Coenzyme Q10 is present in almost every cell of the body, and it is most abundant in organs with high energy needs - the heart, liver, kidneys and skeletal muscles. It is simultaneously a link in the 'energy conveyor' of mitochondria and a fat-soluble antioxidant. The editorial team explains how this molecule is arranged, what it does and where it comes from in the body.
What coenzyme Q10 is
Coenzyme Q10, or ubiquinone, is a fat-soluble compound whose molecule consists of a quinone ring and a long side chain of ten isoprene units. It is precisely this number of units that gives the figure '10' in the name. In other organisms variants with a different chain length occur, for example Q9 in rodents or Q6 in yeast.
The name 'ubiquinone' comes from the English ubiquitous - 'everywhere present': the substance is indeed found in almost all cells. It was discovered in 1957 in the mitochondria of a bull's heart, and later Peter Mitchell, explaining the mechanism of ATP synthesis, gave it a central place in his chemiosmotic theory, for which he received the Nobel Prize in Chemistry in 1978.
Coenzyme Q10 is not a vitamin in the classical sense, since the body is able to synthesize it on its own. Therefore it is sometimes called a 'vitamin-like substance'. Dietary intake exists, but, as is believed, it constitutes only a small fraction of the total pool in the body.
Because of its long lipophilic 'tail', coenzyme Q10 is located inside cell membranes - primarily the inner membrane of mitochondria, as well as the membranes of other organelles and blood lipoproteins. This position determines both of its main functions (Crane, 2001).
The role in mitochondrial energetics
Mitochondria produce the main part of the cell's energy in the form of ATP through the process of oxidative phosphorylation. It takes place on the inner membrane of mitochondria, where the protein complexes of the respiratory chain are located. Coenzyme Q10 plays the role of a mobile electron carrier between them.
Electrons obtained from the oxidation of nutrients enter complex I (from NADH) and complex II (from succinate). Coenzyme Q accepts these electrons, converting into the reduced form, diffuses in the membrane to complex III and passes the electrons further. From there they pass through cytochrome c to complex IV and finally to oxygen.
During this transfer, complexes I, III and IV pump protons across the membrane, creating an electrochemical gradient. It is the energy of this gradient that ATP synthase uses to produce ATP. Without coenzyme Q10, electrons from complexes I and II could not reach complex III, and energy production would drop sharply.
In addition to the respiratory chain, coenzyme Q participates in the oxidation of fatty acids, in the synthesis of pyrimidines (through the enzyme dihydroorotate dehydrogenase) and in other redox reactions. This explains why a severe genetic deficiency of coenzyme Q10 simultaneously affects the muscles, nervous system and kidneys.
Antioxidant function: ubiquinone and ubiquinol
Coenzyme Q10 exists in three redox states: fully oxidized ubiquinone, intermediate semiquinone and fully reduced ubiquinol. In the body these forms are constantly converting into one another, and it is precisely this ability that makes the molecule both an electron carrier and an antioxidant (Littarru, Tiano, 2007).
| Form | State | Main role | Where it predominates |
|---|---|---|---|
| Ubiquinone (CoQ10) | Oxidized | Accepts electrons in the respiratory chain | Most supplements; partly tissues |
| Semiquinone | Intermediate | A short-lived state during electron transfer | Mitochondria |
| Ubiquinol (CoQ10H₂) | Reduced | Antioxidant in membranes and lipoproteins | Blood plasma of healthy people |
Ubiquinol directly neutralizes free radicals in the lipid layer of membranes and protects low-density lipoproteins from oxidation. In addition, it is able to restore vitamin E (alpha-tocopherol) from its oxidized form, that is, it supports the work of another key fat-soluble antioxidant.
In the blood plasma of healthy people, most of the coenzyme Q10 is in the reduced form - ubiquinol. The ratio of the reduced and oxidized forms is sometimes used as a marker of oxidative stress in studies.
It is important that both forms interconvert in the body. Ubiquinone taken in is largely reduced to ubiquinol after absorption. Therefore the difference between supplements with these forms concerns mostly the features of absorption rather than which of them 'works' in the cell.
Synthesis, sources and causes of deficiency
The body synthesizes coenzyme Q10 in all tissues. The quinone ring is formed from the amino acid tyrosine, and the isoprene chain - through the mevalonate pathway, the same one that leads to the synthesis of cholesterol. B-group vitamins, in particular B6, are also needed for the synthesis reactions.
From food a person obtains coenzyme Q10 mainly from meat (especially heart and liver), fatty fish, some oils and nuts. It is believed that a typical diet provides only a few milligrams per day, so the main part of the coenzyme in the body is of its own production.
- Age.The content of coenzyme Q10 in a number of tissues, in particular in the heart, declines with age (Kalén et al., 1989).
- Statins.They block the enzyme HMG-CoA reductase in the mevalonate pathway and therefore reduce the level of coenzyme Q10 in the blood.
- Primary deficiency.Rare genetic disorders of synthesis enzymes, which manifest with severe neurological, muscular and renal symptoms.
- Chronic diseases.Reduced levels have been described in heart failure and some mitochondrial diseases.
For a healthy young person with a complete diet, a clinical deficiency of coenzyme Q10 as a rule does not occur. That is precisely why the question of the benefit of supplements for athletes is a separate and more complex one than a simple 'filling of a shortage'.
Absorption and medical use
The large molecule and high lipophilicity make the absorption of coenzyme Q10 slow and incomplete. It is absorbed in the small intestine together with fats with the participation of bile, enters the lymph as part of chylomicrons and is then distributed by lipoproteins. The plasma concentration after intake reaches a peak after several hours (Bhagavan, Chopra, 2006).
Intake with food, especially with fats, improves absorption. Solubilized forms and ubiquinol in some studies gave higher plasma concentrations than ordinary ubiquinone powder. At the same time, penetration into tissues, especially into the mitochondria of healthy organs, after taking supplements is limited.
The most substantial clinical data were obtained in cardiology. In the randomized Q-SYMBIO study (Mortensen et al., 2014), 420 patients with chronic heart failure received 300 mg of coenzyme Q10 per day or placebo for two years; in the coenzyme group the frequency of serious cardiovascular events was lower. The results require confirmation in larger studies, but became the best-known argument in favor of the supplement.
Other directions studied are statin-induced myopathy, migraine, primary deficiencies of coenzyme Q10 and mitochondrial diseases. For primary deficiency, prescribing coenzyme Q10 is part of the treatment; for the other conditions the evidence base is heterogeneous.
Editorial conclusions
Coenzyme Q10 is a key electron carrier in the respiratory chain of mitochondria and an important fat-soluble antioxidant that protects membranes and lipoproteins from oxidation.
The body synthesizes it on its own through the mevalonate pathway, so the level of the coenzyme can be lowered by age, statins, genetic defects and some chronic illnesses.
Absorption from supplements is slow and depends on fats in food and the form of the product, and the most convincing clinical data were obtained in patients with heart failure rather than in healthy people.
Next we recommend reading our materials on the benefit of coenzyme Q10 for athletes from the standpoint of the evidence base, on its side effects and on how to take it correctly.
References
- Crane FL. Biochemical functions of coenzyme Q10. J Am Coll Nutr. 2001;20(6):591–598.
- Littarru GP, Tiano L. Bioenergetic and antioxidant properties of coenzyme Q10: recent developments. Mol Biotechnol. 2007;37(1):31–37.
- Bhagavan HN, Chopra RK. Coenzyme Q10: absorption, tissue uptake, metabolism and pharmacokinetics. Free Radic Res. 2006;40(5):445–453.
- Kalén A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Lipids. 1989;24(7):579–584.
- Mortensen SA, Rosenfeldt F, Kumar A, et al. The effect of coenzyme Q10 on morbidity and mortality in chronic heart failure: results from Q-SYMBIO: a randomized double-blind trial. JACC Heart Fail. 2014;2(6):641–649.
- Mitchell P. Coupling of phosphorylation to electron and hydrogen transfer by a chemi-osmotic type of mechanism. Nature. 1961;191:144–148.
Andriy Melnyk
A strength-sports coach and author of programs for beginner and intermediate levels. Writes about training planning.
