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| Coenzyme Q10 (CoQ10 ), also known as ubiquinone, is a naturally occurring biochemical cofactor (coenzyme) and an antioxidant produced by the human body. It can also be obtained from dietary sources, such as meat, fish, seed oils, vegetables, and dietary supplements. CoQ10 is found in many organisms, including animals and bacteria.
CoQ10 plays a role in mitochondrial oxidative phosphorylation, aiding in the production of adenosine triphosphate (ATP), which is involved in energy transfer within cells. The structure of CoQ10 consists of a benzoquinone moiety and an isoprenoid side chain, with the "10" referring to the number of isoprenyl chemical subunits in its tail.
Although a ubiquitous molecule in human tissues, CoQ10 is not a dietary nutrient and does not have a recommended intake level, and its use as a supplement is not approved in the United States for any health or anti-disease effect.
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Read full article at Wikipedia
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InChI=1S/C59H90O4/c1- 44(2)24-15-25-45(3)26-16-27-46(4)28-17-29-47(5)30-18-31-48(6)32-19-33-49(7)34-20-35-50(8)36-21-37-51(9)38-22-39-52(10)40-23-41-53(11)42-43-55-54(12)56(60)58(62-13)59(63-14)57(55)61/h24,26,28,30,32,34,36,38,40,42H,15-23,25,27,29,31,33,35,37,39,41,43H2,1-14H3/b45-26+,46-28+,47-30+,48-32+,49-34+,50-36+,51-38+,52-40+,53-42+ |
| ACTIUHUUMQJHFO-UPTCCGCDSA-N |
| COC1=C(OC)C(=O)C(C\C=C(/C)CC\C=C(/C)CC\C=C(/C)CC\C=C(/C)CC\C=C(/C)CC\C=C(/C)CC\C=C(/C)CC\C=C(/C)CC\C=C(/C)CCC=C(C)C)=C(C)C1=O |
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Homo sapiens
(NCBI:txid9606)
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See:
DOI
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antioxidant
A substance that opposes oxidation or inhibits reactions brought about by dioxygen or peroxides.
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human metabolite
Any mammalian metabolite produced during a metabolic reaction in humans (Homo sapiens).
ferroptosis inhibitor
Any substance that inhibits the process of ferroptosis (a type of programmed cell death dependent on iron and characterized by the accumulation of lipid peroxides) in organisms.
Escherichia coli metabolite
Any bacterial metabolite produced during a metabolic reaction in Escherichia coli.
(via ubiquinones )
mouse metabolite
Any mammalian metabolite produced during a metabolic reaction in a mouse (Mus musculus).
(via ubiquinones )
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View more via ChEBI Ontology
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2-[(2E,6E,10E,14E,18E,22E,26E,30E,34E)-3,7,11,15,19,23,27,31,35,39-decamethyltetraconta-2,6,10,14,18,22,26,30,34,38-decaen-1-yl]-5,6-dimethoxy-3-methylcyclohexa-2,5-diene-1,4-dione
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2-((all-E)-3,7,11,15,19,23,27,31,35,39-decamethyl-2,6,10,14,18,22,26,30,34,38-tetracontadecaenyl)-5,6-dimethoxy-3-methyl-p-benzoquinone
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ChemIDplus
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2-[(2E,6E,10E,14E,18E,22E,26E,30E,34E)-3,7,11,15,19,23,27,31,35,39-decamethyltetraconta-2,6,10,14,18,22,26,30,34,38-decaen-1-yl]-5,6-dimethoxy-3-methyl-1,4-benzoquinone
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ChEBI
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Adelir
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KEGG DRUG
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all-trans-ubiquinone
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ChEBI
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coenzyme Q10
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ChemIDplus
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Coenzyme Q10
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KEGG COMPOUND
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CoQ
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ChEBI
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CoQ10
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ChEBI
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Q
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ChEBI
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Q 199
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ChemIDplus
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Q10
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ChEBI
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Ubidecarenone
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KEGG COMPOUND
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ubiquinone
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ChEBI
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ubiquinone 10
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ChemIDplus
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ubiquinone 50
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ChemIDplus
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UBIQUINONE-10
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PDBeChem
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Ubiquinone-10
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KEGG COMPOUND
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ubiquinone-10
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UniProt
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4445197
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ChemSpider
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4607
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DrugCentral
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C00002866
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KNApSAcK
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C11378
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KEGG COMPOUND
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Coenzyme_Q10
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Wikipedia
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D01065
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KEGG DRUG
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FDB013228
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FooDB
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HMDB0001072
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HMDB
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LMPR02010001
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LIPID MAPS
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U10
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PDBeChem
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UBIQUINONE-10
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MetaCyc
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| View more database links |
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1900141
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Beilstein Registry Number
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Beilstein
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1900141
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Reaxys Registry Number
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Reaxys
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303-98-0
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CAS Registry Number
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NIST Chemistry WebBook
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303-98-0
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CAS Registry Number
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ChemIDplus
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Sharma A, Fonarow GC, Butler J, Ezekowitz JA, Felker GM (2016)
Coenzyme Q10 and Heart Failure: A State-of-the-Art Review.
Circulation. Heart failure 9, e002639 [PubMed:27012265]
[show Abstract]
Heart failure (HF) with either preserved or reduced ejection fraction is associated with increased morbidity and mortality. Evidence-based therapies are often limited by tolerability, hypotension, electrolyte disturbances, and renal dysfunction. Coenzyme Q10 (CoQ10) may represent a safe therapeutic option for patients with HF. CoQ10 is a highly lipophilic molecule with a chemical structure similar to vitamin K. Although being a common component of cellular membranes, CoQ10's most prominent role is to facilitate the production of adenosine triphosphate in the mitochondria by participating in redox reactions within the electron transport chain. Numerous trials during the past 30 years examining CoQ10 in patients with HF have been limited by small numbers and lack of contemporary HF therapies. The recent publication of the Q-SYMBIO randomized controlled trial demonstrated a reduction in major adverse cardiovascular events with CoQ10 supplementation in a contemporary HF population. Although having limitations, this study has renewed interest in evaluating CoQ10 supplementation in patients with HF. Current literature suggests that CoQ10 is relatively safe with few drug interactions and side effects. Furthermore, it is already widely available as an over-the-counter supplement. These findings warrant future adequately powered randomized controlled trials of CoQ10 supplementation in patients with HF. This state-of-the-art review summarizes the literature about the mechanisms, clinical data, and safety profile of CoQ10 supplementation in patients with HF. | Zaki NM (2016)
Strategies for oral delivery and mitochondrial targeting of CoQ10.
Drug delivery 23, 1868-1881 [PubMed:25544601]
[show Abstract]
Coenzyme Q10 (CoQ10), also known as ubiquinone or ubidecarenone, is a powerful, endogenously produced, intracellularly existing lipophilic antioxidant. It combats reactive oxygen species (ROS) known to be responsible for a variety of human pathological conditions. Its target site is the inner mitochondrial membrane (IMM) of each cell. In case of deficiency and/or aging, CoQ10 oral supplementation is warranted. However, CoQ10 has low oral bioavailability due to its lipophilic nature, large molecular weight, regional differences in its gastrointestinal permeability and involvement of multitransporters. Intracellular delivery and mitochondrial target ability issues pose additional hurdles. To maximize CoQ10 delivery to its biopharmaceutical target, numerous approaches have been undertaken. The review summaries the current research on CoQ10 bioavailability and highlights the headways to obtain a satisfactory intracellular and targeted mitochondrial delivery. Unresolved questions and research gaps were identified to bring this promising natural product to the forefront of therapeutic agents for treatment of different pathologies. | Saha SP, Whayne TF (2016)
Coenzyme Q-10 in Human Health: Supporting Evidence?
Southern medical journal 109, 17-21 [PubMed:26741866]
[show Abstract]
Coenzyme Q-10 (CoQ10) is a widely used alternative medication or dietary supplement and one of its roles is as an antioxidant. It naturally functions as a coenzyme and component of oxidative phosphorylation in mitochondria. Decreased levels have been demonstrated in diseased myocardium and in Parkinson disease. Farnesyl pyrophosphate is a critical intermediate for CoQ10 synthesis and blockage of this step may be important in statin myopathy. Deficiency of CoQ10 also has been associated with encephalomyopathy, severe infantile multisystemic disease, cerebellar ataxia, nephrotic syndrome, and isolated myopathy. Although supplementation with CoQ10 has been reported to be beneficial in treating hypertension, congestive heart failure, statin myopathy, and problems associated with chemotherapy for cancer treatement, this use of CoQ10 as a supplement has not been confirmed in randomized controlled clinical trials. Nevertheless, it appears to be a safe supplementary medication where usage in selected clinical situations may not be inappropriate. This review is an attempt to actualize the available information on CoQ10 and define its potential benefit and appropriate usage. | Villalba JM, Parrado C, Santos-Gonzalez M, Alcain FJ (2010)
Therapeutic use of coenzyme Q10 and coenzyme Q10-related compounds and formulations.
Expert opinion on investigational drugs 19, 535-554 [PubMed:20367194]
[show Abstract]
Importance of the fieldCoenzyme Q(10) (CoQ(10)) is found in blood and in all organs. CoQ(10) deficiencies are due to autosomal recessive mutations, ageing-related oxidative stress and carcinogenesis processes, and also statin treatment. Many neurodegenerative disorders, diabetes, cancer and muscular and cardiovascular diseases have been associated with low CoQ(10) levels, as well as different ataxias and encephalomyopathies.Areas covered in this reviewWe review the efficacy of a variety of commercial formulations which have been developed to solubilise CoQ(10) and promote its better absorption in vivo, and its use in the therapy of pathologies associated with low CoQ(10) levels, with emphasis in the results of the clinical trials. Also, we review the use of its analogues idebenone and MitoQ.What the reader will gainThis review covers the most relevant aspects related with the therapeutic use of CoQ(10), including existing formulations and their effects on its bioavailability.Take home messageCoQ(10) does not cause serious adverse effects in humans and new formulations have been developed that increase CoQ(10) absorption. Oral CoQ(10) is a viable antioxidant strategy in many diseases, providing a significant to mild symptomatic benefit. Idebenone and MitoQ are promising substitutive CoQ(10)-related drugs which are well tolerated and safe. | Skough K, Krossén C, Heiwe S, Theorell H, Borg K (2008)
Effects of resistance training in combination with coenzyme Q10 supplementation in patients with post-polio: a pilot study.
Journal of rehabilitation medicine 40, 773-775 [PubMed:18843432]
[show Abstract]
ObjectiveCoenzyme Q10 supplementation leads to increased muscle metabolism in patients with post-polio syndrome. The aim of this study was to investigate the effect of resistance training in combination with oral supplementation with coenzyme Q10 in patients with post-polio syndrome regarding muscle strength and endurance as well as functional capacity and health-related quality of life.DesignParallel randomized, controlled, double-blind pilot study.Patients and methodsA total of 14 patients (8 women and 6 men) with post-polio syndrome participated in a 12-week muscular resistance training, 3 days/week. The patients were randomized for oral supplementation with coenzyme Q10, 200 mg/day, or placebo. Measurements used were: sit-stand-sit test, timed up & go test, 6-minute walk test, muscle strength measurement by means of dynamic dynamometer and short-form (SF)-36 questionnaire.ResultsMuscle strength, muscle endurance and quality of life regarding mental health increased statistically significantly in all 14 patients. There was no significant difference between the coenzyme Q10 and placebo groups regarding muscle strength, muscle endurance and quality of life.ConclusionThere was no effect of coenzyme Q10 supplementation during resistance training on post-polio syndrome symptoms. Thus, supplementation with coenzyme Q10 has no beneficial effect on muscle function in patients with post-polio syndrome. | Molyneux SL, Young JM, Florkowski CM, Lever M, George PM (2008)
Coenzyme Q10: is there a clinical role and a case for measurement?
The Clinical biochemist. Reviews 29, 71-82 [PubMed:18787645]
[show Abstract]
Coenzyme Q(10) (CoQ(10)) is an essential cofactor in the mitochondrial electron transport pathway, and is also a lipid-soluble antioxidant. It is endogenously synthesised via the mevalonate pathway, and some is obtained from the diet. CoQ(10) supplements are available over the counter from health food shops and pharmacies. CoQ(10) deficiency has been implicated in several clinical disorders, including but not confined to heart failure, hypertension, Parkinson's disease and malignancy. Statin, 3-hydroxy-3- methyl-glutaryl (HMG)-CoA reductase inhibitor therapy inhibits conversion of HMG-CoA to mevalonate and lowers plasma CoQ(10) concentrations. The case for measurement of plasma CoQ(10) is based on the relationship between levels and outcomes, as in chronic heart failure, where it may identify individuals most likely to benefit from supplementation therapy. During CoQ(10) supplementation plasma CoQ(10) levels should be monitored to ensure efficacy, given that there is variable bioavailability between commercial formulations, and known inter-individual variation in CoQ(10) absorption. Knowledge of biological variation and reference change values is important to determine whether a significant change in plasma CoQ(10) has occurred, whether a reduction for example following statin therapy or an increase following supplementation. Emerging evidence will determine whether CoQ(10) does indeed have an important clinical role and in particular, whether there is a case for measurement. | Young AJ, Johnson S, Steffens DC, Doraiswamy PM (2007)
Coenzyme Q10: a review of its promise as a neuroprotectant.
CNS spectrums 12, 62-68 [PubMed:17192765]
[show Abstract]
Coenzyme Q10 (CoQ10) is a powerful antioxidant that buffers the potential adverse consequences of free radicals produced during oxidative phosphorylation in the inner mitochondrial membrane. Oxidative stress, resulting in glutathione loss and oxidative DNA and protein damage, has been implicated in many neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and Huntington's disease. Experimental studies in animal models suggest that CoQ10 may protect against neuronal damage that is produced by ischemia, atherosclerosis and toxic injury. Though most have tended to be pilot studies, there are published preliminary clinical trials showing that CoQ10 may offer promise in many brain disorders. For example, a 16-month randomized, placebo-controlled pilot trial in 80 subjects with mild Parkinson's disease found significant benefits for oral CoQ10 1,200 mg/day to slow functional deterioration. However, to date, there are no published clinical trials of CoQ10 in Alzheimer's disease. Available data suggests that oral CoQ10 seems to be relatively safe and tolerated across the range of 300-2,400 mg/day. Randomized controlled trials are warranted to confirm CoQ10's safety and promise as a clinically effective neuroprotectant. | Singh U, Devaraj S, Jialal I (2007)
Coenzyme Q10 supplementation and heart failure.
Nutrition reviews 65, 286-293 [PubMed:17605305]
[show Abstract]
Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in the Western world. Oxidative stress appears to play a pivotal role in atherosclerosis. Coenzyme Q10 (CoQ10), one of the most important antioxidants, is synthesized de novo by every cell in the body. Its biosynthesis decreases with age and its deficit in tissues is associated with degenerative changes of aging, thus implicating a possible therapeutic role of CoQl0 in human diseases. There is evidence to support the therapeutic value of CoQ10 as an adjunct to standard medical therapy in congestive heart failure. However, much further research is required, especially in the use of state-of-the-art techniques to assess functional outcomes in patients with congestive heart failure. | Hojerová J (2000)
[Coenzyme Q10--its importance, properties and use in nutrition and cosmetics].
Ceska a Slovenska farmacie : casopis Ceske farmaceuticke spolecnosti a Slovenske farmaceuticke spolecnosti 49, 119-123 [PubMed:10953455]
[show Abstract]
Coenzyme Q10, or ubiquinone, is a nutrient--a vitamin-like substance which plays a crucial role in the generation of cellular energy an in free radical scavenging in the human body. After the age of 35 to 40, the organism begins to lose its ability to synthesize Co Q10 from food and its deficiency develops. Ageing, poor eating habits, stress and infection--they all affect our ability to provide adequate amounts of Co Q10. Therefore Co Q10 supplementation may be very helpful for the organism. The present summarizing study reports the history of the discovery and research, properties, biochemical effects, dosage of Co Q10 deficiency in the human body. A possible use of Co Q10 as a dietary supplement and an ingredient for topical cosmetic products is described. | Ernster L, Dallner G (1995)
Biochemical, physiological and medical aspects of ubiquinone function.
Biochimica et biophysica acta 1271, 195-204 [PubMed:7599208]
[show Abstract]
This presentation is a brief review of current knowledge concerning some biochemical, physiological and medical aspects of the function of ubiquinone (coenzyme Q) in mammalian organisms. In addition to its well-established function as a component of the mitochondrial respiratory chain, ubiquinone has in recent years acquired increasing attention with regard to its function in the reduced form (ubiquinol) as an antioxidant. Ubiquinone, partly in the reduced form, occurs in all cellular membranes as well as in blood serum and in serum lipoproteins. Ubiquinol efficiently protects membrane phospholipids and serum low-density lipoprotein from lipid peroxidation, and, as recent data indicate, also mitochondrial membrane proteins and DNA from free-radical induced oxidative damage. These effects of ubiquinol are independent of those of exogenous antioxidants, such as vitamin E, although ubiquinol can also potentiate the effect of vitamin E by regenerating it from its oxidized form. Tissue ubiquinone levels are regulated through the mevalonate pathway, increasing upon various forms of oxidative stress, and decreasing during aging. Drugs inhibiting cholesterol biosynthesis via the mevalonate pathway may inhibit or stimulate ubiquinone biosynthesis, depending on their site of action. Administration of ubiquinone as a dietary supplement seems to lead primarily to increased serum levels, which may account for most of the reported beneficial effects of ubiquinone intake in various instances of experimental and clinical medicine. | Watts TL (1995)
Coenzyme Q10 and periodontal treatment: is there any beneficial effect?
British dental journal 178, 209-213 [PubMed:7718355]
[show Abstract]
Many dentists have been surprised by recent media claims of periodontal benefits with a purportedly revolutionary dietary supplement. The research literature on coenzyme Q10's periodontal effects does not extend to the international English language dental literature, which perhaps explains the surprise. A review of the available literature does not give any ground for the claims made, and selected papers are discussed to show that there is actually some evidence that coenzyme Q10 has no place in periodontal treatment. | CRANE FL, HATEFI Y, LESTER RL, WIDMER C (1957)
Isolation of a quinone from beef heart mitochondria.
Biochimica et biophysica acta 25, 220-221 [PubMed:13445756] |
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2010-04-29
