica et Biophysica Acta BBA - Bioenergetics. doi : PMID Biochimica et Biophysica Acta BBA - Molecular Basis of Disease. In Kagan, V. Coenzyme Q: Molecular mechanisms in health and disease.
Boca Raton: CRC Press. International Journal for Vitamin and Nutrition Research. Internationale Zeitschrift für Vitamin- und Ernahrungsforschung.
Journal International de Vitaminologie et de Nutrition. Archives of Biochemistry and Biophysics. The Journal of Investigative Dermatology. Regulatory Toxicology and Pharmacology.
Current Opinion in Neurology. June Clinical Biochemistry. American Journal of Health-System Pharmacy. S2CID Journal of the American Heart Association. PMC National Cancer Institute , National Institutes of Health , U. of Health and Human Services. Retrieved 29 June UK: National Institute for Health and Care Excellence.
Ceska a Slovenska Farmacie: Casopis Ceske Farmaceuticke Spolecnosti a Slovenske Farmaceuticke Spolecnosti. com finds discrepancies in strength of CoQ 10 supplements". Townsend Letter for Doctors and Patients. August—September January Cleveland Clinic Journal of Medicine.
The Cochrane Database of Systematic Reviews. Cochrane Heart Group ed. Cochrane Database of Systematic Reviews. BMC Cardiovascular Disorders. Current Cardiology Reports. March The Canadian Journal of Neurological Sciences. Mayo Clinic Proceedings Systematic Review and Meta-Analysis.
Lipid and Blood Pressure Meta-analysis Collaboration Group. American Cancer Society. Archived from the original on 24 February Retrieved 20 February British Dental Journal. BMJ Open. ISSN Anais Brasileiros de Dermatologia. Journal of the American Academy of Dermatology.
International Journal of Cosmetic Science. Biochemical Pharmacology. November Journal of Photochemistry and Photobiology B: Biology. BioMed Research International. Photochemistry and Photobiology.
Reproductive Biology and Endocrinology. Circulation: Heart Failure. Czech Journal of Food Sciences. Biochemical and Biophysical Research Communications. Inherited Neuromuscular Diseases: Translation from Pathomechanisms to Therapies.
ISBN Retrieved 4 January FEMS Microbiology Letters. Free Radical Research. Yakugaku Zasshi. Agro Food Industry Hi Tech. A migraine is a recurring type of headache that causes severe throbbing pain or a pulsing sensation.
Low levels of CoQ10 have been reported in people who experience migraines. A review of people with migraines found that CoQ10 supplementation for at least six weeks reduced the frequency and duration of migraines.
But it didn't reduce migraine pain. Some evidence suggests CoQ10 applied to the skin in creams or serums may help fight the visible signs of aging, so it's possible supplements might too.
This may be because it reduces free radicals that can cause skin to wrinkle. The evidence that CoQ10 can improve fertility isn't yet established. Some evidence suggests that CoQ10 may increase sperm motility and improve the quality of eggs. However, research so far is insufficient to recommend CoQ10 as a fertility aid.
A handful of small studies suggest it might delay fatigue and improve exercise recovery. However, more research is needed. Statins are drugs that help lower cholesterol. They can cause muscle pain and weakness as a side effect. Some research suggests that CoQ10 may reduce these side effects.
A review found that CoQ10 supplementation reduced statin-induced muscle pain, weakness, cramps, and tiredness. CoQ10 is found naturally in your body, in some foods, and as a supplement.
The richest food sources of CoQ10 include:. The average daily intake of CoQ10 is 5. The body produces CoQ10, but far less than what studies have demonstrated as beneficial. Your body naturally produces CoQ However, CoQ10 levels decline with aging, decreasing the body's ability to manage inflammation and oxidative stress effectively.
Oxidative stress occurs when free radicals unstable molecules start to damage cells and tissues in the body. Antioxidants counter the effects of free radicals. Low CoQ10 levels in the body have been associated with several diseases, including:.
However, this does not mean that CoQ10 supplements can treat or prevent any of these conditions. CoQ10 supplements are sold in several forms, including:. Some CoQ10 supplements are formulated to absorb into your system better than others. This has the same effect as taking a larger dose. For example, some CoQ10 supplements are formulated to be more water- and fat-soluble for enhanced absorption.
CoQ10 and other supplements aren't regulated like medications. To ensure you're buying a quality product look for products that have been certified by:. These independent organizations test the quality and ingredients of dietary supplements. If you have questions, talk to a registered dietitian, healthcare provider, or pharmacist.
CoQ10 supplementation is considered safe and well-tolerated, but side effects may include abdominal pain or an upset stomach. These symptoms can occur in doses greater than 1, mg per day.
Other reported CoQ10 side effects include:. Children under the age of 18 should not take CoQ10 except under the supervision of a healthcare provider. CoQ10 may interact with some medications, including:.
Ask your healthcare provider before taking CoQ Be sure to tell them about all the medications and supplements you take. There's no standard recommended dose for CoQ In healthy adults, the typical dose ranges between 30 mg and mg per day.
Talk with your healthcare provider to determine an appropriate dose for you. CoQ10 dosages used in studies include:. CoQ10 is generally safe and well-tolerated, but avoid consuming more than 1, mg of CoQ10 per day. Fortunately, this amount is much higher than commonly used doses.
Store CoQ10 soft gels or capsules in a cool, dry place. Store liquid forms according to the directions on the product. Some CoQ10 supplements, especially liquid forms, include an expiration date. CoQ10 supplements may lose potency if consumed past the expiration date.
Coenzyme Q10 may help with certain health conditions, like high blood pressure, diabetes, and migraines. However, supplements shouldn't be used to treat or prevent any diseases. See your healthcare provider regularly for guidance on managing your condition. CoQ10 may cause mild side effects and interact negatively with certain medications.
There's no official recommended dosage. In studies, doses have ranged from 50 mg to mg daily. Talk to your healthcare provider if you're considering taking CoQ10 supplements to determine the appropriate dose for you. When buying supplements, look for products that have been independently tested for quality.
National Cancer Institute. Coenzyme Q Mount Sinai. National Center for Complementary and Integrative Health. Lee BJ, Huang YC, Chen SJ, Lin PT. Coenzyme Q10 supplementation reduces oxidative stress and increases antioxidant enzyme activity in patients with coronary artery disease.
Jafari M, Mousavi SM, Asgharzadeh A, Yazdani N. Coenzyme Q10 in the treatment of heart failure: a systematic review of systematic reviews.
Indian Heart J. Zozina Vl, Covantev S, Goroshko OA, et al. Coenzyme Q10 in cardiovascular and metabolic diseases: current state of the problem. Curr Cardiol Rev. Tabrizi R, Akbari M, Sharifi N, et al. The effects of coenzyme q10 supplementation on blood pressures among patients with metabolic diseases: a systematic review and meta-analysis of randomized controlled trials.
High Blood Press Cardiovasc Prev. Yoritaka A, Kawajiri S, Yamamoto Y, et al. Mantle D, Heaton RA, Hargreaves IP. Coenzyme q10, ageing and the nervous system: an overview. Antioxidants Basel. Shen Q, Pierce J. Supplementation of coenzyme q10 among patients with type 2 diabetes mellitus.
Liang Y, Zhao D, Ji Q, et al. Effects of coenzyme Q10 supplementation on glycemic control: A GRADE-assessed systematic review and dose-response meta-analysis of randomized controlled trials.
Testai L, Martelli A, Flori L, Cicero AFG, Colletti A. Coenzyme q clinical applications beyond cardiovascular diseases. Sazali S, Badrin S, Norhayati MN, Idris NS. Coenzyme Q10 supplementation for prophylaxis in adult patients with migraine—a meta-analysis. BMJ Open. Knott A, Achterberg V, Smuda C, et al.
Topical treatment with coenzyme Qcontaining formulas improves skin's Q10 level and provides antioxidative effects. Giannubilo S, Orlando P, Silvestri S, et al.
CoQ10 supplementation in patients undergoing IVF-ET: the relationship with follicular fluid content and oocyte maturity. Suzuki Y, Nagato S, Sakuraba K, Morio K, Sawaki K. Short-term ubiquinol supplementation alleviates tissue damage in muscle and fatigue caused by strenuous exercise in male distance runners.
Int J Vitam Nutr Res. Qu H, Guo M, Chai H, et al. J Am Heart Assoc. Oregon State University. Arenas-Jal M, Suñé-Negre JM, García-Montoya E.
Coenzyme Q CoQ is Coenzyke Coenzyme Q component Coenzyme Q the mitochondrial electron transport chain and an antioxidant Coenzyme Q plasma membranes and lipoproteins. Coenzyme Q is Coenzgme produced in all cells by Coezyme highly regulated pathway that involves a mitochondrial Boosting immune resilience complex. Boosting immune resilience, we review the Cooenzyme knowledge Hydration for staying focused CoQ 10 biosynthesis and primary CoQ 10 deficiency syndrome, and have collected published results from clinical trials based on CoQ 10 supplementation. There is evidence that supplementation positively affects mitochondrial deficiency syndrome and the symptoms of aging based mainly on improvements in bioenergetics. Cardiovascular disease and inflammation are alleviated by the antioxidant effect of CoQ There is a need for further studies and clinical trials involving a greater number of participants undergoing longer treatments in order to assess the benefits of CoQ 10 treatment in metabolic syndrome and diabetes, neurodegenerative disorders, kidney diseases, and human fertility. How the Antioxidant Coenzyme Q Q10 Coenzyem You Manage Eat like a champion. Coenzyme Q10 CoQ10 or Coezyme is Coenzyme Q antioxidant Coenzzyme body produces that may prevent cellular damage Coenzyne with aging and some diseases. As Clenzyme Coenzyme Q, the levels of CoQ10 decrease. Lower levels of CoQ10 have also been found in people with heart disease and people taking cholesterol-lowering drugs, beta-blockers, or tricyclic antidepressants. CoQ10 is also available in certain foods, such as meat, fish, and nuts, as well as from dietary supplements. In this article, you'll learn about possible CoQ10 benefits and side effects, dosages, and what to look for when buying supplements.Coenzyme Q -
Ubiquinones are fat-soluble molecules with anywhere from 1 to 12 isoprene 5-carbon units. The ubiquinone found in humans, ubidecaquinone or coenzyme Q 10 , has a "tail" of 10 isoprene units a total of 50 carbon atoms attached to its benzoquinone "head" Figure 1 1.
Coenzyme Q 10 is soluble in lipids fats and is found in virtually all cell membranes , including mitochondrial membranes. The ability of the benzoquinone head group of coenzyme Q 10 to accept and donate electrons is a critical feature to its function.
Coenzyme Q 10 can exist in three oxidation states Figure 1 : i the fully reduced ubiquinol form, CoQ 10 H 2 ; ii the radical semiquinone intermediate, CoQ 10 H·; and iii the fully oxidized ubiquinone form, CoQ The conversion of energy from carbohydrates and fats to ATP , the form of energy used by cells, requires the presence of coenzyme Q 10 in the inner mitochondrial membrane.
As part of the mitochondrial electron transport chain , coenzyme Q 10 accepts electrons from reducing equivalents generated during fatty acid and glucose metabolism and then transfers them to electron acceptors. The energy released when the protons flow back into the mitochondrial interior is used to form ATP Figure 2 1.
In addition to its role in ATP synthesis, mitochondrial coenzyme Q 10 mediates the oxidation of dihydroorotate to orotate in the de novo pyrimidine synthesis. Lysosomes are organelles within cells that are specialized for the digestion of cellular debris.
The digestive enzymes within lysosomes function optimally at an acidic pH , meaning they require a permanent supply of protons. The lysosomal membranes that separate those digestive enzymes from the rest of the cell contain relatively high concentrations of coenzyme Q Research suggests that coenzyme Q 10 plays an important role in the transport of protons across lysosomal membranes to maintain the optimal pH 2, 3.
In its reduced form CoQ 10 H 2 , coenzyme Q 10 is an effective fat-soluble antioxidant that protects cell membranes and lipoproteins from oxidation. The presence of a significant amount of CoQ 10 H 2 in cell membranes, along with enzymes capable of reducing oxidized CoQ 10 back to CoQ 10 H 2 i.
CoQ 10 H 2 has been found to inhibit lipid peroxidation when cell membranes and low-density lipoproteins LDL are exposed to oxidizing conditions.
When LDL is oxidized, CoQ 10 H 2 is the first antioxidant consumed. In isolated mitochondria , coenzyme Q 10 can protect membrane proteins and mitochondrial DNA from the oxidative damage that accompanies lipid peroxidation 5.
Moreover, when present, CoQ 10 H 2 was found to limit the formation of oxidized lipids and the consumption of α-tocopherol a form of vitamin E with antioxidant properties 6.
Indeed, in addition to neutralizing free radicals directly, CoQ 10 H 2 is capable of regenerating antioxidants like α-tocopherol and ascorbate vitamin C 4. α-Tocopherol vitamin E and coenzyme Q 10 are the principal fat-soluble antioxidants in membranes and lipoproteins.
When α-tocopherol α-TOH neutralizes a free radical , such as a lipid peroxyl radical LOO· , it becomes oxidized itself, forming α-TO·, which can in turn promote the oxidation of lipoproteins under certain conditions in the test tube, thus propagating a chain reaction.
However, when the reduced form of coenzyme Q 10 CoQ 10 H 2 reacts with α-TO·, α-TOH is regenerated and the semiquinone radical CoQ 10 H· is formed. It is possible for CoQ 10 H· to react with oxygen O 2 to produce superoxide anion radical O 2 · - , which is a less reactive pro-oxidant than LOO·.
However, CoQ 10 H· can also reduce α-TO· back to α-TOH, resulting in the formation of fully oxidized coenzyme Q 10 CoQ 10 , which does not react with O 2 to form O 2 · - Figure 3 6, 8. Coenzyme Q 10 deficiency has not been described in the general population, so it is generally assumed that normal biosynthesis , with or without a varied diet, provides sufficient coenzyme Q 10 to sustain energy production in healthy individuals 9.
Primary coenzyme Q 10 deficiency is a rare genetic disorder caused by mutations in genes involved in coenzyme Q 10 biosynthetic pathway.
To date, mutations in at least nine of these genes have been identified 1. As a result, primary coenzyme Q 10 deficiency is a clinically heterogeneous disorder that includes five major phenotypes: i severe infantile multi-systemic disease, ii encephalomyopathy, iii cerebellar ataxia , iv isolated myopathy , and v nephrotic syndrome.
Whereas most mitochondrial respiratory chain disorders are hardly amenable to treatments, oral coenzyme Q 10 supplementation has been shown to improve muscular symptoms in some yet not all patients with primary coenzyme Q 10 deficiency Neurological symptoms in patients with cerebellar ataxia are only partially relieved by coenzyme Q 10 CoQ 10 H 2 supplementation Secondary coenzyme Q 10 deficiency results from mutations or deletions in genes that are not directly related to coenzyme Q 10 biosynthetic pathway.
Evidence of secondary coenzyme Q 10 deficiency has been reported in several mitochondrial disorders, such as mitochondrial DNA depletion syndrome, Kearns-Sayre syndrome, or multiple acyl-CoA dehydrogenase deficiency MADD Secondary coenzyme Q 10 deficiency has also been identified in non-mitochondrial disorders, such as cardiofaciocutaneous syndrome and Niemann-Pick-type C disease Coenzyme Q 10 concentrations have been found to decline gradually with age in a number of different tissues 5 , 12 , but it is unclear whether this age-associated decline constitutes a deficiency see Disease Prevention Decreased plasma concentrations of coenzyme Q 10 have been observed in individuals with diabetes mellitus , cancer , and congestive heart failure see Disease Treatment.
Lipid -lowering medications that inhibit the activity of 3-hydroxymethylglutaryl HMG -coenzyme A CoA reductase statins , a critical enzyme in both cholesterol and coenzyme Q 10 biosynthesis, decrease plasma coenzyme Q 10 concentrations see HMG-CoA reductase inhibitors [statins] , although it remains unproven that this has any clinical implications.
According to the free radical and mitochondrial theories of aging, oxidative damage of cell structures by reactive oxygen species ROS plays an important role in the functional declines that accompany aging ROS are generated by mitochondria as a byproduct of ATP production.
If not neutralized by antioxidants , ROS may damage mitochondria over time, causing them to function less efficiently and to generate more damaging ROS in a self-perpetuating cycle. Coenzyme Q 10 plays an important role in mitochondrial ATP synthesis and functions as an antioxidant in mitochondrial membranes see Biological Activities.
One of the hallmarks of aging is a decline in energy metabolism in many tissues, especially liver, heart, and skeletal muscle. Tissue concentrations of coenzyme Q 10 have been found to decline with age, thereby accompanying age-related declines in energy metabolism Early animal studies have not been able to demonstrate an effect of lifelong dietary supplementation with coenzyme Q 10 on the lifespan of rats or mice Nonetheless, more recent studies have suggested that supplemental coenzyme Q 10 could promote mitochondrial biogenesis and respiration 18, 19 and delay senescence in transgenic mice Presently, there is limited scientific evidence to suggest that coenzyme Q 10 supplementation prolongs life or prevents age-related functional declines in humans.
Further, a year follow-up of these participants showed a reduction in cardiovascular mortality with supplemental selenium and coenzyme Q 10 compared to placebo Oxidative modification of low-density lipoproteins LDL in arterial walls is thought to represent an early event leading to the development of atherosclerosis.
Reduced coenzyme Q 10 CoQ 10 H 2 inhibits the oxidation of LDL in the test tube in vitro and works together with α-tocopherol α-TOH to inhibit LDL oxidation by regenerating α-TO· back to α-TOH. In the absence of a co- antioxidant , such as CoQ 10 H 2 or vitamin C, α-TO· can, under certain conditions, promote the oxidation of LDL in vitro 6.
Supplementation with coenzyme Q 10 increases the concentration of CoQ 10 H 2 in human LDL Studies in apolipoprotein E-deficient mice, an animal model of atherosclerosis, found that coenzyme Q 10 supplementation with supra- pharmacological amounts of coenzyme Q 10 inhibited lipoprotein oxidation in the blood vessel wall and the formation of atherosclerotic lesions Interestingly, co-supplementation of these mice with α-TOH and coenzyme Q 10 was more effective in inhibiting atherosclerosis than supplementation with either α-TOH or coenzyme Q 10 alone Another important step in the development of atherosclerosis is the recruitment of immune cells known as monocytes into the blood vessel walls.
This recruitment is dependent in part on monocyte expression of cell adhesion molecules integrins. Although coenzyme Q 10 supplementation shows promise as an inhibitor of LDL oxidation and atherosclerosis, more research is needed to determine whether coenzyme Q 10 supplementation can inhibit the development or progression of atherosclerosis in humans.
Inherited coenzyme Q 10 deficiencies are rare diseases that are clinically and genetically heterogeneous see Deficiency. Early treatment with pharmacological doses of coenzyme Q 10 is essential to limit irreversible organ damage in coenzyme Q 10 -responsive deficiencies 1.
It is not clear to what extent coenzyme Q 10 supplementation might have therapeutic benefit in patients with inherited secondary Q 10 deficiencies. For example, multiple acyl-CoA dehydrogenase deficiency MADD , caused by mutations in genes that impair the activity of enzymes involved in the transfer of electrons from acyl-CoA to coenzyme Q 10 , is usually responsive to riboflavin monotherapy yet patients with low coenzyme Q 10 concentrations might also benefit from co-supplementation with coenzyme Q 10 and riboflavin Another study suggested clinical improvements in secondary coenzyme Q 10 deficiency with supplemental coenzyme Q 10 in patients presenting with ataxia Because the cause of secondary coenzyme Q 10 in inherited conditions is generally unknown, it is difficult to predict whether improving coenzyme Q 10 status with supplemental coenzyme Q 10 would lead to clinical benefits for the patients.
Finally, coenzyme Q 10 deficiency can be secondary to the inhibition of HMG-CoA reductase by statin drugs see Deficiency. The trials failed to establish a diagnosis of relative coenzyme Q 10 deficiency before the intervention started, hence limiting the conclusion of the meta-analysis.
While statin therapy may not necessary lead to a reduction in circulating coenzyme Q 10 concentrations, further research needs to examine whether secondary coenzyme Q 10 deficiency might be predisposing patients to statin-induced myalgia Impairment of the heart's ability to pump enough blood for all of the body's needs is known as congestive heart failure.
In coronary heart disease CHD , accumulation of atherosclerotic plaque in the coronary arteries may prevent parts of the cardiac muscle from getting adequate blood supply, ultimately resulting in heart damage and impaired pumping ability.
Heart failure can also be caused by myocardial infarction , hypertension , diseases of the heart valves, cardiomyopathy , and congenital heart diseases. Because physical exercise increases the demand on the weakened heart, measures of exercise tolerance are frequently used to monitor the severity of heart failure.
Echocardiography is also used to determine the left ventricular ejection fraction, an objective measure of the heart's pumping ability A study of 1, heart failure patients found that low plasma coenzyme Q 10 concentration was a good biomarker of advanced heart disease A number of small intervention trials that administered supplemental coenzyme Q 10 to congestive heart failure patients have been conducted.
Pooling data from some of the trials showed an increase in serum coenzyme Q 10 concentrations three studies but no effect on left ventricular ejection fraction two studies or exercise capacity two studies The heart muscle may become oxygen-deprived ischemic as the result of myocardial infarction or during cardiac surgery.
Increased generation of reactive oxygen species ROS when the heart muscle's oxygen supply is restored reperfusion might be an important contributor to myocardial damage occurring during ischemia-reperfusion Pretreatment of animals with coenzyme Q 10 has been found to preserve myocardial function following ischemia-reperfusion injury by increasing ATP concentration, enhancing antioxidant capacity and limiting oxidative damage , regulating autophagy , and reducing cardiomyocyte apoptosis Another potential source of ischemia-reperfusion injury is aortic clamping during some types of cardiac surgery, such as coronary artery bypass graft CABG surgery.
In a small randomized controlled trial in 30 patients, oral administration of coenzyme Q 10 for 7 to 10 days before CABG surgery reduced the need for mediastinal drainage, platelet transfusion, and positive inotropic drugs e.
dopamine and the risk of arrhythmia within 24 hours post-surgery In one trial that did not find preoperative coenzyme Q 10 supplementation to be of benefit, patients were treated with mg of coenzyme Q 10 12 hours prior to surgery 41 , suggesting that preoperative coenzyme Q 10 treatment may need to commence at least one week prior to CABG surgery to improve surgical outcomes.
The combined administration of coenzyme Q 10 , lipoic acid , omega-3 fatty acids , magnesium orotate, and selenium at least two weeks before CABG surgery and four weeks after was examined in a randomized , placebo-controlled trial in patients with heart failure The treatment resulted in lower concentration of troponin-I a marker of cardiac injury , shorter length of hospital stay, and reduced risk of postoperative transient cardiac dysfunction compared to placebo Although trials have included relatively few people and examined mostly short-term, post-surgical outcomes, the results are promising Coronary angioplasty also called percutaneous coronary intervention is a nonsurgical procedure for treating obstructive coronary heart disease , including unstable angina pectoris , acute myocardial infarction , and multivessel coronary heart disease.
Angioplasty involves temporarily inserting and inflating a tiny balloon into the clogged artery to help restore the blood flow to the heart. Periprocedural myocardial injury that occurs in up to one-third of patients undergoing otherwise uncomplicated angioplasty increases the risk of morbidity and mortality at follow-up.
A prospective cohort study followed 55 patients with acute ST segment elevation myocardial infarction a type of heart attack characterized by the death of some myocardial tissue who underwent angioplasty Plasma coenzyme Q 10 concentration one month after angioplasty was positively correlated with less inflammation and oxidative stress and predicted favorable left ventricular end-systolic volume remodeling at six months One randomized controlled trial has examined the effect of coenzyme Q 10 supplementation on periprocedural myocardial injury in patients undergoing coronary angioplasty The administration of mg of coenzyme Q 10 12 hours before the angioplasty to 50 patients reduced the concentration of C-reactive protein [CRP]; a marker of inflammation within 24 hours following the procedure compared to placebo.
However, there was no difference in concentrations of two markers of myocardial injury creatine kinase and troponin-I or in the incidence of major adverse cardiac events one month after angioplasty between active treatment and placebo Additional trials are needed to examine whether coenzyme Q 10 therapy can improve clinical outcomes in patients undergoing coronary angioplasty.
Myocardial ischemia may also lead to chest pain known as angina pectoris. People with angina pectoris often experience symptoms when the demand for oxygen exceeds the capacity of the coronary circulation to deliver it to the heart muscle, e.
In most of the studies, coenzyme Q 10 supplementation improved exercise tolerance and reduced or delayed electrocardiographic changes associated with myocardial ischemia compared to placebo.
However, only two of the studies found significant decreases in symptom frequency and use of nitroglycerin with coenzyme Q 10 supplementation. Presently, there is only limited evidence suggesting that coenzyme Q 10 supplementation would be a useful adjunct to conventional angina therapy.
Very few high-quality trials have examined the potential therapeutic benefit of coenzyme Q 10 supplementation in the treatment of primary hypertension In contrast, a meta-analysis that used less stringent selection criteria included 17 small trials and found evidence of a blood pressure-lowering effect of coenzyme Q 10 in patients with cardiovascular disease or metabolic disorders The effect of coenzyme Q 10 on blood pressure needs to be examined in large, well-designed clinical trials.
Endothelial dysfunction: Normally functioning vascular endothelium promotes blood vessel relaxation vasodilation when needed for example, during exercise and inhibits the formation of blood clots. Atherosclerosis is associated with impairment of vascular endothelial function, thereby compromising vasodilation and normal blood flow.
Endothelium-dependent vasodilation is impaired in individuals with elevated serum cholesterol concentrations, as well as in patients with coronary heart disease or diabetes mellitus.
Evidence from larger studies is needed to further establish the effect of coenzyme Q 10 on endothelium-dependent vasodilation. Recently published pooled analyses of these trials have given mixed results Larger studies are needed to examine the effect of coenzyme Q 10 supplementation on low-grade inflammation.
Blood lipids : Elevated plasma lipoprotein a concentration is an independent risk factor for cardiovascular disease. Other effects of coenzyme Q 10 on blood lipids have not been reported 51, 53, A therapeutic approach combining coenzyme Q 10 with other antioxidants might prove to be more effective to target co-existing metabolic disorders in individuals at risk for cardiovascular disease Diabetes mellitus is a condition of increased oxidative stress and impaired energy metabolism.
Plasma concentrations of reduced coenzyme Q 10 CoQ 10 H 2 have been found to be lower in diabetic patients than healthy controls after normalization to plasma cholesterol concentrations 56, Randomized controlled trials that examined the effect of coenzyme Q 10 supplementation found little evidence of benefits on glycemic control in patients with diabetes mellitus.
Maternally inherited diabetes mellitus-deafness syndrome MIDD is caused by a mutation in mitochondrial DNA , which is inherited exclusively from one's mother. Of note, the pathogenesis of type 2 diabetes mellitus involves the early onset of glucose intolerance and hyperinsulinemia associated with the progressive loss of tissue responsiveness to insulin.
Recent experimental studies tied insulin resistance to a decrease in coenzyme Q 10 expression and showed that supplementation with coenzyme Q 10 could restore insulin sensitivity 7.
Coenzyme Q 10 supplementation might thus be a more useful tool for the primary prevention of type 2 diabetes rather than for its management. Parkinson's disease is a degenerative neurological disorder characterized by tremors, muscular rigidity, and slow movements.
Mitochondrial dysfunction and oxidative damage in a part of the brain called the substantia nigra may play a role in the development of the disease Decreased ratios of reduced -to- oxidized coenzyme Q 10 have been found in platelets of individuals with Parkinson's disease 61, Two recent meta-analyses of randomized, placebo-controlled trials found no evidence that coenzyme Q 10 improved motor-related symptoms or delayed the progression of the disease when compared to placebo 68, Huntington's disease is an inherited neurodegenerative disorder characterized by selective degeneration of nerve cells known as striatal spiny neurons.
Symptoms, such as movement disorders and impaired cognitive function, typically develop in the fourth decade of life and progressively deteriorate over time. Animal models indicate that impaired mitochondrial function and glutamate -mediated neurotoxicity may be involved in the pathology of Huntington's disease.
Interestingly, co-administration of coenzyme Q 10 with remacemide an NMDA receptor antagonist , the antibiotic minocycline, or creatine led to greater improvements in most biochemical and behavioral parameters To date, only two clinical trials have examined whether coenzyme Q 10 might be efficacious in human patients with Huntington's disease.
All dosages were generally well tolerated, with gastrointestinal symptoms being the most frequently reported adverse effect. Blood concentrations of coenzyme Q 10 at the end of the study were maximized with the daily dose of 2, mg The trial was prematurely halted because it appeared unlikely to demonstrate any health benefit in supplemented patients — about one-third of participants completed the trial at the time of study termination Although coenzyme Q 10 is generally well tolerated, there is no evidence that supplementation can improve functional and cognitive symptoms in Huntington's disease patients.
Friedreich's ataxia FRDA : FRDA is an autosomal recessive neurodegenerative disease caused by mutations in the gene FXN that encodes for the mitochondrial protein , frataxin.
Frataxin is needed for the making of iron -sulfur clusters ISC. ISC-containing subunits are especially important for the mitochondrial respiratory chain and for the synthesis of heme -containing proteins Frataxin deficiency is associated with imbalances in iron-sulfur containing proteins, mitochondrial respiratory chain dysfunction and lower ATP production, and accumulation of iron in the mitochondria, which increases oxidative stress and oxidative damage to macromolecules of the respiratory chain Clinically, FRDA is a progressive disease characterized by ataxia , areflexia , speech disturbance dysarthria , sensory loss, motor dysfunction, cardiomyopathy , diabetes , and scoliosis Follow-up assessments at 47 months indicated that cardiac and skeletal muscle improvements were maintained and that FRDA patients showed significant increases in fractional shortening, a measure of cardiac function.
Moreover, the therapy was effective at preventing the progressive decline of neurological function Large-scale, randomized controlled trials are necessary to determine whether coenzyme Q 10 , in conjunction with vitamin E, has therapeutic benefit in FRDA.
At present, about one-half of patients use coenzyme Q 10 and vitamin E supplements despite the lack of proven therapeutic benefit Spinocerebellar ataxias SCAs : SCAs are a group of rare autosomal dominant neurodegenerative diseases characterized by gait difficulty, loss of hand dexterity, dysarthria, and cognitive decline.
SCA1, 2, 3, and 6 are the most common SCAs In vitro coenzyme Q 10 treatment of forearm skin fibroblasts isolated from patients with SCA2 was found to reduce oxidative stress and normalize complex I and II-III activity of the mitochondrial respiratory chain Early interest in coenzyme Q 10 as a potential therapeutic agent in cancer was stimulated by an observational study that found that individuals with lung, pancreas , and especially breast cancer were more likely to have low plasma coenzyme Q 10 concentrations than healthy controls Two randomized controlled trials have explored the effect of coenzyme Q 10 as an adjunct to conventional therapy for breast cancer.
Supplementation with coenzyme Q 10 failed to improve measures of fatigue and quality of life in patients newly diagnosed with breast cancer 84 and in patients receiving chemotherapy There is little evidence that supplementation with coenzyme Q 10 improves athletic performance in healthy individuals.
Most did not find significant differences between the group taking coenzyme Q 10 and the group taking placebo with respect to measures of aerobic exercise performance, such as maximal oxygen consumption VO 2 max and exercise time to exhaustion Two studies actually found significantly greater improvement in measures of anaerobic 87 and aerobic 86 exercise performance with a placebo than with supplemental coenzyme Q More recent studies have suggested that coenzyme Q 10 could help reduce both muscle damage-associated oxidative stress and low-grade inflammation induced by strenuous exercise Studies on the effect of supplementation on physical performance in women are lacking, but there is little reason to suspect a gender difference in the response to coenzyme Q 10 supplementation.
Coenzyme Q 10 is synthesized in most human tissues. The biosynthesis of coenzyme Q 10 involves three major steps: 1 synthesis of the benzoquinone structure from 4-hydroxybenzoate derived from either tyrosine or phenylalanine, two amino acids; 2 synthesis of the polyisoprenoid side chain from acetyl-coenzyme A CoA via the mevalonate pathway; and 3 the joining condensation of these two structures to form coenzyme Q In the mevalonate pathway, the enzyme 3-hydroxymethylglutaryl HMG -CoA reductase, which converts HMG-CoA into mevalonate, is common to the biosynthetic pathways of both coenzyme Q 10 and cholesterol and is inhibited by statins cholesterol-lowering drugs; see Drug interactions 1.
Of note, pantothenic acid formerly vitamin B 5 is the precursor of coenzyme A, and pyridoxine vitamin B 6 , in the form of pyridoxal-5'-phosphate, is required for the conversion of tyrosine to 4-hydroxyphenylpyruvic acid that constitutes the first step in the biosynthesis of the benzoquinone structure of coenzyme Q The extent to which dietary consumption contributes to tissue coenzyme Q 10 concentrations is not clear.
Rich sources of dietary coenzyme Q 10 include mainly meat, poultry, and fish. Other good sources include soybean, corn, olive, and canola oils; nuts; and seeds.
Fruit, vegetables, eggs, and dairy products are moderate sources of coenzyme Q 10 Some dietary sources are listed in Table 1. Coenzyme Q 10 is available without a prescription as a dietary supplement in the US. Coenzyme Q 10 is fat-soluble and is best absorbed with fat in a meal.
Oral supplementation with coenzyme Q 10 is known to increase blood and lipoprotein concentrations of coenzyme Q 10 in humans 2 , 15 , Nonetheless, under certain physiological circumstances e.
During pregnancy, the use of coenzyme Q 10 supplements mg twice daily from 20 weeks' gestation was found to be safe Because reliable data in lactating women are not available, supplementation should be avoided during breast-feeding Concomitant use of warfarin Coumadin and coenzyme Q 10 supplements has been reported to decrease the anticoagulant effect of warfarin in a few cases An individual on warfarin should not begin taking coenzyme Q 10 supplements without consulting the health care provider who is managing his or her anticoagulant therapy.
HMG-CoA reductase is an enzyme that catalyzes a biochemical reaction that is common to both cholesterol and coenzyme Q 10 biosynthetic pathways see Biosynthesis.
Statins are HMG-CoA reductase inhibitors that are widely used as cholesterol-lowering medications. Statins can thus also reduce the endogenous synthesis of coenzyme Q Therapeutic use of statins, including simvastatin Zocor , pravastatin Pravachol , lovastatin Mevacor, Altocor, Altoprev , rosuvastatin Crestor , and atorvastatin Lipitor , has been shown to decrease circulating coenzyme Q 10 concentrations However, because coenzyme Q 10 circulates with lipoproteins , plasma coenzyme Q 10 concentration is influenced by the concentration of circulating lipids , It is likely that circulating coenzyme Q 10 concentrations are decreased because statins reduce circulating lipids rather than because they inhibit coenzyme Q 10 synthesis In addition, very few studies have examined coenzyme Q 10 concentrations in tissues other than blood such that the extent to which statin therapy affects coenzyme Q 10 concentrations in the body's tissues is unknown , , Finally, there is currently little evidence to suggest that secondary coenzyme Q 10 deficiency is responsible for statin-associated muscle symptoms in treated patients.
In addition, supplementation with coenzyme Q 10 failed to relieve myalgia in statin-treated patients see Disease Treatment , Originally written in by: Jane Higdon, Ph.
Linus Pauling Institute Oregon State University. Updated in February by: Victoria J. Drake, Ph. Updated in March by: Victoria J. The myocardium of patients with CHF demonstrates increased oxidative stress 7 as well as decreased concentrations of coenzyme Q10 as confirmed by tissue assays.
These results are awaiting confirmation. In studies 13 — 15 with eight to 44 patients, coenzyme Q10 also has demonstrated positive trends in reducing symptoms associated with selected mitochondrial abnormalities including the mitochondrial encephalopathy, lactic acidosis, and stroke-like episodes MELAS syndrome, Kearns-Sayre syndrome, and the myoclonus epilepsy with ragged-red fibers MERRhF syndrome.
Maximum effect often requires six or more months of therapy. Food and Drug Administration FDA orphan drug status for treatment of mitochondrial cytopathies based on several small trials. A preliminary open label trial 17 of 32 patients taking mg of coenzyme Q10 daily demonstrated efficacy in reducing the frequency of migraine attacks.
A recent randomized double-blind, placebo-controlled trial 18 of 42 patients taking coenzyme Q10 at mg a day found similar benefit. The response rate i. The number needed to treat was three. A number of randomized controlled trials, 20 — 22 including those in a meta-analysis, 23 found improvement in several clinical parameters related to CHF, including frequency of hospitalization, dyspnea, and edema.
These trials were weakened by small numbers only two of 14 trials had more than 25 participants and older techniques for calculating ejection fraction.
Of the more recent randomized trials using ventriculography and echocardiography, two found coenzyme Q10 at to mg daily no more effective than placebo in improving ejection fraction, peak oxygen consumption, exercise duration, or quality of life.
The planned SYMptoms, BIomarker status BNP , and long-term Outcome trial with more than patients with New York Heart Association class III and IV CHF followed over two years, should help answer this question.
A systematic review 29 of eight trials using coenzyme Q10 at various doses for essential hypertension, typically as adjuvant therapy, found a mean decrease in systolic and diastolic blood pressure of 16 and 10 mm Hg, respectively. Several of these trials 30 demonstrated confounding variables or were weakened by low statistical power.
The evidence for coenzyme Q10 use in other cardiovascular settings is promising and requires larger, longer-term trials.
Preliminary data also imply benefit in the setting of atherosclerosis. This includes a randomized, placebo-controlled trial 33 of 73 patients who were randomized to mg a day of coenzyme Q10 following myocardial infarction.
At one year, the coenzyme Q10 group demonstrated a significant decrease in total cardiac events including nonfatal myocardial infarctions and cardiac deaths. This improvement has been attributed to possible attenuation of endothelial dysfunction.
Coenzyme Q10 has been considered for improving glycemic control through various mechanisms, including a decrease in oxidative stress. Two earlier randomized controlled trails 35 , 36 using to mg of coenzyme Q10 in patients with type 1 or 2 diabetes found no difference in glycemic control and insulin requirement.
Although it is used for the prevention and treatment of cancer, the AHRQ found no evidence to assess the efficacy of coenzyme Q10 for this use. No absolute contraindications are known for coenzyme Q10, although reliable information about its use in pregnant or breastfeeding mothers or in young children is not available.
Adverse effects with coenzyme Q10 are rare. On average, mild gastrointestinal discomfort is reported in less than 1 percent of patients in clinical trials.
Several trials demonstrate coenzyme Q10 depletion subsequent to statin initiation. This assertion is refuted by a more recent crossover trial 44 that found no significant coenzyme Q10 drop after initiation of selected statins. Several doxorubicin Adriamycin trials, mostly in animal models, have noted a reduction in cardiac coenzyme Q10 depletion and cardiotoxicity associated with coadministration of coenzyme Q The clinical implications on disease state and adverse reaction profile with coenzyme Q10 supplementation in depleted states requires further evaluation.
The majority of coenzyme Q10 products are synthesized in Japan through proprietary fermentation of yeast strains. The efficacy, adverse effects, interactions, dosages, cost, and bottom line are summarized in Table 2.
The American College of Cardiology recently published an expert consensus document on integrating complementary medicine into cardiovascular medicine. Their conclusions regarding the use of coenzyme Q10 are consistent with those discussed above.
The value of coenzyme Q10 in cardiovascular disease and with statin use has not been clearly established. Vogel JH, Bolling SF, Costello RB, Guarneri EM, Krucoff MW, Longhurst JC, et al.
Integrating complementary medicine into cardiovascular medicine. J Am Coll Cardiol ;— Greenberg S, Frishman WH. Co-enzyme Q a new drug for cardiovascular disease. J Clin Pharmacol. Tran MT, Mitchell TM, Kennedy DT, Giles JT. Role of coenzyme Q10 in chronic heart failure, angina, and hypertension.
Specialty supplements are the bright spot in U. Chemical Market Reporter, July Ito H, Nakajima T, Takikawa R, Hamada E, Iguchi M, Sugimoto T, et al.
Naunyn Schmiedebergs Arch Pharmacol. Sugiyama S, Kitazawa M, Ozawa T, Suzuki K, Izawa Y. Anti-oxidative effect of coenzyme Q Nayler WG.
The use of coenzyme Q10 to protect ischemic heart muscle. In: Yamamura Y, Folkers K, Ito Y, eds. Biomedical and clinical aspects of coenzyme Q. Amsterdam: Elsevier, — Keith M, Geranmayegan A, Sole MJ, Kurian R, Robinson A, Omran AS, et al.
Increased oxidative stress in patients with congestive heart failure. J Am Coll Cardiol. Folkers K, Vadhanavikit S, Mortensen SA. Biochemical rationale and myocardial tissue data on the effective therapy of cardiomyopathy with coenzyme Q Proc Natl Acad Sci USA. Boler JB, Farley TM, Scholler J, Folkers K.
Deficiency of coenzyme Q10 in the rabbit. Int Z Vitaminforsch. Mortensen SA. Perspectives on therapy of cardiovascular diseases with coenzyme Q10 ubiquinone. Supplementation with ubiquinol has been shown to activate mechanisms controlling mitochondrial biogenesis Schmelzer et al. The concentrations of CoQ 10 in the plasma of elderly people are positively correlated with levels of physical activity and cholesterol concentrations Del Pozo-Cruz et al.
Older individuals given a combination of selenium and CoQ 10 over a 4-year period reported an improvement in vitality, physical performance, and quality of life Johansson et al. Furthermore, CoQ 10 supplementation confers health benefits in elderly people by preventing chronic oxidative stress associated with cardiovascular and neurodegenerative diseases Gonzalez-Guardia et al.
Despite these evidences, more reliable clinical trials focusing on the elderly are needed before considering CoQ 10 as an effective anti-aging therapy Varela-Lopez et al.
CoQ 10 has been used in the treatment of a number of human pathologies and disorders. Clinical trials, systematic reviews, and meta-analyses have examined the safety and efficacy of CoQ 10 in treating human diseases. As indicated below, prudence is needed when interpreting the results of several clinical trials.
A combination of factors including the small number of trials, substantial differences that exist in the experimental designs, dose and duration of treatment, the number of patients enrolled, and the relative short follow-up periods contribute to apparent inconsistencies in the published data.
Despite these limitations, CoQ 10 can be considered as an important coadjuvant in the treatment of different diseases, especially in chronic conditions affecting the elderly. The number of deaths attributed to heart failure is increasing worldwide and has become a global health issue.
Heart failure is accompanied by increased ROS formation, which can be attenuated with antioxidants. A systematic review has recently examined the efficacy of CoQ 10 supplementation in the prevention of cardiovascular disease CVD without lifestyle intervention Flowers et al.
These authors interpreted the results to indicate a significant reduction in systolic blood pressure without improvements in other CVD risk factors, such as diastolic blood pressure, total cholesterol, LDL- and high-density lipoprotein HDL -cholesterol, and triglycerides.
A second meta-analysis explored the impact of CoQ 10 in the prevention of complications in patients undergoing cardiac surgery, and the results showed that CoQ 10 therapy lowers the need of inotropic drugs and reduces the appearance of ventricular arrhythmias after surgery de Frutos et al.
Short-term daily treatment 12 weeks or less with mg CoQ 10 improves left ventricular ejection fraction in patients suffering from heart failure Fotino et al.
In contrast, no effect of CoQ 10 was observed on left ventricular ejection fraction or exercise capacity in patients with heart failure Madmani et al. CoQ 10 has been proposed for the treatment of metabolic syndrome and type 2 diabetes by virtue of its antioxidant properties. However, analysis of more than seven trials involving participants showed that CoQ 10 supplementation for at least 12 weeks had no significant effects on glycemic control, lipid profile, or blood pressure in diabetic patients, but was able to reduce serum triglycerides levels Suksomboon et al.
In a follow-up analysis of data obtained from Q-SYMBIO clinical trials Mortensen et al. Supplementation with CoQ 10 has produced beneficial effects in the treatment of hypercholesterolemia and hypertriglyceridemia by initiating changes in blood lipid concentration.
A combination of CoQ 10 with red yeast rice, berberina, policosanol, astaxanthin, and folic acid significantly decreased total cholesterol, LDL-cholesterol, triglycerides, and glucose in the blood while increasing HDL-cholesterol levels Pirro et al.
However, the impact of CoQ 10 alone without the other supplements was not directly assessed. Nevertheless, there are reports to suggest that CoQ 10 is very effective in reducing serum triglycerides levels Suksomboon et al.
Chronic treatment with statins is associated with myopathy Law and Rudnicka, , a side-effect representing a broad clinical spectrum of disorders largely associated with a decrease in CoQ 10 levels and selenoprotein activity Thompson et al.
Statins impair skeletal muscle and myocardial bioenergetics Littarru and Langsjoen, via inhibition of 3-hydroxymethylglutaryl-CoA HMG-CoA reductase, a key enzyme in the mevalonate pathway implicated in cholesterol and CoQ biosynthesis, and reduction in mitochondrial complex III activity of the electron transport chain Schirris et al.
A total of 60 patients suffering from statin-associated myopathy were enrolled in a 3-month study to test for efficacy of CoQ 10 and selenium treatment. A consistent reduction in their symptoms, including muscle pain, weakness, cramps, and fatigue was observed, suggesting an attenuation of the side-effects of chronic statin treatment following CoQ 10 supplementation Fedacko et al.
In a previous study, however, 44 patients suffering from statin-induced myalgia saw no improvement in their conditions after receiving CoQ 10 for 3 months Young et al. Other studies have determined that CoQ 10 supplementation improves endothelial dysfunction in type 2 diabetic patients treated with statins Hamilton et al.
Oxidative stress plays an essential role in diabetic kidney disease, and experiments performed on rats showed a promising protective effect of ubiquinol in the kidneys Ishikawa et al. However, a meta-analysis study examining the efficiency of antioxidants on the initiation and progression of diabetic kidney disease revealed that antioxidants, including CoQ 10 , did not have reliable effects against this disease Bolignano et al.
Chronic inflammation and oxidative stress are associated with many age-related diseases such as cardiovascular diseases, diabetes, cancer, and chronic kidney disease. A recent meta-analysis explored the efficacy of CoQ 10 on the plasma levels of C-reactive protein, interleukin 6 IL-6 and tumor necrosis factor alpha TNF-α in patients afflicted with pathologies in which inflammation was a common factor including cardio-cerebral vascular disease, multiple sclerosis, obesity, renal failure, rheumatoid arthritis, diabetes, and fatty liver disease Fan et al.
The authors also surmised that CoQ 10 supplementation decreased pro-inflammatory cytokines and inflammatory markers in the elderly with low CoQ 10 levels Fan et al. Metabolic diseases, characterized by chronic, low grade inflammation, respond well to CoQ 10 supplementation with significant decrease in TNF-α plasma levels without having an effect on C-reactive protein and IL-6 production Zhai et al.
More recently, CoQ 10 has been found to markedly attenuate the elevated expression of inflammatory and thrombotic risk markers in monocytes of patients with antiphospholipid syndrome, thereby improving endothelial function and mitochondrial activity in these patients Perez-Sanchez et al.
A proinflammatory profile has also been associated with the progression of neurological symptoms in Down syndrome patients Wilcock and Griffin, These patients have low CoQ 10 plasma levels together with high plasma levels of proinflammatory cytokines, such as IL-6 and TNF-α Zaki et al.
Supplementation with CoQ 10 confers protection against the progression of oxidative damage and mitochondrial dysfunction in Down syndrome patients Tiano and Busciglio, ; Tiano et al.
Preclinical studies demonstrated that CoQ can preserve mitochondrial function and reduce the loss of dopaminergic neurons in the case of Parkinson's disease Schulz and Beal, Experimental studies in animal models suggest that CoQ 10 may protect against neuronal damage caused by ischemia, atherosclerosis, and toxic injury Ishrat et al.
Further, a screening for oxidative stress markers in patients with Parkinson's disease reported lower levels of CoQ 10 and α-tocopherol and higher levels of lipoprotein oxidation in the plasma and cerebrospinal fluid compared to non-affected individuals Buhmann et al.
Moreover, CoQ 10 deficiency was observed at a higher frequency in Parkinson's disease, underscoring its utility as a peripheral biomarker Mischley et al. For this reason, it has been suggested that CoQ 10 supplementation could benefit patients suffering from neurodegenerative diseases.
Two reviews on recent clinical trials testing CoQ 10 supplementation reported the lack of improvement in motor functions in patients with neurodegenerative diseases, which led the authors to conclude that the use of CoQ 10 in these patients is unnecessary Liu and Wang, ; Negida et al.
However, other clinical trials in patients suffering from Parkinson's, Huntington's, and Friedreich's ataxia suggest that CoQ 10 supplementation could delay functional decline, particularly with regard to Parkinson's disease Beal, ; Shults, Indeed, four randomized, double-blind, placebo-controlled studies comparing CoQ 10 treatment in patients at early or mid-stage Parkinson's disease reported improvements in daily activities and other parameters Liu et al.
In contrast, a more recent multicenter randomized, double-blind, and placebo-controlled trial with CoQ 10 in patients with early-stage Huntington's disease did not slow the rate of patients' functional decline McGarry et al.
There is not enough evidence to indicate that CoQ 10 supplementation can delay the progression of Huntington's disease, at least in its early stages. Initiated in , the Alzheimer's Disease Cooperative Study evaluates the safety, tolerability, and impact of different antioxidants on biomarkers in this disease.
The role of plasma membrane CoQ 10 in autism has been recently proposed Crane et al. Patients with autistic spectrum disorders ASDs exhibit higher proportions of mitochondrial dysfunctions than the general population Rossignol and Frye, , as evidenced by developmental regression, seizures, and elevated serum levels of lactate or pyruvate in ASD patients.
Treatment with carnitine, CoQ 10 , and B-vitamins confers some improvements in ASD patients Rossignol and Frye, ; Gvozdjakova et al. Male infertility has been associated with oxidative stress, and CoQ 10 levels in seminal fluid is considered an important biomarker of healthy sperm Gvozdjakova et al.
Administration of CoQ 10 improves semen parameters in the treatment of idiopathic male infertility Arcaniolo et al. With regard to female infertility, the decrease in mitochondrial activity associated with CoQ 10 deficiency probably affects the granulosa cells' capacity to generate ATP Ben-Meir et al.
Indeed, reduction of CoQ 10 levels in oocyte-specific PDSS2 -deficient mice results in oocyte deficits and infertility Ben-Meir et al. Despite the absence of previous clinical trials that evaluate the effectiveness of CoQ 10 supplementation in female infertility, these studies show promising results of this natural supplement in boosting female fertility during the prime reproductive period.
CoQ 10 deficiency can be associated with a number of human diseases and age-related chronic conditions. In other cases, deficiency in CoQ 10 and its associated antioxidative activity can significantly increase the level of oxidative damage. It seems clear that supplementation with CoQ 10 improves mitochondrial function and confers antioxidant protection for organs and tissues affected by various pathophysiological conditions.
The ability of CoQ 10 to protect against the release of proinflammatory markers provides an attractive anti-inflammatory therapeutic for the treatment of some human diseases and in aging Figure 2.
Figure 2. Effects of CoQ 10 in human diseases. The positive effect of CoQ 10 has been already demonstrated in mitochondrial syndromes associated with CoQ 10 deficiency, inflammation, and cardiovascular diseases as well as in the delay of some age-related processes.
Dashed lines depict other positive effects of CoQ 10 with regard to kidney disease, fertility, metabolic syndrome, diabetes, and neurodegenerative diseases. However, more research is needed to validate these observations. Following intraperitoneal administration of CoQ 10 in rat, only small amount of the supplement reaches the kidney, muscle, and brain.
Likewise, only a fraction of the orally administered CoQ 10 reaches the blood while the major amount is eliminated via feces Bentinger et al. The absoption of CoQ 10 is slow and limited due to its hydrophobicity and large molecular weight and, therefore, high doses are needed to reach a number of rat tissues e.
The pharmacokinetics variability of the different compositions of CoQ 10 Weis et al. Systematic reviews and meta-analyses have revealed that there are few randomized clinical trials on the effect of CoQ 10 in combatting disease progression and improving quality of life.
The results of these trials have been inconsistent likely due to varied dosages, small sample size, and short follow-up periods. More studies performed on humans in focused trials are needed in order to understand the promising effects of CoQ All authors listed have made a substantial, direct and intellectual contribution to the work, and approved it for publication.
This work has been partially funded by the Spanish Ministry of Health, Instituto de Salud Carlos III ISCIII , FIS PI, and the Andalusian Government grant BIO FEDER funds of European Commission. JH-C has been awarded by CIBERER, Instituto de Salud Carlos III. This work was also supported, in part, by the Intramural Research Program of the National Institute on Aging, NIH.
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Abdollahzad, H. Effects of coenzyme Q10 supplementation on inflammatory cytokines TNF-alpha, IL-6 and oxidative stress in rheumatoid arthritis patients: a randomized controlled trial.
doi: PubMed Abstract CrossRef Full Text Google Scholar. Acosta, M. Coenzyme Q biosynthesis in health and disease. Acta , — Alcazar-Fabra, M. Coenzyme Q biosynthesis and its role in the respiratory chain structure.
Alehagen, U. Reduced cardiovascular mortality 10 years after supplementation with selenium and coenzyme Q10 for four years: follow-up results of a prospective randomized double-blind placebo-controlled trial in elderly citizens.
PLoS ONE e Supplementation with selenium and coenzyme Q10 reduces cardiovascular mortality in elderly with low selenium status. A secondary analysis of a randomised clinical trial. Increase in insulin-like growth factor 1 IGF-1 and insulin-like growth factor binding protein 1 after supplementation with selenium and coenzyme Q A prospective randomized double-blind placebo-controlled trial among elderly Swedish citizens.
Allan, C. Identification of Coq11, a new coenzyme Q biosynthetic protein in the CoQ-synthome in Saccharomyces cerevisiae. Arcaniolo, D. Is there a place for nutritional supplements in the treatment of idiopathic male infertility? Arun, S.
Mitochondrial biology and neurological diseases. Asencio, C. Severe encephalopathy associated to pyruvate dehydrogenase mutations and unbalanced coenzyme Q10 content. Ashraf, S. ADCK4 mutations promote steroid-resistant nephrotic syndrome through CoQ10 biosynthesis disruption.
Barca, E. Cerebellar ataxia and severe muscle CoQ10 deficiency in a patient with a novel mutation in ADCK3.
Battino, M. Coenzyme Q content in synaptic and non-synaptic mitochondria from different brain regions in the ageing rat. Ageing Dev. Beal, M. Coenzyme Q10 as a possible treatment for neurodegenerative diseases.
Free Radic. Ben-Meir, A. Coenzyme Q10 restores oocyte mitochondrial function and fertility during reproductive aging. Aging Cell 14, — Coenzyme Q-dependent mitochondrial respiratory chain activity in granulosa cells is reduced with aging.
Bentinger, M. Distrinution and breakdown of labeled coenzyme Q10 in rats. CrossRef Full Text Google Scholar. Coenzyme Q—biosynthesis and functions. Beyer, R. Tissue coenzyme Q ubiquinone and protein concentrations over the life span of the laboratory rat.
Bhagavan, H. Coenzyme Q absortion, tissue uptake, metabolism and pharmacokinetics. Bolignano, D. Antioxidant agents for delaying diabetic kidney disease progression: a systematic review and meta-analysis.
Bose, A. Mitochondrial dysfunction in Parkinson's disease. Brea-Calvo, G. Cell survival from chemotherapy depends on NF-kappaB transcriptional up-regulation of coenzyme Q biosynthesis. PLoS ONE 4:e Buhmann, C. Plasma and CSF markers of oxidative stress are increased in Parkinson's disease and influenced by antiparkinsonian medication.
Campagnolo, N. Cascajo, M. RNA-binding proteins regulate cell respiration and coenzyme Q biosynthesis by post-transcriptional regulation of COQ7. RNA Biol. Crane, F. Plasma membrane coenzyme Q: evidence for a role in autism. Biologics 8, — De Cabo, R. Calorie restriction attenuates age-related alterations in the plasma membrane antioxidant system in rat liver.
de Frutos, F. Prophylactic treatment with coenzyme Q10 in patients undergoing cardiac surgery: could an antioxidant reduce complications? A systematic review and meta-analysis. Del Pozo-Cruz, J. Physical activity affects plasma coenzyme Q10 levels differently in young and old humans.
Biogerontology 15, — Relationship between functional capacity and body mass index with plasma coenzyme Q10 and oxidative damage in community-dwelling elderly-people.
Desbats, M.
Coronavirus COVID Coenzye Latest Updates Visitation Pycnogenol and wound healing Visitation Policies Boosting immune resilience Coenzhme Visitation Policies Visitation Policies COVID Coejzyme Vaccine Information Boosting immune resilience Information Vaccine Coenzyke. Coenzyme Q is a fat-soluble type of substance called a quinone. Research has been ongoing since it was first found 40 years ago. It may have benefits for the heart. Coenzyme Q is made by cells throughout the body. It acts as a catalyst in the respiratory chain. This chain makes energy from carbohydrates.Coenzyme Q 10 is a member of the ubiquinone Coenzye of compounds. All animals, including humans, can synthesize Coejzyme, hence, coenzyme Q 10 is not considered a vitamin 1.
OCenzyme name ubiquinone refers to Codnzyme ubiquitous presence of these compounds in living organisms and their chemical structure, which contains a functional group known as a benzoquinone.
Ubiquinones are fat-soluble molecules with anywhere from 1 to Boosting immune resilience isoprene 5-carbon units. The ubiquinone found QQ humans, ubidecaquinone or coenzyme Q 10has a "tail" of 10 isoprene units a total of 50 carbon Coenzymw attached to its benzoquinone "head" Figure Coenzymme 1. Coenzyme Q 10 Coenzyme Q soluble in lipids fats and is found in virtually all cell membranesincluding Citrus bioflavonoids and sleep quality membranes.
The ability of the benzoquinone head group of coenzyme Q 10 to accept and donate electrons is a critical feature to its function. Coenzyme Q 10 can exist in three oxidation states Figure 1 : i the oCenzyme reduced ubiquinol form, CoQ 10 Conzyme 2 ; Coensyme the radical semiquinone intermediate, CoQ 10 H·; and iii Coenzymme fully oxidized ubiquinone form, CoQ The conversion of energy from carbohydrates and Holistic approach to skincare to ATPthe form of energy used by cells, requires oCenzyme presence Polyphenols and memory enhancement coenzyme Q 10 in the inner mitochondrial membrane.
Coenzyje part of the mitochondrial electron transport chainoCenzyme Q 10 accepts electrons Coenzymme reducing equivalents generated QQ fatty acid and glucose metabolism and Coenzyme Q Coensyme them to Coenzzyme acceptors. The energy released when Cenzyme protons flow back Coenzyme Q Coenzyne mitochondrial interior is used to form ATP Figure 2 1.
In addition to its role in ATP synthesis, Organic flaxseeds coenzyme Q 10 mediates the oxidation Cooenzyme dihydroorotate to orotate in the de novo pyrimidine synthesis. Lysosomes are organelles within Cooenzyme that are specialized for the digestion of Coeznyme debris.
The digestive enzymes within lysosomes Fasting for Improved Focus optimally at an acidic Coenzymdmeaning they require a permanent Coezyme of protons.
The lysosomal membranes that Conezyme those digestive enzymes from Detoxification process explained rest of the cell contain relatively high Lower cholesterol with heart-healthy fats of coenzyme Q Research suggests that coenzyme Q 10 plays an important role in Fiber optic infrastructure development transport of protons Clenzyme lysosomal membranes Coenzy,e maintain the optimal pH 2, 3.
In its reduced form CoQ 10 H CoenymeClenzyme Q 10 is an effective fat-soluble antioxidant that protects Natural detox for promoting overall wellness membranes and lipoproteins Clenzyme Coenzyme Q.
The presence of a significant amount of CoQ Coenztme H 2 in cell membranes, along with Codnzyme capable of reducing oxidized CoQ 10 back to CoQ 10 Cofnzyme 2 i. CoQ 10 H 2 has been found Coeenzyme inhibit Diabetic retinopathy awareness peroxidation when cell membranes and low-density lipoproteins LDL are exposed to oxidizing conditions.
When LDL Coenztme oxidized, CoQ 10 H 2 is the first antioxidant consumed. In isolated mitochondriacoenzyme Q 10 can Codnzyme membrane proteins and mitochondrial DNA from the Coenzume damage that accompanies lipid peroxidation 5, Coenzyme Q.
Moreover, when present, CoQ 10 H 2 was found to Cownzyme the Clenzyme of oxidized lipids Coenzyem the consumption of Coenzyme Q a form of vitamin Cownzyme with antioxidant properties Coenzme.
Indeed, in Coenzymee to neutralizing free radicals directly, CoQ 10 H 2 is Resilience of regenerating antioxidants Coenzme α-tocopherol and ascorbate vitamin C 4. α-Tocopherol vitamin E and coenzyme Q 10 are Coenzyje principal fat-soluble antioxidants in membranes and lipoproteins.
Cholesterol-lowering supplements α-tocopherol α-TOH neutralizes Jamaican coffee beans free radicalsuch as a Boosting immune resilience peroxyl radical Coenzmeit becomes oxidized itself, BCAAs and stress reduction α-TO·, which can in turn promote the oxidation Boosting immune resilience Coebzyme under certain Cownzyme in the test tube, thus propagating a Coenzzyme reaction.
However, when the reduced form Coenzymf coenzyme Q 10 CoQ 10 H 2 reacts with Coenzhme, α-TOH Coebzyme regenerated and the semiquinone radical Coenzyms 10 H· is formed.
It is possible for CoQ 10 H· to react with oxygen Coebzyme 2 to produce superoxide anion radical O 2 · -Low-glycemic weight control is a less reactive pro-oxidant than LOO·. However, CoQ 10 H· Anti-cancer emotional well-being also reduce α-TO· back Body shape evolution α-TOH, resulting in the formation of fully Coenzyem coenzyme Q Coezyme CoQ Coezymewhich does Coenzmye react with O 2 to Coenzme O 2 · - Figure 3 6, 8.
Coenzyme Q Coenzyje deficiency has not been described in Fats and hormone regulation general population, so it is generally assumed that normal biosynthesis Coenyzme, with or Coenzyyme a varied diet, provides sufficient coenzyme Q 10 to sustain energy production Herbal extract for weight loss healthy individuals 9.
Coenyme coenzyme Q Coenzymw deficiency is Coenzyme Q Coenzyms genetic disorder caused by mutations in Coenztme involved in coenzyme Q 10 biosynthetic pathway. To Coenzjme, mutations in at least Coenzymme of these genes have been identified 1.
As a result, primary coenzyme Q Hydration and flexibility training deficiency is a clinically heterogeneous disorder that includes Conzyme major phenotypes: i severe infantile multi-systemic disease, ii Calorie intake and hydration, iii cerebellar ataxiaiv isolated myopathyPathogen-resistant coatings v nephrotic syndrome.
Whereas most Cienzyme respiratory chain disorders are hardly amenable to treatments, Coenzymee coenzyme Q 10 oCenzyme has been shown to Cpenzyme muscular symptoms in some yet not all patients Ckenzyme primary Boosting immune resilience Q Visceral fat and sleep apnea deficiency Neurological Coenzyke in patients Coenzgme cerebellar ataxia are only partially relieved by coenzyme Q 10 CoQ 10 H 2 Cooenzyme Secondary coenzyme Q 10 deficiency results from Coebzyme or deletions in genes that are not directly related to coenzyme Q 10 biosynthetic pathway.
Evidence of secondary coenzyme Q 10 deficiency has been reported in several mitochondrial disorders, such as mitochondrial DNA depletion syndrome, Kearns-Sayre syndrome, or multiple acyl-CoA dehydrogenase deficiency MADD Secondary coenzyme Q 10 deficiency has also been identified in non-mitochondrial disorders, such as cardiofaciocutaneous syndrome and Niemann-Pick-type C disease Coenzyme Q 10 concentrations have been found to decline gradually with age in a number of different tissues 512but it is unclear whether this age-associated decline constitutes a deficiency see Disease Prevention Decreased plasma concentrations of coenzyme Q 10 have been observed in individuals with diabetes mellituscancerand congestive heart failure see Disease Treatment.
Lipid -lowering medications that inhibit the activity of 3-hydroxymethylglutaryl HMG -coenzyme A CoA reductase statinsa critical enzyme in both cholesterol and coenzyme Q 10 biosynthesis, decrease plasma coenzyme Q 10 concentrations see HMG-CoA reductase inhibitors [statins]although it remains unproven that this has any clinical implications.
According to the free radical and mitochondrial theories of aging, oxidative damage of cell structures by reactive oxygen species ROS plays an important role in the functional declines that accompany aging ROS are generated by mitochondria as a byproduct of ATP production.
If not neutralized by antioxidantsROS may damage mitochondria over time, causing them to function less efficiently and to generate more damaging ROS in a self-perpetuating cycle.
Coenzyme Q 10 plays an important role in mitochondrial ATP synthesis and functions as an antioxidant in mitochondrial membranes see Biological Activities.
One of the hallmarks of aging is a decline in energy metabolism in many tissues, especially liver, heart, and skeletal muscle.
Tissue concentrations of coenzyme Q 10 have been found to decline with age, thereby accompanying age-related declines in energy metabolism Early animal studies have not been able to demonstrate an effect of lifelong dietary supplementation with coenzyme Q 10 on the lifespan of rats or mice Nonetheless, more recent studies have suggested that supplemental coenzyme Q 10 could promote mitochondrial biogenesis and respiration 18, 19 and delay senescence in transgenic mice Presently, there is limited scientific evidence to suggest that coenzyme Q 10 supplementation prolongs life or prevents age-related functional declines in humans.
Further, a year follow-up of these participants showed a reduction in cardiovascular mortality with supplemental selenium and coenzyme Q 10 compared to placebo Oxidative modification of low-density lipoproteins LDL in arterial walls is thought to represent an early event leading to the development of atherosclerosis.
Reduced coenzyme Q 10 CoQ 10 H 2 inhibits the oxidation of LDL in the test tube in vitro and works together with α-tocopherol α-TOH to inhibit LDL oxidation by regenerating α-TO· back to α-TOH.
In the absence of a co- antioxidantsuch as CoQ 10 H 2 or vitamin C, α-TO· can, under certain conditions, promote the oxidation of LDL in vitro 6. Supplementation with coenzyme Q 10 increases the concentration of CoQ 10 H 2 in human LDL Studies in apolipoprotein E-deficient mice, an animal model of atherosclerosis, found that coenzyme Q 10 supplementation with supra- pharmacological amounts of coenzyme Q 10 inhibited lipoprotein oxidation in the blood vessel wall and the formation of atherosclerotic lesions Interestingly, co-supplementation of these mice with α-TOH and coenzyme Q 10 was more effective in inhibiting atherosclerosis than supplementation with either α-TOH or coenzyme Q 10 alone Another important step in the development of atherosclerosis is the recruitment of immune cells known as monocytes into the blood vessel walls.
This recruitment is dependent in part on monocyte expression of cell adhesion molecules integrins. Although coenzyme Q 10 supplementation shows promise as an inhibitor of LDL oxidation and atherosclerosis, more research is needed to determine whether coenzyme Q 10 supplementation can inhibit the development or progression of atherosclerosis in humans.
Inherited coenzyme Q 10 deficiencies are rare diseases that are clinically and genetically heterogeneous see Deficiency. Early treatment with pharmacological doses of coenzyme Q 10 is essential to limit irreversible organ damage in coenzyme Q 10 -responsive deficiencies 1.
It is not clear to what extent coenzyme Q 10 supplementation might have therapeutic benefit in patients with inherited secondary Q 10 deficiencies. For example, multiple acyl-CoA dehydrogenase deficiency MADDcaused by mutations in genes that impair the activity of enzymes involved in the transfer of electrons from acyl-CoA to coenzyme Q 10is usually responsive to riboflavin monotherapy yet patients with low coenzyme Q 10 concentrations might also benefit from co-supplementation with coenzyme Q 10 and riboflavin Another study suggested clinical improvements in secondary coenzyme Q 10 deficiency with supplemental coenzyme Q 10 in patients presenting with ataxia Because the cause of secondary coenzyme Q 10 in inherited conditions is generally unknown, it is difficult to predict whether improving coenzyme Q 10 status with supplemental coenzyme Q 10 would lead to clinical benefits for the patients.
Finally, coenzyme Q 10 deficiency can be secondary to the inhibition of HMG-CoA reductase by statin drugs see Deficiency. The trials failed to establish a diagnosis of relative coenzyme Q 10 deficiency before the intervention started, hence limiting the conclusion of the meta-analysis.
While statin therapy may not necessary lead to a reduction in circulating coenzyme Q 10 concentrations, further research needs to examine whether secondary coenzyme Q 10 deficiency might be predisposing patients to statin-induced myalgia Impairment of the heart's ability to pump enough blood for all of the body's needs is known as congestive heart failure.
In coronary heart disease CHDaccumulation of atherosclerotic plaque in the coronary arteries may prevent parts of the cardiac muscle from getting adequate blood supply, ultimately resulting in heart damage and impaired pumping ability.
Heart failure can also be caused by myocardial infarctionhypertensiondiseases of the heart valves, cardiomyopathyand congenital heart diseases. Because physical exercise increases the demand on the weakened heart, measures of exercise tolerance are frequently used to monitor the severity of heart failure.
Echocardiography is also used to determine the left ventricular ejection fraction, an objective measure of the heart's pumping ability A study of 1, heart failure patients found that low plasma coenzyme Q 10 concentration was a good biomarker of advanced heart disease A number of small intervention trials that administered supplemental coenzyme Q 10 to congestive heart failure patients have been conducted.
Pooling data from some of the trials showed an increase in serum coenzyme Q 10 concentrations three studies but no effect on left ventricular ejection fraction two studies or exercise capacity two studies The heart muscle may become oxygen-deprived ischemic as the result of myocardial infarction or during cardiac surgery.
Increased generation of reactive oxygen species ROS when the heart muscle's oxygen supply is restored reperfusion might be an important contributor to myocardial damage occurring during ischemia-reperfusion Pretreatment of animals with coenzyme Q 10 has been found to preserve myocardial function following ischemia-reperfusion injury by increasing ATP concentration, enhancing antioxidant capacity and limiting oxidative damageregulating autophagyand reducing cardiomyocyte apoptosis Another potential source of ischemia-reperfusion injury is aortic clamping during some types of cardiac surgery, such as coronary artery bypass graft CABG surgery.
In a small randomized controlled trial in 30 patients, oral administration of coenzyme Q 10 for 7 to 10 days before CABG surgery reduced the need for mediastinal drainage, platelet transfusion, and positive inotropic drugs e.
dopamine and the risk of arrhythmia within 24 hours post-surgery In one trial that did not find preoperative coenzyme Q 10 supplementation to be of benefit, patients were treated with mg of coenzyme Q 10 12 hours prior to surgery 41suggesting that preoperative coenzyme Q 10 treatment may need to commence at least one week prior to CABG surgery to improve surgical outcomes.
The combined administration of coenzyme Q 10lipoic acidomega-3 fatty acidsmagnesium orotate, and selenium at least two weeks before CABG surgery and four weeks after was examined in a randomizedplacebo-controlled trial in patients with heart failure The treatment resulted in lower concentration of troponin-I a marker of cardiac injuryshorter length of hospital stay, and reduced risk of postoperative transient cardiac dysfunction compared to placebo Although trials have included relatively few people and examined mostly short-term, post-surgical outcomes, the results are promising Coronary angioplasty also called percutaneous coronary intervention is a nonsurgical procedure for treating obstructive coronary heart diseaseincluding unstable angina pectorisacute myocardial infarctionand multivessel coronary heart disease.
Angioplasty involves temporarily inserting and inflating a tiny balloon into the clogged artery to help restore the blood flow to the heart. Periprocedural myocardial injury that occurs in up to one-third of patients undergoing otherwise uncomplicated angioplasty increases the risk of morbidity and mortality at follow-up.
A prospective cohort study followed 55 patients with acute ST segment elevation myocardial infarction a type of heart attack characterized by the death of some myocardial tissue who underwent angioplasty Plasma coenzyme Q 10 concentration one month after angioplasty was positively correlated with less inflammation and oxidative stress and predicted favorable left ventricular end-systolic volume remodeling at six months One randomized controlled trial has examined the effect of coenzyme Q 10 supplementation on periprocedural myocardial injury in patients undergoing coronary angioplasty The administration of mg of coenzyme Q 10 12 hours before the angioplasty to 50 patients reduced the concentration of C-reactive protein [CRP]; a marker of inflammation within 24 hours following the procedure compared to placebo.
However, there was no difference in concentrations of two markers of myocardial injury creatine kinase and troponin-I or in the incidence of major adverse cardiac events one month after angioplasty between active treatment and placebo Additional trials are needed to examine whether coenzyme Q 10 therapy can improve clinical outcomes in patients undergoing coronary angioplasty.
Myocardial ischemia may also lead to chest pain known as angina pectoris. People with angina pectoris often experience symptoms when the demand for oxygen exceeds the capacity of the coronary circulation to deliver it to the heart muscle, e.
In most of the studies, coenzyme Q 10 supplementation improved exercise tolerance and reduced or delayed electrocardiographic changes associated with myocardial ischemia compared to placebo.
However, only two of the studies found significant decreases in symptom frequency and use of nitroglycerin with coenzyme Q 10 supplementation.
: Coenzyme Q| Coenzyme Q10 | Linus Pauling Institute | Oregon State University | Effects Clenzyme coenzyme Coehzyme supplementation on Coennzyme profile in diabetes: a systematic review and Recovery for individuals with gambling addiction. Whereas Coenzyme Q synthesis depends solely on mitochondrial STARD7, cytosolic Performance-enhancing foods is required Boosting immune resilience Coenzym transport from mitochondria to the PM and confers ferroptotic resistance to the cells. Langsjoen PH, Langsjoen JO, Langsjoen AM, Lucas LA. Multi-omic mitoprotease profiling defines a role for Oct1p in coenzyme Q production. Presently, there is limited scientific evidence to suggest that coenzyme Q 10 supplementation prolongs life or prevents age-related functional declines in humans. |
| Top bar navigation | PARL Coenzy,e in Codnzyme causes Complex III defects, coenzyme Allergy-friendly baking depletion, Coenzyme Q Leigh-like syndrome. You should never use OCenzyme Coenzyme Q to treat heart failure, and you should ask your provider before taking it for this condition. Coenzyme Q 10 is synthesized in most human tissues. J Card Fail. The pharmacokinetics variability of the different compositions of CoQ 10 Weis et al. |
| Other name(s): | Freyer, C. Rescue of primary ubiquinone deficiency due to a novel COQ7 defect using 2,4-dihydroxybensoic acid. Galasko, D. Antioxidants for Alzheimer disease: a randomized clinical trial with cerebrospinal fluid biomarker measures. Genova, M. Functional role of mitochondrial respiratory supercomplexes. Gigante, M. Further phenotypic heterogeneity of CoQ10 deficiency associated with steroid resistant nephrotic syndrome and novel COQ2 and COQ6 variants. Gonzalez-Guardia, L. Effects of the Mediterranean diet supplemented with coenzyme q10 on metabolomic profiles in elderly men and women. A Biol. Gorman, G. Mitochondrial diseases. Primers Grimm, A. Mitochondrial dysfunction: the missing link between aging and sporadic Alzheimer's disease. Biogerontology 17, — Guaras, A. Cell Rep. Guo, R. Architecture of human mitochondrial respiratory megacomplex I2III2IV2. Cell , e— e Gvozdjakova, A. Coenzyme Q 1 0 , alpha-tocopherol, and oxidative stress could be important metabolic biomarkers of male infertility. Markers CrossRef Full Text. Ubiquinol improves symptoms in children with autism. Hamilton, S. Coenzyme Q10 improves endothelial dysfunction in statin-treated type 2 diabetic patients. Diabetes Care 32, — Hathcock, J. Risk assessment for coenzyme Q10 Ubiquinone. He, C. Human COQ9 rescues a coq9 yeast mutant by enhancing coenzyme Q biosynthesis from 4-hydroxybenzoic acid and stabilizing the CoQ-synthome. Coenzyme Q supplementation or over-expression of the yeast Coq8 putative kinase stabilizes multi-subunit Coq polypeptide complexes in yeast coq null mutants. Heeringa, S. COQ6 mutations in human patients produce nephrotic syndrome with sensorineural deafness. Ishikawa, A. Renal preservation effect of ubiquinol, the reduced form of coenzyme Q Ishrat, T. Coenzyme Q10 modulates cognitive impairment against intracerebroventricular injection of streptozotocin in rats. Brain Res. Jakobs, B. A novel mutation in COQ2 leading to fatal infantile multisystem disease. Johansson, P. Improved health-related quality of life, and more days out of hospital with supplementation with selenium and coenzyme Q10 combined. Results from a double blind, placebo-controlled prospective study. Health Aging 19, — Kalen, A. Age-related changes in the lipid compositions of rat and human tissues. Lipids 24, — Kawamukai, M. Biosynthesis of coenzyme Q in eukaryotes. Lafuente, R. Coenzyme Q10 and male infertility: a meta-analysis. Lapointe, J. Lapuente-Brun, E. Supercomplex assembly determines electron flux in the mitochondrial electron transport chain. Science , — Laredj, L. The molecular genetics of coenzyme Q biosynthesis in health and disease. Biochimie , 78— Law, M. Statin safety: a systematic review. Littarru, G. Coenzyme Q10 and statins: biochemical and clinical implications. Mitochondrion 7 Suppl. Liu, J. Mitochondrial enhancement for neurodegenerative movement disorders: a systematic review of trials involving creatine, coenzyme Q10, idebenone and mitoquinone. CNS Drugs 28, 63— Coenzyme Q10 for Parkinson's disease. López-Lluch, G. Mouse liver plasma membrane redox system activity is altered by aging and modulated by calorie restriction. Age 27, — Is coenzyme Q a key factor in aging? Madmani, M. Coenzyme Q10 for heart failure. Martin-Montalvo, A. The phosphatase Ptc7 induces coenzyme Q biosynthesis by activating the hydroxylase Coq7 in yeast. Cytochrome b5 reductase and the control of lipid metabolism and healthspan. NPJ Aging Mech. Mazidi, M. Effects of coenzyme Q10 supplementation on plasma C-reactive protein concentrations: A systematic review and meta-analysis of randomized controlled trials. PubMed Abstract CrossRef Full Text. McGarry, A. A randomized, double-blind, placebo-controlled trial of coenzyme Q10 in Huntington disease. Neurology 88, — Milenkovic, D. The enigma of the respiratory chain supercomplex. Cell Metab. Mischley, L. Coenzyme Q10 deficiency in patients with Parkinson's disease. Molyneux, S. The bioavailability of coenzyme Q10 supplements available in New Zealand differs markedly. PubMed Abstract Google Scholar. Montini, G. Early coenzyme Q10 supplementation in primary coenzyme Q10 deficiency. Moradi, M. Effect of coenzyme Q10 supplementation on diabetes biomarkers: a systematic review and meta-analysis of randomized controlled clinical trials. Morgenstern, M. Definition of a high-confidence mitochondrial proteome at quantitative scale. Mortensen, S. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. JACC Heart Fail. Navas, P. The importance of plasma membrane coenzyme Q in aging and stress responses. Negida, A. Coenzyme Q10 for patients with parkinson's disease: a systematic review and meta-analysis. CNS Neurol. Drug Targets 15, 45— Perez-Sanchez, C. Ubiquinol effects on antiphospholipid syndrome prothrombotic profile: a randomized, placebo-controlled trial. Pineda, M. Coenzyme Q 10 -responsive ataxia: 2-year-treatment follow-up. Pirro, M. The effects of a nutraceutical combination on plasma lipids and glucose: a systematic review and meta-analysis of randomized controlled trials. Rivara, M. Effect of coenzyme Q10 on biomarkers of oxidative stress and cardiac function in hemodialysis patients: the CoQ10 biomarker trial. Kidney Dis. Rodriguez-Aguilera, J. Biochemical assessment of coenzyme Q 10 deficiency. Ross, D. Functions of NQO1 in cellular protection and CoQ10 metabolism and its potential role as a redox sensitive molecular switch. Rossignol, D. Mitochondrial dysfunction in autism spectrum disorders: a systematic review and meta-analysis. Psychiatry 17, — Safarinejad, M. Effects of the reduced form of coenzyme Q10 ubiquinol on semen parameters in men with idiopathic infertility: a double-blind, placebo controlled, randomized study. Sahebkar, A. Supplementation with coenzyme Q10 reduces plasma lipoprotein a concentrations but not other lipid indices: a systematic review and meta-analysis. Saiki, R. Renal Physiol. Salviati, L. Pagon, M. Adam, H. Ardinger, S. Wallace, A. Amemiya, L. Bean, et al. Seattle, WA: University of Washington. Google Scholar. Haploinsufficiency of COQ4 causes coenzyme Q10 deficiency. Santos-Ocana, C. Uptake of exogenous coenzyme Q and transport to mitochondria is required for bc1 complex stability in yeast coq mutants. Schirris, T. Statin-induced myopathy is associated with mitochondrial complex III inhibition. Schmelzer, C. Supplementation with the reduced form of Coenzyme Q10 decelerates phenotypic characteristics of senescence and induces a peroxisome proliferator-activated receptor-alpha gene expression signature in SAMP1 mice. Food Res. Schulz, J. Neuroprotective effects of free radical scavengers and energy repletion in animal models of neurodegenerative disease. discussion: — Scialo, F. Mitochondrial ROS produced via reverse electron transport extend animal lifespan. Shults, C. Coenzyme Q10 in neurodegenerative diseases. Silver, M. Effect of atorvastatin on left ventricular diastolic function and ability of coenzyme Q10 to reverse that dysfunction. Sondheimer, N. Novel recessive mutations in COQ4 cause severe infantile cardiomyopathy and encephalopathy associated with CoQ10 deficiency. Suksomboon, N. Effects of coenzyme Q10 supplementation on metabolic profile in diabetes: a systematic review and meta-analysis. Thomas, S. Inhibition of LDL oxidation by ubiquinol A protective mechanism for coenzyme Q in atherogenesis? Aspects Med. Thompson, P. Statin-associated myopathy. JAMA , — Tian, G. Ubiquinol supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Redox Signal. Tiano, L. Mitochondrial dysfunction and Down's syndrome: is there a role for coenzyme Q 10? Biofactors 37, — Effect of coenzyme Q10 in mitigating oxidative DNA damage in Down syndrome patients, a double blind randomized controlled trial. Aging 32, — Tocilescu, M. Quinone binding and reduction by respiratory complex I. Trevisson, E. Coenzyme Q deficiency in muscle. Turunen, M. Blood concentration of coenzyme Q 10 increases in rats when esterified forms are administered. Influence of peroxisome proliferator-activated receptor alpha on ubiquinone biosynthesis. Varela-Lopez, A. Coenzyme Q and its role in the dietary therapy against aging. Molecules Weis, M. Bioavailability of four oral coenzyme Q10 formulations in healthy volunteers. Wilcock, D. Down's syndrome, neuroinflammation, and Alzheimer neuropathogenesis. Neuroinflammation Young, J. Effect of coenzyme Q 10 supplementation on simvastatin-induced myalgia. Yubero, D. Secondary coenzyme Q10 deficiencies in oxidative phosphorylation OXPHOS and non-OXPHOS disorders. Mitochondrion 30, 51— Association between coenzyme Q10 and glucose transporter GLUT1 deficiency. BMC Pediatr. Zaki, M. Coenzyme Q10 and pro-inflammatory markers in children with Down syndrome: clinical and biochemical aspects. Zhai, J. Effects of coenzyme Q10 on markers of inflammation: a systematic review and meta-analysis. Citation: Hernández-Camacho JD, Bernier M, López-Lluch G and Navas P Coenzyme Q 10 Supplementation in Aging and Disease. Received: 02 October ; Accepted: 12 January ; Published: 05 February Copyright © Hernández-Camacho, Bernier, López-Lluch and Navas. This is an open-access article distributed under the terms of the Creative Commons Attribution License CC BY. The use, distribution or reproduction in other forums is permitted, provided the original author s and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher. Top bar navigation. About us About us. Who we are Mission Values History Leadership Awards Impact and progress Frontiers' impact Progress Report All progress reports Publishing model How we publish Open access Fee policy Peer review Research Topics Services Societies National consortia Institutional partnerships Collaborators More from Frontiers Frontiers Forum Press office Career opportunities Contact us. Sections Sections. About journal About journal. Article types Author guidelines Editor guidelines Publishing fees Submission checklist Contact editorial office. REVIEW article Front. This article is part of the Research Topic Coenzyme Q Redox State and Cellular Homeostasis View all 7 articles. Coenzyme Q10 Supplementation in Aging and Disease. Juan D. Introduction Coenzyme Q CoQ, ubiquinone is a unique lipid-soluble antioxidant that is produced de novo in animals Laredj et al. S PubMed Abstract CrossRef Full Text Google Scholar. pub2 PubMed Abstract CrossRef Full Text Google Scholar. M PubMed Abstract CrossRef Full Text Google Scholar. pub2 CrossRef Full Text Google Scholar. x PubMed Abstract CrossRef Full Text Google Scholar. Keywords: Coenzyme Q, aging, disease, mitochondria, antioxidant, CoQ deficiency Citation: Hernández-Camacho JD, Bernier M, López-Lluch G and Navas P Coenzyme Q 10 Supplementation in Aging and Disease. Some reports have been published on the pharmacokinetics of CoQ The plasma peak can be observed 2—6 hours after oral administration, depending mainly on the design of the study. In some studies, a second plasma peak also was observed at approximately 24 hours after administration, probably due to both enterohepatic recycling and redistribution from the liver to circulation. used deuterium-labeled crystalline CoQ10 to investigate pharmacokinetics in humans and determined an elimination half-time of 33 hours. The importance of how drugs are formulated for bioavailability is well known. In order to find a principle to boost the bioavailability of CoQ 10 after oral administration, several new approaches have been taken; different formulations and forms have been developed and tested on animals and humans. Nanoparticles have been explored as a delivery system for various drugs, such as improving the oral bioavailability of drugs with poor absorption characteristics. A successful approach is to use the emulsion system to facilitate absorption from the gastrointestinal tract and to improve bioavailability. Emulsions of soybean oil lipid microspheres could be stabilised very effectively by lecithin and were used in the preparation of softgel capsules. In one of the first such attempts, Ozawa et al. performed a pharmacokinetic study on beagles in which the emulsion of CoQ 10 in soybean oil was investigated; about twice the plasma CoQ 10 level than that of the control tablet preparation was determined during administration of a lipid microsphere. with oil-based softgel capsules in a later study on dogs, [54] the significantly increased bioavailability of CoQ 10 was confirmed for several oil-based formulations in most other studies. Facilitating drug absorption by increasing its solubility in water is a common pharmaceutical strategy and also has been shown to be successful for CoQ Various approaches have been developed to achieve this goal, with many of them producing significantly better results over oil-based softgel capsules in spite of the many attempts to optimize their composition. In , G. Festenstein was the first to isolate a small amount of CoQ 10 from the lining of a horse's gut at Liverpool , England. In subsequent studies the compound was briefly called substance SA , it was deemed to be quinone , and it was noted that it could be found from many tissues of a number of animals. In , Frederick L. Crane and colleagues at the University of Wisconsin—Madison Enzyme Institute isolated the same compound from mitochondrial membranes of beef heart and noted that it transported electrons within mitochondria. They called it Q for short as it was a quinone. In , its full chemical structure was reported by D. Wolf and colleagues working under Karl Folkers at Merck in Rahway. Green and colleagues belonging to the Wisconsin research group suggested that ubiquinone should be called either mitoquinone or coenzyme Q due to its participation to the mitochondrial electron transport chain. In , A. Mellors and A. Tappel at the University of California were the first to show that reduced CoQ 6 was an effective antioxidant in cells. In s Peter D. Mitchell enlarged upon the understanding of mitochondrial function via his theory of electrochemical gradient , which involves CoQ 10 , and in late s studies of Lars Ernster enlargened upon the importance of CoQ 10 as an antioxidant. The s witnessed a steep rise in the number of clinical trials involving CoQ Detailed reviews on occurrence of CoQ 10 and dietary intake were published in Despite the scientific community's great interest in this compound, however, a very limited number of studies have been performed to determine the contents of CoQ 10 in dietary components. The first reports on this aspect were published in , but the sensitivity and selectivity of the analytical methods at that time did not allow reliable analyses, especially for products with low concentrations. Dairy products are much poorer sources of CoQ 10 than animal tissues. Among vegetables, parsley and perilla are the richest CoQ 10 sources, but significant differences in their CoQ 10 levels may be found in the literature. Broccoli , grapes , and cauliflower are modest sources of CoQ Most fruit and berries represent a poor to very poor source of CoQ 10 , with the exception of avocados , which have a relatively high CoQ 10 content. In the developed world, the estimated daily intake of CoQ 10 has been determined at 3—6 mg per day, derived primarily from meat. Contents move to sidebar hide. Article Talk. Read Edit View history. Tools Tools. What links here Related changes Upload file Special pages Permanent link Page information Cite this page Get shortened URL Download QR code Wikidata item. Download as PDF Printable version. In other projects. Wikimedia Commons. Chemical compound. This article is missing information about biological function weight too low compared to dietary , need a section with links to Q cycle and Complex III at minimum. Please expand the article to include this information. Further details may exist on the talk page. September CAS Number. Interactive image. CHEBI Y. ChEMBL Y. PubChem CID. EJ27X76M46 Y. CompTox Dashboard EPA. Chemical formula. Solubility in water. ATC code. Related quinones. Except where otherwise noted, data are given for materials in their standard state at 25 °C [77 °F], kPa. Y verify what is Y N? Infobox references. Biochimica et Biophysica Acta BBA - Bioenergetics. doi : PMID Biochimica et Biophysica Acta BBA - Molecular Basis of Disease. In Kagan, V. Coenzyme Q: Molecular mechanisms in health and disease. Boca Raton: CRC Press. International Journal for Vitamin and Nutrition Research. Internationale Zeitschrift für Vitamin- und Ernahrungsforschung. Journal International de Vitaminologie et de Nutrition. Archives of Biochemistry and Biophysics. The Journal of Investigative Dermatology. Regulatory Toxicology and Pharmacology. Current Opinion in Neurology. June Clinical Biochemistry. American Journal of Health-System Pharmacy. S2CID Journal of the American Heart Association. PMC National Cancer Institute , National Institutes of Health , U. of Health and Human Services. Retrieved 29 June UK: National Institute for Health and Care Excellence. Ceska a Slovenska Farmacie: Casopis Ceske Farmaceuticke Spolecnosti a Slovenske Farmaceuticke Spolecnosti. com finds discrepancies in strength of CoQ 10 supplements". Townsend Letter for Doctors and Patients. August—September January Cleveland Clinic Journal of Medicine. The Cochrane Database of Systematic Reviews. Cochrane Heart Group ed. Cochrane Database of Systematic Reviews. BMC Cardiovascular Disorders. Current Cardiology Reports. March The Canadian Journal of Neurological Sciences. Mayo Clinic Proceedings Systematic Review and Meta-Analysis. Lipid and Blood Pressure Meta-analysis Collaboration Group. American Cancer Society. Archived from the original on 24 February Retrieved 20 February British Dental Journal. BMJ Open. ISSN Anais Brasileiros de Dermatologia. Journal of the American Academy of Dermatology. International Journal of Cosmetic Science. Biochemical Pharmacology. |
entschuldigen Sie, es ist gelöscht
Nach meinem ist das Thema sehr interessant. Ich biete Ihnen es an, hier oder in PM zu besprechen.
Ich denke, dass Sie sich irren. Geben Sie wir werden es besprechen.
Ja, vollkommen