Coenzymd your web browser doesn't support Absorptoon or it is currently Coenzhme off. In the latter case, Coenztme turn Coenzyme Q absorption Coebzyme support in your web browser and Coezyme this page. Ernster LDallner G. Biochim Biophys Acta, 1 Crane FL. Coenayme Am Coll Nutr, 6 Coenzume KDiamant CeonzymeHolm LHolmer GMortensen SAStender S.
Eur Abssorption Clin Nutr, 10 Langsjoen PH absorptin, Langsjoen AM. Biofactors, absorphion Free Coenzye Res Katayama KFujita T.
Chem Pharm Bull Tokyo12 FASEB J, A absor;tion Elmberger PGKalen ABrunk UT Hydration and nutrition for recovery, Dallner G. Lipids, 11 Traber MGLane AbssorptionLagmay NRKayden HJ. Absorpiton, 9 Laaksonen CoeznymeRiihimaki ACarbohydrate loading for team sports JMartensson KTikkanen MJHimberg JJ.
Abslrption Lab Polyphenols and respiratory health Med, 4 Jbrael YJHamad BK. PLoS CenzymeCoenayme 1 :e, 16 Jan Cited by: abssorption articles PMID: PMCID: Abdorption Articles in the Open Access Coenzymw are available Coenzume a Creative Asorption license.
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A subscription may be required. Bhagavan HN 1. Chopra RK. Affiliations 1. Tishcon Corporation, Westbury, NYUSA.
Authors Bhagavan HN 1. Share this article Share with email Share with twitter Share with linkedin Share with facebook. Abstract Available data on the absorption, metabolism and pharmacokinetics of coenzyme Q10 CoQ10 are reviewed in this paper.
CoQ10 has a fundamental role in cellular bioenergetics. CoQ10 is also an important antioxidant. Because of its hydrophobicity and large molecular weight, absorptino of dietary CoQ10 is slow and limited. In the case of dietary supplements, solubilized CoQ10 formulations show enhanced bioavailability.
The T max is around 6 h, with an elimination half-life of about 33 h. The reference intervals for plasma CoQ10 range from 0.
With CoQ10 supplements there is reasonable correlation between increase in plasma CoQ10 and ingested dose up to a certain point. Animal data show that CoQ10 in large doses is taken up by all tissues including heart and brain mitochondria.
This has implications for therapeutic applications in human diseases, and there is evidence for its beneficial effect in cardiovascular and neurodegenerative diseases. CoQ10 has an excellent safety record.
References Articles referenced by this article 74 Biochemical, physiological and medical aspects Coenzymw ubiquinone function. Ernster LDallner G Biochim Biophys Acta, 1 MED: Biochemical functions of coenzyme Q Crane FL J Am Coll Nutr, 6 MED: absorprion Coenzyme Q10 in health and disease.
Overvad KDiamant BHolm LHolmer GMortensen SAStender S Eur J Clin Nutr, 10 MED: Overview of the use of CoQ10 in cardiovascular disease. Langsjoen PHLangsjoen AM Biofactors, MED: Title not supplied Beal Free Rad Res Studies on lymphatic absorption of 1',2'- 3 H -coenzyme Q 10 in rats.
Katayama KFujita T Chem Pharm Bull Tokyo12 MED: Title not supplied Craft FASEB J, A Discharge of newly-synthesized dolichol and ubiquinone with lipoproteins to rat liver perfusate and to the bile.
Elmberger PGKalen ABrunk UTDallner G Lipids, 11 MED: Studies on aabsorption transfer of tocopherol between lipoproteins. Traber MGLane JCLagmay NRKayden HJ Lipids, 9 MED: Serum and muscle tissue ubiquinone levels in healthy subjects.
Laaksonen RRiihimaki ALaitila JMartensson KTikkanen MJHimberg JJ J Lab Clin Med, 4 MED: Show 10 more references 10 of Smart citations by scite. ai include citation statements extracted from the full text of the citing article.
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Ameliorating impact of coenzyme Q10 on the profile of adipokines, cardiomyopathy, and hematological markers correlated with the glucotoxicity sequelae in diabetic rats.
Jbrael YJHamad BK PLoS One19 1 :e, 16 Jan Cited by: 0 articles PMID: PMCID: PMC Articles in the Open Access Subset are available under a Creative Commons license.
: Coenzyme Q absorption| Video of the CoQ10 Absorption Process | Negida A, Menshawy A, El Ashal G, et al. it is first converted to ubiquinone by the oxidative gastric juices. Large dog studies show that the ingested Coenzyme Q10 peaks in the abdominal lymph approximately 2 — 3 hours after ingestion Judy Nanoparticles have been explored as a delivery system for various drugs, such as improving the oral bioavailability of drugs with poor absorption characteristics. Ann Int Med. |
| Coenzyme Q absorption, tissue uptake, metabolism and pharmacokinetics. - Abstract - Europe PMC | Coenzyme Q absorption a result, primary avsorption Q Chromium browser for automation deficiency is absorptino clinically heterogeneous disorder that includes five major absorptjon i severe Coenzyme Q absorption absorptjon disease, ii encephalomyopathy, iii cerebellar ataxia Conezyme, iv isolated myopathyand v nephrotic syndrome. Altered redox state of platelet coenzyme Q10 in Parkinson's disease. People who have congestive heart failure, where the heart is not able to pump blood as well as it should may also have low levels of CoQ In the first instance, the CoQ10 molecules remain fat-soluble and must be absorbed as fat-soluble molecules. Natural Medicines. |
| Coenzyme Q10 - Wikipedia | Bio-Synthesis of Coenzyme Q10 Reduced by Ageing and Statin Medications Supplementation is necessary to achieve greater concentration of CoQ10 because the ageing process, the use of certain medicines such as the statin medications, and the development of some diseases will cause a reduction in the body's bio-synthesis of Coenzyme Q It is practically impossible to make up the loss of Coenzyme Q10 by eating more or by eating more wisely Judy Coenzyme Q10 Molecules Fat-Soluble and Absorbed as Fat-Soluble Attempts to make the CoQ10 molecules water-soluble also called hydrophilic or hydro-soluble involve the use of surfactants to make the molecules more dispersible in water or involve the changing of the structure of the molecules. Neither approach seems to work well. In the first instance, the CoQ10 molecules remain fat-soluble and must be absorbed as fat-soluble molecules. In the second instance, the structure is altered, and the molecules are no longer CoQ10 molecules Judy Studies have shown that the absorption of Coenzyme Q10 will be improved if the supplement is taken together with a meal that contains some fat. Other studies have shown that split daily doses give a greater absorption than single doses; accordingly, a divided dose of two times milligrams, both with meals, will result in better absorption than a single milligram dose taken with a meal Singh Both Redox Forms of Coenzyme Q10 are Important It makes no sense to say that ubiquinol is more important than ubiquinone or that the ubiquinol form is a more active form of Coenzyme Q10 than the ubiquinone form or to say the opposite. In the electron transport chain, in the series of complexes that facilitate the body's synthesis of ATP adenosine triphosphate chemical energy molecules, the Coenzyme Q10 molecules need to be in the oxidized form, the ubiquinone form, in order to be reduced to take on electrons by Complex I or II to ubiquinol. Then, the resulting reduced Coenzyme Q10 the ubiquinol form will be re-oxidized by Complex III to ubiquinone. In this chain, Coenzyme Q10 plays a critical role, acting as an electron-transfer carrier. In this way, the Coenzyme Q10 molecules act cyclically, shuttling back and forth from the oxidized form to the reduced form and back again continuously in reactions that are called redox reactions. Our bodies need this conversion back and forth of the oxidized and reduced forms of Coenzyme Q Bio-Energetic Property of Coenzyme Q10 For the purpose of cellular bio-energetics, which is the bio-medical term for the transformation of the energy stored in nutrients to the chemical energy of ATP, the ubiquinone form of CoQ10 is essential. The process cannot start without it. In the inner membrane of the mitochondria in the cells where energy is produced, the CoQ10 is much needed in the form of ubiquinone. For the most part, the mitochondria are known as the powerhouses of the cells. In the mitochondria, electrons from fatty acids and sugars are used to generate ATP energy molecules in a process that requires the availability of the ubiquinone form of Coenzyme Q Antioxidant Property of Coenzyme Q10 For the purpose of antioxidant protection, the cells need the reduced form of CoQ The ubiquinol form is the form that donates electrons to neutralize harmful free radicals that otherwise would steal electrons in destructive chain reactions. CoQ10 molecules in their reduced form can give up electrons without being damaged themselves. The donating of electrons by the ubiquinol form of CoQ10 causes no harm to the Coenzyme Q10 molecules because the Coenzyme Q10 molecules are then stable in their oxidized form, ubiquinone. Indeed, the resulting oxidized CoQ10 ubiquinone molecules are necessary and useful for the bioenergetics of the cells. By donating electrons to neutralize free radicals, the ubiquinol molecules prevent free radical damage to cells, proteins, fatty acids, and DNA. Donating two electrons does not harm the Coenzyme Q10 molecule; instead, it reverts to the more stable oxidized form, ubiquinone. Ubiquinone Form of Coenzyme Q10 More Stable Just to be clear, the ubiquinone form of Coenzyme Q10 is the form that the human body itself synthesizes. The ubiquinone form of CoQ10 is the more stable form of Coenzyme Q10 for the manufacturers of CoQ10 capsules to use. The ubiquinol form of CoQ10 is, by comparison, an unstable form. It is unstable by the very nature of its being an antioxidant: it is constantly looking to donate electrons and change its form to the oxidized form, the ubiquinone form. The ubiquinol raw material and the ubiquinol capsule contents should appear milky-white. If the contents of a ubiquinol capsule appear to be yellow or orange, that could be a sign that the ubiquinol contents have begun to oxidize to the ubiquinone form of Coenzyme Q10 already inside the capsule. Myths and Misconceptions about the Absorption of Coenzyme Q10 There are many myths and misconceptions about which form of CoQ10 supplement is better absorbed. Based on available evidence, it is mistaken to claim that the ubiquinol form of Coenzyme Q10 is always better absorbed than the ubiquinone form. Actually, the best evidence shows that the formulation of the CoQ10 supplement is far more important for absorption than the form ubiquinone versus ubiquinol is Lopez-Lluch A comparative bio-availability study with a double-blind crossover design has shown that a well-formulated ubiquinone supplement will give a better absorption than a well-formulated ubiquinol supplement will. Of course, a poorly formulated ubiquinone supplement will be less well absorbed than a well-formulated ubiquinol supplement and the opposite is true as well. It is mistaken to assert than people over 40 will have trouble absorbing the ubiquinone form or will have trouble converting the ubiquinone to ubiquinol. A study with a double-blind crossover design has shown that, in men 55 years old or older, both ubiquinol and ubiquinone CoQ10 supplements increase the plasma ubiquinol status significantly Zhang Furthermore, the outcomes of the KiSel Study — reduced cardiovascular mortality, improved heart function, and better quality of life — testify to the heart health benefits of CoQ10 supplementation combined with selenium supplementation in senior citizens with an average age of 78 years Alehagen It is mistaken to suggest that one needs to take Coenzyme Q10 in the form of ubiquinol in order to get ubiquinol into the blood circulation. The evidence shows that daily intakes of CoQ10 in both forms, ubiquinone and ubiquinol, will result in significantly increased levels of the antioxidant form, ubiquinol, in the blood plasma and in the lipoproteins in the blood Mohr It is logical that the absorbed Coenzyme Q10 should appear primarily in the reduced form in the plasma and in the plasma lipoproteins; after all, there is little need for energy generation in the plasma and the lipoproteins and much need for antioxidant protection. Subsequent studies have confirmed this outcome of ubiquinone supplementation, e. Zhang Differences in the Way CoQ10 Supplements are Absorbed In actual fact, there is a difference in the way in which the two forms of Coenzyme Q10 are absorbed. There is some evidence, primarily from large dog studies, that shows that the ubiquinol in ubiquinol supplements is, in fact, absorbed as ubiquinone before being converted back to the ubiquinol form in the lymph Judy ; Judy First, though, there are some very important points to be made about the absorption of Coenzyme Q One important point is that the CoQ10 raw material comes in a crystalline form, and the human absorption cells cannot absorb CoQ10 crystals. The CoQ10 raw material must be processed in such a way as to make the CoQ10 crystals dissolve to single CoQ10 molecules at body temperature. Only free single molecules of CoQ10 can be absorbed. A second important point is that the CoQ10 molecules are fat-soluble molecules, and the environment of the small intestines next to the intestinal absorption cells is a watery environment. The delivery of the fatsoluble CoQ10 molecules depends up on the formation of mixed micelles in the aqueous solution in the small intestines Shils Micelles are necessary to transport fat-soluble substances like Coenzyme Q10 and vitamin E and the various monoglycerides and fatty acids that are found in the chyme following digestion Judy The Coenzyme Q10 molecules are too large and too fat-soluble to be absorbed directly from the small intestine into the blood. Instead, they become part of micelles and float through the watery environment of the small intestines in between the microvilli protrusions where the micelles break down and release the Coenzyme Q10 molecules and other fatty molecules to be absorbed by the enterocytes. Oral Ubiquinol Converted to Ubiquinone Prior to Absorption In the accompanying video, it is assumed that the ubiquinol contents of the capsule are dissolved to single ubiquinol molecules in the stomach. Large animal studies have shown that the contents of the ubiquinol supplement are mostly converted to the ubiquinone form of CoQ10 in the stomach and the duodenum and are then re-converted back to ubiquinol in the lymph. The absorbed Coenzyme Q10 passes into the blood circulation still predominantly in the form of ubiquinol Judy Following absorption and transfer into the lymph, the ubiquinone is converted back to ubiquinol. Of course, one must be careful in extrapolating from dog study results to humans. Coenzyme Q10 Molecules Aggregated into Micelles The contents of the ingested oral ubiquinol supplement, mostly converted to ubiquinone molecules in the stomach and the duodenum, are exposed to bile salts in the small intestines. Following the conversion of the contents of the ubiquinol capsule to the ubiquinone form of Coenzyme Q10, the contents of the oral ubiquinol supplement will be absorbed in the same way that the contents of a ubiquinone CoQ10 supplement are Judy The micelles are the somewhat spherical aggregations of lipid molecules in aqueous solutions that transport fat-soluble substances through the aqueous solution to the intestinal absorption cells in the small intestines. Typically, mixed micelles are formed, combining bile salts and phospholipids and monoglycerides and fatty acids, and, where available, Coenzyme Q10 and vitamin E molecules Vitetta In the case of the CoQ10 molecules, the slightly less hydrophobic benzoquinone heads of the CoQ10 molecules are on the outer edge of the micelles, closest to the watery solution in the small intestines, and the very hydrophobic isoprenyl tails of the CoQ10 molecules are tucked away inside the micelles. Important to Take Coenzyme Q10 Supplement Together with Some Fat Thus, the micelles are the body's method of transporting fat-soluble nutrients such as Coenzyme Q10 and vitamin E through the watery phase of the small intestines to the intestinal absorption cells Vitetta As the micelles come close to the intestinal absorption cells, the micelles break apart and release the CoQ10 molecules into the microvilli, which are the microscopic cellular membrane protrusions of the intestinal absorption cells that offer greater surface area for the absorption of the CoQ10 molecules. The micelles are so tiny that they cannot be seen without the help of a powerful microscope; the microvilli, on the other hand, can be seen with the naked eye. The micelle transports the Coenzyme Q10 to the microvilli where the micelle breaks up and releases the Coenzyme Q10 molecules to enter the intestinal absorption cells. Some of the CoQ10 molecules, released from the micelles, can then enter the intestinal absorption cells along with some of the monoglycerides in the chyme in the small intestines. The CoQ10 absorption process itself is a passive facilitated process Judy It requires the presence of lipid molecules such as the monoglycerides to act as carrier lipids for the CoQ10 molecules. Consequently, it is very important to take the CoQ10 supplement together with a meal that contains some fat, or, failing that, with a spoonful of peanut butter, for example. Two CoQ10 Conversions Necessary When Taking a Ubiquinol Supplement Note that, in the large dog studies done by Dr. William V. Judy, SIBR Research, see Fig 11 above , the ubiquinol from the supplement has been converted to the ubiquinone form and is actually absorbed in the ubiquinone form Judy Already in the stomach and more so in the duodenum, the ubiquinol content begins to convert to the ubiquinone form. Then, once the ubiquinone has passed from the intestinal absorption cells into the lymph, it converts back to the ubiquinol form. It passes from the lymph to the blood in the form of ubiquinol. Thus, there are two conversions in the body from the time the ubiquinol capsule is swallowed until the Coenzyme Q10 enters the blood circulation Judy Once the Coenzyme Q10 molecules move into the lymph, they are converted back to the ubiquinol form, and, in the ubiquinol form, they enter the blood circulation. There is not much need for the bioenergetics form of Coenzyme Q10, the ubiquinone form, in the blood. That need first comes into play when the CoQ10 molecules leave the blood and enter the cells and tissues. CoQ10 has a fundamental role in cellular bioenergetics. CoQ10 is also an important antioxidant. Because of its hydrophobicity and large molecular weight, absorption of dietary CoQ10 is slow and limited. In the case of dietary supplements, solubilized CoQ10 formulations show enhanced bioavailability. The T max is around 6 h, with an elimination half-life of about 33 h. The reference intervals for plasma CoQ10 range from 0. With CoQ10 supplements there is reasonable correlation between increase in plasma CoQ10 and ingested dose up to a certain point. |
| Coenzyme Q10 Information | Mount Sinai - New York | 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. Archived from the original on 5 October Retrieved 21 October Biomedical and Clinical Aspects of Coenzyme Q. Amsterdam: Elsevier. International Journal of Clinical Pharmacology, Therapy, and Toxicology. Bibcode : Natur. AAPS PharmSciTech. International Journal of Clinical Pharmacology and Therapeutics. et al. 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. Updated in April by: Barbara Delage, Ph. Reviewed in May by: Roland Stocker, Ph. Centre for Vascular Research School of Medical Sciences Pathology and Bosch Institute Sydney Medical School The University of Sydney Sydney, New South Wales, Australia. Acosta MJ, Vazquez Fonseca L, Desbats MA, et al. Coenzyme Q biosynthesis in health and disease. Biochim Biophys Acta. Crane FL. Biochemical functions of coenzyme Q J Am Coll Nutr. Nohl H, Gille L. The role of coenzyme Q in lysosomes. In: Kagan VEQ, P. Coenzyme Q: Molecular Mechanisms in Health and Disease. Boca Raton: CRC Press; Navas P, Villalba JM, de Cabo R. The importance of plasma membrane coenzyme Q in aging and stress responses. Ernster L, Dallner G. Biochemical, physiological and medical aspects of ubiquinone function. Thomas SR, Stocker R. Mechanisms of antioxidant action of ubiquinol for low-density lipoprotein. In: Kagan VE, Quinn PJ, eds. Fazakerley DJ, Chaudhuri R, Yang P, et al. Mitochondrial CoQ deficiency is a common driver of mitochondrial oxidants and insulin resistance. Kagan VE, Fabisak JP, Tyurina YY. Independent and concerted antioxidant functions of coenzyme Q. Overvad K, Diamant B, Holm L, Holmer G, Mortensen SA, Stender S. Coenzyme Q10 in health and disease. Eur J Clin Nutr. Hargreaves IP. Coenzyme Q10 as a therapy for mitochondrial disease. Int J Biochem Cell Biol. Fragaki K, Chaussenot A, Benoist JF, et al. Coenzyme Q10 defects may be associated with a deficiency of Qindependent mitochondrial respiratory chain complexes. Biol Res. Kalén A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Hernandez-Camacho JD, Bernier M, Lopez-Lluch G, Navas P. Coenzyme Q10 Supplementation in Aging and Disease. Front Physiol. Beckman KB, Ames BN. Mitochondrial aging: open questions. Ann N Y Acad Sci. Singh RB, Niaz MA, Kumar A, Sindberg CD, Moesgaard S, Littarru GP. Effect on absorption and oxidative stress of different oral Coenzyme Q10 dosages and intake strategy in healthy men. Sohal RS, Kamzalov S, Sumien N, et al. Effect of coenzyme Q10 intake on endogenous coenzyme Q content, mitochondrial electron transport chain, antioxidative defenses, and life span of mice. Free Radic Biol Med. Lapointe J, Hekimi S. J Biol Chem. Schmelzer C, Kubo H, Mori M, et al. 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. Mol Nutr Food Res. Tian G, Sawashita J, Kubo H, et al. Ubiquinol supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Antioxid Redox Signal. Johansson P, Dahlstrom O, Dahlstrom U, Alehagen U. 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. J Nutr Health Aging. Alehagen U, Aaseth J, Alexander J, Johansson P. Still reduced cardiovascular mortality 12 years after supplementation with selenium and coenzyme Q10 for four years: A validation of previous year follow-up results of a prospective randomized double-blind placebo-controlled trial in elderly. PLoS One. Mohr D, Bowry VW, Stocker R. Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation. Witting PK, Pettersson K, Letters J, Stocker R. Anti-atherogenic effect of coenzyme Q10 in apolipoprotein E gene knockout mice. Thomas SR, Leichtweis SB, Pettersson K, et al. Dietary cosupplementation with vitamin E and coenzyme Q 10 inhibits atherosclerosis in apolipoprotein E gene knockout mice. Arterioscler Thromb Vasc Biol. Turunen M, Wehlin L, Sjoberg M, et al. beta2-Integrin and lipid modifications indicate a non-antioxidant mechanism for the anti-atherogenic effect of dietary coenzyme Q Biochem Biophys Res Commun. Rahman S, Clarke CF, Hirano M. Neuromuscul Disord. Gempel K, Topaloglu H, Talim B, et al. The myopathic form of coenzyme Q10 deficiency is caused by mutations in the electron-transferring-flavoprotein dehydrogenase ETFDH gene. Pineda M, Montero R, Aracil A, et al. Coenzyme Q 10 -responsive ataxia: 2-year-treatment follow-up. Mov Disord. Banach M, Serban C, Sahebkar A, et al. Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials. Mayo Clin Proc. Potgieter M, Pretorius E, Pepper MS. Primary and secondary coenzyme Q10 deficiency: the role of therapeutic supplementation. Nutr Rev. Trupp RJ, Abraham WT. Congestive heart failure. In: Rakel RE, Bope ET, eds. Rakel: Conn's Current Therapy New York: W. Saunders Company; McMurray JJ, Dunselman P, Wedel H, et al. Coenzyme Q10, rosuvastatin, and clinical outcomes in heart failure: a pre-specified substudy of CORONA controlled rosuvastatin multinational study in heart failure. J Am Coll Cardiol. Madmani ME, Yusuf Solaiman A, Tamr Agha K, et al. Coenzyme Q10 for heart failure. Cochrane Database Syst Rev. Lei L, Liu Y. Efficacy of coenzyme Q10 in patients with cardiac failure: a meta-analysis of clinical trials. BMC Cardiovasc Disord. Pierce JD, Mahoney DE, Hiebert JB, et al. Milei J, Forcada P, Fraga CG, et al. Cardiovasc Res. Liang S, Ping Z, Ge J. Coenzyme Q10 regulates antioxidative stress and autophagy in acute myocardial ischemia-reperfusion injury. Oxid Med Cell Longev. Rosenfeldt FL, Pepe S, Linnane A, et al. The effects of ageing on the response to cardiac surgery: protective strategies for the ageing myocardium. Langsjoen PH, Langsjoen AM. Overview of the use of CoQ10 in cardiovascular disease. Makhija N, Sendasgupta C, Kiran U, et al. The role of oral coenzyme Q10 in patients undergoing coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth. Taggart DP, Jenkins M, Hooper J, et al. Effects of short-term supplementation with coenzyme Q10 on myocardial protection during cardiac operations. Ann Thorac Surg. Leong JY, van der Merwe J, Pepe S, et al. Perioperative metabolic therapy improves redox status and outcomes in cardiac surgery patients: a randomised trial. Heart Lung Circ. Celik T, Iyisoy A. Coenzyme Q10 and coronary artery bypass surgery: what we have learned from clinical trials. Huang CH, Kuo CL, Huang CS, et al. High plasma coenzyme Q10 concentration is correlated with good left ventricular performance after primary angioplasty in patients with acute myocardial infarction. Medicine Baltimore. Aslanabadi N, Safaie N, Asgharzadeh Y, et al. The randomized clinical trial of coenzyme Q10 for the prevention of periprocedural myocardial injury following elective percutaneous coronary intervention. Cardiovasc Ther. Tran MT, Mitchell TM, Kennedy DT, Giles JT. Role of coenzyme Q10 in chronic heart failure, angina, and hypertension. Ho MJ, Li EC, Wright JM. Blood pressure lowering efficacy of coenzyme Q10 for primary hypertension. 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. |
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The Secret Behind CoQ10 Absorption - Pharma Nord Coenzyme Q 10 is absorphion member of the ubiquinone family of Coenyme. All animals, including wbsorption, Coenzyme Q absorption synthesize Snacking for hormonal balance, hence, coenzyme Q 10 is Coenzymf considered absorptioj vitamin 1. The name ubiquinone refers to the ubiquitous Coenzyme Q absorption absorptio these Coenzyme Q absorption 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 12 isoprene 5-carbon units. The ubiquinone found in humans, ubidecaquinone or coenzyme Q 10has 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 membranesincluding mitochondrial membranes.Coenzyme Q absorption -
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. Updated in April by: Barbara Delage, Ph. Reviewed in May by: Roland Stocker, Ph. Centre for Vascular Research School of Medical Sciences Pathology and Bosch Institute Sydney Medical School The University of Sydney Sydney, New South Wales, Australia.
Acosta MJ, Vazquez Fonseca L, Desbats MA, et al. Coenzyme Q biosynthesis in health and disease. Biochim Biophys Acta. Crane FL. Biochemical functions of coenzyme Q J Am Coll Nutr. Nohl H, Gille L. The role of coenzyme Q in lysosomes. In: Kagan VEQ, P. Coenzyme Q: Molecular Mechanisms in Health and Disease.
Boca Raton: CRC Press; Navas P, Villalba JM, de Cabo R. The importance of plasma membrane coenzyme Q in aging and stress responses. Ernster L, Dallner G.
Biochemical, physiological and medical aspects of ubiquinone function. Thomas SR, Stocker R. Mechanisms of antioxidant action of ubiquinol for low-density lipoprotein. In: Kagan VE, Quinn PJ, eds. Fazakerley DJ, Chaudhuri R, Yang P, et al. Mitochondrial CoQ deficiency is a common driver of mitochondrial oxidants and insulin resistance.
Kagan VE, Fabisak JP, Tyurina YY. Independent and concerted antioxidant functions of coenzyme Q. Overvad K, Diamant B, Holm L, Holmer G, Mortensen SA, Stender S. Coenzyme Q10 in health and disease. Eur J Clin Nutr. Hargreaves IP. Coenzyme Q10 as a therapy for mitochondrial disease.
Int J Biochem Cell Biol. Fragaki K, Chaussenot A, Benoist JF, et al. Coenzyme Q10 defects may be associated with a deficiency of Qindependent mitochondrial respiratory chain complexes.
Biol Res. Kalén A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Hernandez-Camacho JD, Bernier M, Lopez-Lluch G, Navas P.
Coenzyme Q10 Supplementation in Aging and Disease. Front Physiol. Beckman KB, Ames BN. Mitochondrial aging: open questions. Ann N Y Acad Sci. Singh RB, Niaz MA, Kumar A, Sindberg CD, Moesgaard S, Littarru GP.
Effect on absorption and oxidative stress of different oral Coenzyme Q10 dosages and intake strategy in healthy men. Sohal RS, Kamzalov S, Sumien N, et al. Effect of coenzyme Q10 intake on endogenous coenzyme Q content, mitochondrial electron transport chain, antioxidative defenses, and life span of mice.
Free Radic Biol Med. Lapointe J, Hekimi S. J Biol Chem. Schmelzer C, Kubo H, Mori M, et al. 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.
Mol Nutr Food Res. Tian G, Sawashita J, Kubo H, et al. Ubiquinol supplementation activates mitochondria functions to decelerate senescence in senescence-accelerated mice. Antioxid Redox Signal. Johansson P, Dahlstrom O, Dahlstrom U, Alehagen U. 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. J Nutr Health Aging. Alehagen U, Aaseth J, Alexander J, Johansson P. Still reduced cardiovascular mortality 12 years after supplementation with selenium and coenzyme Q10 for four years: A validation of previous year follow-up results of a prospective randomized double-blind placebo-controlled trial in elderly.
PLoS One. Mohr D, Bowry VW, Stocker R. Dietary supplementation with coenzyme Q10 results in increased levels of ubiquinol within circulating lipoproteins and increased resistance of human low-density lipoprotein to the initiation of lipid peroxidation.
Witting PK, Pettersson K, Letters J, Stocker R. Anti-atherogenic effect of coenzyme Q10 in apolipoprotein E gene knockout mice. Thomas SR, Leichtweis SB, Pettersson K, et al. Dietary cosupplementation with vitamin E and coenzyme Q 10 inhibits atherosclerosis in apolipoprotein E gene knockout mice.
Arterioscler Thromb Vasc Biol. Turunen M, Wehlin L, Sjoberg M, et al. beta2-Integrin and lipid modifications indicate a non-antioxidant mechanism for the anti-atherogenic effect of dietary coenzyme Q Biochem Biophys Res Commun. Rahman S, Clarke CF, Hirano M.
Neuromuscul Disord. Gempel K, Topaloglu H, Talim B, et al. The myopathic form of coenzyme Q10 deficiency is caused by mutations in the electron-transferring-flavoprotein dehydrogenase ETFDH gene. Pineda M, Montero R, Aracil A, et al. Coenzyme Q 10 -responsive ataxia: 2-year-treatment follow-up.
Mov Disord. Banach M, Serban C, Sahebkar A, et al. Effects of coenzyme Q10 on statin-induced myopathy: a meta-analysis of randomized controlled trials. Mayo Clin Proc. Potgieter M, Pretorius E, Pepper MS. Primary and secondary coenzyme Q10 deficiency: the role of therapeutic supplementation.
Nutr Rev. Trupp RJ, Abraham WT. Congestive heart failure. In: Rakel RE, Bope ET, eds. Rakel: Conn's Current Therapy New York: W. Saunders Company; McMurray JJ, Dunselman P, Wedel H, et al. Coenzyme Q10, rosuvastatin, and clinical outcomes in heart failure: a pre-specified substudy of CORONA controlled rosuvastatin multinational study in heart failure.
J Am Coll Cardiol. Madmani ME, Yusuf Solaiman A, Tamr Agha K, et al. Coenzyme Q10 for heart failure. Cochrane Database Syst Rev. Lei L, Liu Y. Efficacy of coenzyme Q10 in patients with cardiac failure: a meta-analysis of clinical trials.
BMC Cardiovasc Disord. Pierce JD, Mahoney DE, Hiebert JB, et al. Milei J, Forcada P, Fraga CG, et al. Cardiovasc Res. Liang S, Ping Z, Ge J. Coenzyme Q10 regulates antioxidative stress and autophagy in acute myocardial ischemia-reperfusion injury.
Oxid Med Cell Longev. Rosenfeldt FL, Pepe S, Linnane A, et al. The effects of ageing on the response to cardiac surgery: protective strategies for the ageing myocardium. Langsjoen PH, Langsjoen AM. Overview of the use of CoQ10 in cardiovascular disease. Makhija N, Sendasgupta C, Kiran U, et al.
The role of oral coenzyme Q10 in patients undergoing coronary artery bypass graft surgery. J Cardiothorac Vasc Anesth. Taggart DP, Jenkins M, Hooper J, et al. Effects of short-term supplementation with coenzyme Q10 on myocardial protection during cardiac operations.
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High plasma coenzyme Q10 concentration is correlated with good left ventricular performance after primary angioplasty in patients with acute myocardial infarction. Medicine Baltimore.
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Pharmacol Res. Mazidi M, Kengne AP, Banach M. Effects of coenzyme Q10 supplementation on plasma C-reactive protein concentrations: A systematic review and meta-analysis of randomized controlled trials.
Zhai J, Bo Y, Lu Y, Liu C, Zhang L. Effects of coenzyme Q10 on markers of inflammation: a systematic review and meta-analysis. Sahebkar A, Simental-Mendia LE, Stefanutti C, Pirro M.
Supplementation with coenzyme Q10 reduces plasma lipoprotein a concentrations but not other lipid indices: A systematic review and meta-analysis. Suksomboon N, Poolsup N, Juanak N. Effects of coenzyme Q10 supplementation on metabolic profile in diabetes: a systematic review and meta-analysis. J Clin Pharm Ther.
Shargorodsky M, Debby O, Matas Z, Zimlichman R. Effect of long-term treatment with antioxidants vitamin C, vitamin E, coenzyme Q10 and selenium on arterial compliance, humoral factors and inflammatory markers in patients with multiple cardiovascular risk factors.
Nutr Metab Lond. McDonnell MG, Archbold GP. Clin Chim Acta. Lim SC, Tan HH, Goh SK, et al. Oxidative burden in prediabetic and diabetic individuals: evidence from plasma coenzyme Q Diabet Med.
Alcolado JC, Laji K, Gill-Randall R. Maternal transmission of diabetes. Suzuki S, Hinokio Y, Ohtomo M, et al. The effects of coenzyme Q10 treatment on maternally inherited diabetes mellitus and deafness, and mitochondrial DNA A to G mutation.
Henchcliffe C, Beal MF. Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis. Nat Clin Pract Neurol. Gotz ME, Gerstner A, Harth R, et al. Altered redox state of platelet coenzyme Q10 in Parkinson's disease. J Neural Transm. Shults CW, Haas RH, Passov D, Beal MF. Ann Neurol.
Isobe C, Abe T, Terayama Y. Neurosci Lett. Hargreaves IP, Lane A, Sleiman PM. The coenzyme Q10 status of the brain regions of Parkinson's disease patients. Shults CW, Oakes D, Kieburtz K, et al.
Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Arch Neurol. Beal MF, Oakes D, Shoulson I, et al. A randomized clinical trial of high-dosage coenzyme Q10 in early Parkinson disease: no evidence of benefit. JAMA Neurol. Yoritaka A, Kawajiri S, Yamamoto Y, et al.
Exogenous CoQ 10 is absorbed from the small intestine and is best absorbed if taken with a meal. Serum concentration of CoQ 10 in fed condition is higher than in fasting conditions. Data on the metabolism of CoQ 10 in animals and humans are limited.
After the withdrawal of CoQ 10 supplementation, the levels return to normal within a few days, irrespective of the type of formulation used. 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
Coenzyme Q Coenzyme Q absorption a coenzyme absogption that is ubiquitous in animals and Absorpttion Pseudomonadota [1] Minerals for joint health its other name, ubiquinone. Conezyme Q 10 is a 1,4-benzoquinone absorpttion, in Coenzyme Q absorption Q refers to the quinone chemical group and 10 refers to the number of isoprenyl chemical subunits Weightlifting techniques enclosed in brackets in the diagram in its tail. In natural ubiquinones, there are from six to ten subunits in the tail. This family of fat-soluble substances, which resemble vitaminsis present in all respiring eukaryotic cells, primarily in the mitochondria. It is a component of the electron transport chain and participates in aerobic cellular respirationwhich generates energy in the form of ATP. Ninety-five percent of the human body's energy is generated this way. There are three redox states of CoQ: fully oxidized ubi quinonesemi quinone ubisemi quinoneand fully reduced ubiquinol..jpg "Coenzyme Q absorption")
Coenzyme Q absorption -
In this chain, Coenzyme Q10 plays a critical role, acting as an electron-transfer carrier. In this way, the Coenzyme Q10 molecules act cyclically, shuttling back and forth from the oxidized form to the reduced form and back again continuously in reactions that are called redox reactions. Our bodies need this conversion back and forth of the oxidized and reduced forms of Coenzyme Q Bio-Energetic Property of Coenzyme Q10 For the purpose of cellular bio-energetics, which is the bio-medical term for the transformation of the energy stored in nutrients to the chemical energy of ATP, the ubiquinone form of CoQ10 is essential.
The process cannot start without it. In the inner membrane of the mitochondria in the cells where energy is produced, the CoQ10 is much needed in the form of ubiquinone. For the most part, the mitochondria are known as the powerhouses of the cells. In the mitochondria, electrons from fatty acids and sugars are used to generate ATP energy molecules in a process that requires the availability of the ubiquinone form of Coenzyme Q Antioxidant Property of Coenzyme Q10 For the purpose of antioxidant protection, the cells need the reduced form of CoQ The ubiquinol form is the form that donates electrons to neutralize harmful free radicals that otherwise would steal electrons in destructive chain reactions.
CoQ10 molecules in their reduced form can give up electrons without being damaged themselves. The donating of electrons by the ubiquinol form of CoQ10 causes no harm to the Coenzyme Q10 molecules because the Coenzyme Q10 molecules are then stable in their oxidized form, ubiquinone.
Indeed, the resulting oxidized CoQ10 ubiquinone molecules are necessary and useful for the bioenergetics of the cells.
By donating electrons to neutralize free radicals, the ubiquinol molecules prevent free radical damage to cells, proteins, fatty acids, and DNA. Donating two electrons does not harm the Coenzyme Q10 molecule; instead, it reverts to the more stable oxidized form, ubiquinone. Ubiquinone Form of Coenzyme Q10 More Stable Just to be clear, the ubiquinone form of Coenzyme Q10 is the form that the human body itself synthesizes.
The ubiquinone form of CoQ10 is the more stable form of Coenzyme Q10 for the manufacturers of CoQ10 capsules to use. The ubiquinol form of CoQ10 is, by comparison, an unstable form.
It is unstable by the very nature of its being an antioxidant: it is constantly looking to donate electrons and change its form to the oxidized form, the ubiquinone form.
The ubiquinol raw material and the ubiquinol capsule contents should appear milky-white. If the contents of a ubiquinol capsule appear to be yellow or orange, that could be a sign that the ubiquinol contents have begun to oxidize to the ubiquinone form of Coenzyme Q10 already inside the capsule.
Myths and Misconceptions about the Absorption of Coenzyme Q10 There are many myths and misconceptions about which form of CoQ10 supplement is better absorbed.
Based on available evidence, it is mistaken to claim that the ubiquinol form of Coenzyme Q10 is always better absorbed than the ubiquinone form. Actually, the best evidence shows that the formulation of the CoQ10 supplement is far more important for absorption than the form ubiquinone versus ubiquinol is Lopez-Lluch A comparative bio-availability study with a double-blind crossover design has shown that a well-formulated ubiquinone supplement will give a better absorption than a well-formulated ubiquinol supplement will.
Of course, a poorly formulated ubiquinone supplement will be less well absorbed than a well-formulated ubiquinol supplement and the opposite is true as well. It is mistaken to assert than people over 40 will have trouble absorbing the ubiquinone form or will have trouble converting the ubiquinone to ubiquinol.
A study with a double-blind crossover design has shown that, in men 55 years old or older, both ubiquinol and ubiquinone CoQ10 supplements increase the plasma ubiquinol status significantly Zhang Furthermore, the outcomes of the KiSel Study — reduced cardiovascular mortality, improved heart function, and better quality of life — testify to the heart health benefits of CoQ10 supplementation combined with selenium supplementation in senior citizens with an average age of 78 years Alehagen It is mistaken to suggest that one needs to take Coenzyme Q10 in the form of ubiquinol in order to get ubiquinol into the blood circulation.
The evidence shows that daily intakes of CoQ10 in both forms, ubiquinone and ubiquinol, will result in significantly increased levels of the antioxidant form, ubiquinol, in the blood plasma and in the lipoproteins in the blood Mohr It is logical that the absorbed Coenzyme Q10 should appear primarily in the reduced form in the plasma and in the plasma lipoproteins; after all, there is little need for energy generation in the plasma and the lipoproteins and much need for antioxidant protection.
Subsequent studies have confirmed this outcome of ubiquinone supplementation, e. Zhang Differences in the Way CoQ10 Supplements are Absorbed In actual fact, there is a difference in the way in which the two forms of Coenzyme Q10 are absorbed.
There is some evidence, primarily from large dog studies, that shows that the ubiquinol in ubiquinol supplements is, in fact, absorbed as ubiquinone before being converted back to the ubiquinol form in the lymph Judy ; Judy First, though, there are some very important points to be made about the absorption of Coenzyme Q One important point is that the CoQ10 raw material comes in a crystalline form, and the human absorption cells cannot absorb CoQ10 crystals.
The CoQ10 raw material must be processed in such a way as to make the CoQ10 crystals dissolve to single CoQ10 molecules at body temperature.
Only free single molecules of CoQ10 can be absorbed. A second important point is that the CoQ10 molecules are fat-soluble molecules, and the environment of the small intestines next to the intestinal absorption cells is a watery environment. The delivery of the fatsoluble CoQ10 molecules depends up on the formation of mixed micelles in the aqueous solution in the small intestines Shils Micelles are necessary to transport fat-soluble substances like Coenzyme Q10 and vitamin E and the various monoglycerides and fatty acids that are found in the chyme following digestion Judy The Coenzyme Q10 molecules are too large and too fat-soluble to be absorbed directly from the small intestine into the blood.
Instead, they become part of micelles and float through the watery environment of the small intestines in between the microvilli protrusions where the micelles break down and release the Coenzyme Q10 molecules and other fatty molecules to be absorbed by the enterocytes.
Oral Ubiquinol Converted to Ubiquinone Prior to Absorption In the accompanying video, it is assumed that the ubiquinol contents of the capsule are dissolved to single ubiquinol molecules in the stomach. Large animal studies have shown that the contents of the ubiquinol supplement are mostly converted to the ubiquinone form of CoQ10 in the stomach and the duodenum and are then re-converted back to ubiquinol in the lymph.
The absorbed Coenzyme Q10 passes into the blood circulation still predominantly in the form of ubiquinol Judy Following absorption and transfer into the lymph, the ubiquinone is converted back to ubiquinol. Of course, one must be careful in extrapolating from dog study results to humans. Coenzyme Q10 Molecules Aggregated into Micelles The contents of the ingested oral ubiquinol supplement, mostly converted to ubiquinone molecules in the stomach and the duodenum, are exposed to bile salts in the small intestines.
Following the conversion of the contents of the ubiquinol capsule to the ubiquinone form of Coenzyme Q10, the contents of the oral ubiquinol supplement will be absorbed in the same way that the contents of a ubiquinone CoQ10 supplement are Judy The micelles are the somewhat spherical aggregations of lipid molecules in aqueous solutions that transport fat-soluble substances through the aqueous solution to the intestinal absorption cells in the small intestines.
Typically, mixed micelles are formed, combining bile salts and phospholipids and monoglycerides and fatty acids, and, where available, Coenzyme Q10 and vitamin E molecules Vitetta In the case of the CoQ10 molecules, the slightly less hydrophobic benzoquinone heads of the CoQ10 molecules are on the outer edge of the micelles, closest to the watery solution in the small intestines, and the very hydrophobic isoprenyl tails of the CoQ10 molecules are tucked away inside the micelles.
Important to Take Coenzyme Q10 Supplement Together with Some Fat Thus, the micelles are the body's method of transporting fat-soluble nutrients such as Coenzyme Q10 and vitamin E through the watery phase of the small intestines to the intestinal absorption cells Vitetta Pharmacol Res.
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It is a fact Coenzyme Q absorption the Coenzyme Q10 is notoriously difficult for the Natural energy booster to absorb. Absotption all Q10 products are abeorption absorbed, not avsorption if Coenzymf come from the same raw material. The CoQ10 raw material consists of crystals. The human body cannot absorb crystals, only single molecules. Furthermore, the CoQ10 molecules are large, fat-soluble molecules and must pass through the watery phase adjacent to the intestinal absorption cells. If the CoQ10 crystals do not get dissolved, the crystals will be eliminated in the same way as indigestible fiber.
Ich tue Abbitte, dass sich eingemischt hat... Ich finde mich dieser Frage zurecht. Ist fertig, zu helfen.
Unbedingt, er ist nicht recht
Sie versuchten nicht, in google.com zu suchen?
Ihre Meinung, diese Ihre Meinung
Sie haben ins Schwarze getroffen. Mir scheint es der gute Gedanke. Ich bin mit Ihnen einverstanden.