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Coenzyme Q10 (Ubiquinone) : Implications in Clinical Practice

Deepak Langade*, Pratibha Tarapure#, Abhay Jagtap**, Preeti Arora***, Sanjeev Anand***


Coenzyme Q10 (CoQ10) is a lipophilic compound naturally found throughout the body. It is an endogenously synthesized provitamin that serves as a lipid soluble electron carrier in the mitochondrial electron transport.1 The alternative names ubidecarenone and ubiquinone, meaning ubiquitous quinone, allude to the presence of CoQ10 in all cells.2 The cellular effects of CoQ10 may be important in patients with cardiac diseases especially coronary artery disease and congestive cardiac failure. It has been used as an adjunctive therapy for various cardiovascular conditions and in some countries it is available as over-the-counter nutritional supplement.

Coenzyme-Q exists in several forms and can be found in microorganisms, plants and mammals including humans. Co-enzymes q6, q7, q8 are found in yeast and bacteria whereas co enzyme q9 is found in rats and mice. CoQ10 is prevalent in humans, with high endogenous concentration found in the heart, liver, kidney and pancreas. Current CoQ10 supplements are manufactured by the fermentation of beets and sugarcane.

It can be synthesized in the body therefore CoQ10 is not considered to be an essential nutrient. It is present in foods such as beef, poultry and broccoli.3 Other sources of CoQ10 are soy oil, fish oils, peanuts, sardines and mackerel. Dietary intake of CoQ10 is 2-5 mg per day, which is always inadequate to provide levels in the body required to be beneficial in pathological states. The total body content of CoQ10 is 0.4 to 1.5 gm..

Chemically CoQ10 is 2, 3 dimethoxy - 5 methyl - 6 decaprenyl benzoquinones. It is a naturally occurring fat-soluble quinone ubiquitous in eukaryotic cells. (Fig. 1).

CoQ10 is synthesized in almost all tissues in the body from the amino acid “Tyrosine”. The biosynthesis of the compound is multifold, with the isoprenyl side chain deriving from mevolonate, the benzoquinone ring structure from tyrosine, and condensation of these structures through polyprenyl transferase enzyme activity.4 The primary regulation of CoQ10 biosynthesis is the 3 hydroxy-methyl glutaryl coenzyme a, (HMG-COA) reductase reaction that is similar in cholesterol synthesis. (Fig. 2).

CoQ10 was first isolated from beef heart mitochondria by Dr. Frederick Crane of University of Wisconsin, USA in 1957, Professor Morton introduced the name ubiquinone, meaning the ubiquitous quinone.1 In 1958, professor Karl Folkers and coworkers determined the precise chemical tructure of CoQ10 as 2, 3, dimethoxy-5 methyl-6 decaprenyl benzoquinones synthesized and were the first to produce it by fermentation.

In 1960, professor Yamamura of Japan became the first in the world to use coenzyme q7 a related Compound in the treatment of human diseases viz. congestive heart failure.

In 1978, Peter Mitchell received the Noble prize for his contribution to the understanding of biological energy transfer through the formulation of the chemiosmotic theory, which includes the vital proton motive role of CoQ10 in energy transfer systems.

Mechanism of Action

CoQ10 is a lipid soluble benzoquinone with a 10-isoprenyl unit side chain, is structurally similar to vitamin-K5. It is an essential component in the synthesis of ATP and exhibits both anti-oxidants and membrane stabilizing property. CoQ10 acts as a redox link between flavoproteins and cytochromes that are needed for oxidative phosphorylation and synthesis of ATP. It serves as an electron transport carrier during the processes of respiration and oxidative phosphorylation. Thus, it is involved in the manufacture of ATP. CoQ10 directly regulates NADH and succinate dehyrogenase, enabling reversible reactions between these enzymes in the mitochondrial electron transport chain. CoQ10 must be reduced to ubiquinol to wield its anti-oxidative function, and supplementation with CoQ10 may inhibit lipid oxidizability.

Coenzyme-Q participates in the electron transport inside the mitochondria of the cell, thus either hydrogen ions or electrons are gained or lost by CoQ10. It serves as an electron acceptor for one group of enzymes and as an electron donor to the next group of enzymes in the electron transport chain. It helps transport electron from complex-i to complex-ii and from complex-ii to complex-iii. The [H]+ accumulated in the intermembrane space of mitochondria is driven back into the mitochondria matrix via ATP syntheses (complex-v) with formation of ATP.

Other mechanisms of action may include stabilization of calcium dependent slow channels, inhibition of intracellular phospholipases, and alteration of prostaglandin metabolism.5

Physiological role of CoQ10

I. CoQ10 as Energizer
CoQ10 participates in the electron transport inside the mitochondria of the cell, thus either H+ or e- are gained or lost by CoQ10. It serves as an electron acceptor for one group of enzymes and as an electron donor to the next group of enzymes in the electron transport chain.

ATP synthase is like a turbine where higher concentrations of H+ leads to more energy trapping and ATP formation and vice-versa. CoQ10 is the important coenzyme responsible for taking up electrons and pushing H+ into the intermembrane space.

Thus, CoQ10 is an essential component in the ATP synthesis in the mitochondria and high concentrations of CoQ10 can increase the total utilization of energy released by the metabolic processes in the body; whereas deficiency of which may lead to loss of energy generated during the metabolic processes in the form of heat.

It is a central rate-limiting constituent of the mitochondrial respiratory chain, which generates most of the ATP within the cell. Thus CoQ10 acts as an energizer where it improves the efficiency of the cells to utilize all available energy from its sources.

II. Antioxidant effects of CoQ10

It is well known that free radicals cause oxidative damage in various chronic disease states like atherosclerotic heart disease, hypertension, congestive heart failure, diabetes mellitus, ischaemia reperfusion injury, dyslipidaemia and many other conditions.

Free radicals are the substances, which have one or more unpaired electrons. These unpaired electrons can easily react with cell components to cause free radicals injury or oxidative damage. The unutilized oxygen in the body can lead to the formation of free oxygen radicals viz. Suproxide anion (O2-), Hydroxyl radicals (OH-).

Various drugs, chemicals, pesticides, industrial pollutants, tobacco smoke, sunlight and ionizing radiation can generate free radicals; whereas in the body they are being constantly formed in the lysosomes, peroxisomes, endoplasmic reticulum, plasma membrane and the cytoplasm. Free radicals bring about modulation of inflammatory process by regulating prostaglandin synthesis.

Free radicals have high propensity to damage cellular DNA leading to activation of carcinogenesis. They also lead to fatty acid peroxidation and damage to the cell architecture and function. They also damage the various cellular metabolic processes and interfere with ion channels located on the cells.

CoQ10 acts as an antioxidant by decreasing formation of free radicals. It improves the transport of electrons (e-) and protons (H+) and thus prevents the formation of superoxide radicals that would otherwise form from the released O2. It itself is a strong directly acting endogenous antioxidant. It acts as a substrate for free radicals and accepts the free electrons from free radicals; gets converted to reduced CoQ (Ubiquinol), thus rendering free radicals into harmless compounds. Reduced CoQ10 then gives up electrons and gets reactivated again for further activity. CoQ10 is found to regenerate the oxidized Vitamin-E thus converting it into a strong antioxidant.

III. Other possible roles of CoQ

It may be involved in maintenance of cell membrane integrity of RBCs and maintains optimum blood viscosity. It stabilizes the calcium channels and may promote apoptosis in malignant cells and may improve the immune status of patients.


In animal studies CoQ10 has an oral bioavailability of 2-3%. With high doses of dietary CoQ10, the blood concentration in both rats and humans can be increased about 2 to 4-fold. Following ingestion of 100 mg of CoQ10,peak plasma levels occur between 5 and 10 hours. Tmax is approximately 6.5 hours, which indicates slow absorpiton from the GI tract possibly due to the high molecular weight and low water solubility of CoQ10.2 Uptake of dietary CoQ10 in the liver does not affect the synthesis of endogenous CoQ10.

The mean plasma levels after a single 100 mg oral dose of CoQ10 in human subjects is 1.004 ± 0.37 mg/ml. In humans, CoQ10 is found in relatively high concentrations in the heart, liver, kidney, and pancreas.6 The plasma half-life of CoQ10 in different tissues varies between 49-125 hours.7 Following absorption from the GI tract, CoQ10 is taken up by chylomicrons. The major portion of an exogenous dose of CoQ10 is deposited in the liver and packaged into VLDL lipoprotein.

Metabolism and Excretion
It is assumed that metabolism and excretion of exogenous CoQ10 is analogous to endogenously produced CoQ10. The excretion of CoQ10 predominantly occurs via the biliary tract.

Role in pathological conditions

Role in CHF
Coenzyme Q10 supplementation as an adjunct to CHF standard therapy is reported to have positive outcomes, especially in patients with deficient levels of the provitamin. Heart failure often is characterized by an energy depletion status that has been associated with low endogenous CoQ10 levels. The possible usefulness of the CoQ10 in the treatment of CHF may be related to its ability to increase ATP synthesis and enhancement of myocardial contractility.5

As with other muscle types, cardiac muscle fibres require calcium for contraction and relaxation, and more energy is required for relaxation. These cells rely heavily on fat sources of energy and hence contain more mitochondria. Since energy synthesis (ATP Synthesis) from fats requires a higher oxygen concentration, mitochondria function in the cardiac myocytes can be significantly impaired in deficiency of CoQ10. Therefore, administration of CoQ10 increases the energy synthesis in the mitochondria and significantly improves the cardiac function (contraction and relaxation), decreases end diastolic ventricular pressure and improves the ejection fraction in CHF.

Thus, therapy with CoQ10 may be considered to be an efficacious aid in the traditional treatment of chronic congestive heart failure along with other agents used in CHF. CoQ10 administration has shown to reduce the signs and symptoms of CHF like oedema, pulmonary rales, cyanosis, hepatomegaly and breathlessness on exertion.

CoQ10 is also useful in patients with hypertension, cardiac transplantation, cardiac bypass surgery, cardiomyopathies and ischaemic heart disease. In patients of dyslipidaemia who are on statins, which decrease cholesterol synthesis by HMG-CoA reductase inhibition, there is an apparent deficiency of CoQ10 and concurrent CoQ10 administration in such patients significantly improves the cellular function and reduces the complications of dyslipidaemia. CoQ10 also reduces the ischaemia-reperfusion injury seen in patients recovering from myocardial ischaemia. Its antioxidant properties contribute to prevention of lipid peroxidation, which alleviates the oxidative stress inherent in CHF. Patients with severe CHF, i.e. NYHA class III and IV tend to have lower levels of endogenous CoQ10 than that of patients with NYHA class-I CHF or healthy subjects.5 Thus, patients with severe diseases may be more likely to attain a favourable clinical response to CoQ10 supplementation.

Studies reported clinical benefits from short-term (1-4 wks) and long-term (3 months - 6 yrs) therapy with oral CoQ10 supplements, 50-100 mg/day, added to conventional therapy in patients with severe CHF (NYHA class III and IV).4,5,8-11 Two large multicenter, open-label studies evaluated the efficacy and safety of CoQ10 as adjuvant therapy in CHF. The two studies examined a total of more than 4000 patients with varying severity of CHF (i.e. patients with NYHA class II and III and class III and IV CHF) who experienced clinical improvement in signs and symptoms such as cyanosis, oedema, pulmonary rales, dyspnoea, and palpitations.12,13

Role in angina
The mechanism for improved exercise tolerance in patients with stable angina may be due to ischaemic myocardial protection by CoQ10, allowing tissue to reach higher levels of energy expenditure.5 Possible activities of the coenzyme in the maintenance of oxidative phosphorylation, enhancement of ATP synthesis, or reduction of free radicals formation create distinctions between the anti-anginal effects of CoQ10 and the effects of other agents such as nitrates, calcium channel blockers, or b-adrenergic blockers. The ability of exogenous CoQ10 to protect the ischaemic myocardium and reduce or delay signs and symptoms of angina is suggested by six small randomized, double-blind, placebo-controlled studies involving patients with stable angina pectoris.14,15-19 All of these studies determined that CoQ10 dosages of 60-600 mg/day significantly prolonged exercise duration, reduced exercise-induced ischaemic ST-segment depression, and delayed the onset of stable angina pectoris when compared with placebo.

Role in hypertension
These effect of CoQ10 to decrease blood pressure is attributed to the correction of endogenous pro-vitamin deficiency.20,21 In a study of hypertensive rats, a deficiency in the activity of succinate de-hydrogenase CoQ10 reductase in leucocytes was found. Deficient activity of this enzyme can result in decreased levels of CoQ10.22 Having identified same deficiency in human subject with chronic hypertension, investigators conducted a pilot study in which they concluded that increased succinate dehydrogenase CoQ10 reductase activity and subsequent increased CoQ10 level lead to decreases in systolic and diastolic blood pressures.20,23 Statistically significant decreases in systolic and diastolic blood pressure were observed with CoQ10 dosages ranging from 30-360 mg/day in patients with hypertension but these results are not consistent among the trials.20,21,24-29

Male infertility
Three important parameters in infertility are count, morphology and motility of sperm cells. The sperm count and morphology may be adversely affected due to damage by free radicals. The reduced sperm motility is the consequence of decrease in energy production ATP. CoQ10 has been found to be useful in idiopathic asthenozoospermia, which is loss or decrease of sperm motility in semen. In Jan 2004 a study was conducted to evaluate role of CoQ10 in male infertility. In this study subjects with history of primary infertility received 200 mg twice daily of CoQ10 for 6 months. At the end of study period CoQ10 levels in seminal plasma and phosphatidylcholine increased significantly. Motility of sperm cells also increased from 9.13% to 16.34%.

Testicular tissue and sperm viability are particularly vulnerable to peroxidation injury produced by free radicals and reactive oxygen species. Increased lipid peroxidation of sperm leads to its damage and thereby causing infertility. The reasons why sperms are vulnerable to damaging effects of these are: wide surface of the sperm membranes, poor cytoplasmic defense mechanisms, lack of protection in the female genital tract once the sperms are ejaculated. Whenever there is oligoasthenozoospermia, the available sperm also have a high chance of being damaged by free radicals.

Asthenospermia and ATP
The main concentration of mitochondria in the sperm is in its midpiece. The sperm motility is directly dictated by its ability to generate ATP, which in turn is dependent on CoQ10 production. The motility of sperm requires a high-energy expenditure, and hence optimal mitochondrial ATP generation plays an important role in sperm motility.30

Just before ovulation, the quantity of water and mucus increases in the living cells of the cervix in female. The water and salt interact with the glycoproteins present in mucus to form crystal. This is called ferning and, as a result of the latter channels is formed in mucus, which only allows sperms, which are normal, and possess adequate motility, to navigate successfully so as to reach the ovum for fertilization in the optimal 69 minutes of time. CoQ10 encourages better sperm viability due to proving protection against the damaging effects of reactive oxygen species, and also by enhancing sperm motility. The CoQ10 concentration in serum is usually 0.081-1.066 mmol, and good correlation has been demonstrated between these levels and sperm motility/count.31 Due to its lipophillic nature. CoQ10 increases the membrane integrity of sperm and increases defense mechanism of the sperm. Because of its antioxidant and free radical scavenging activity, CoQ10 prevents the sperm from free radical induced damage.

After administration, CoQ10 gets incorporated in the sperm mitochondria during the process of spermatogenesis. Since the complete process of spermatogenesis requires a long time CoQ10 should be administered at least for a period of 10 to 12 weeks

In therapeutic dosages, CoQ10 has proved to be relatively devoid of major side effects. The most common adverse effects are nausea, epigastric pain, diarrhoea, heartburn, and appetite-suppression. However, the prevalence of these adverse effects was less than 1% in reported studies.3,5 Gastrointestinal effects of CoQ10 may be lessened with a dosage reduction or may subside with continued therapy. Asymptomatic elevations in serum lactate dehydrogenase and hepatic enzymes were observed and may occur with oral dosages of CoQ10 in excess of 300 mg/day; however, cases of serious hepatotoxicity have not been reported.6,35 Clinical relapse was noted on withdrawal of CoQ10, whereas reinstatement of therapy resulted in improvement.36-37 In one withdrawal study, subsequent onset of fatigue and dyspnoea indicating clinical relapse occurred in 88% of 16 patients, yet 75% improved and regained their clinical status with resumption of CoQ10.36

Drug interactions
A drug interaction may occur between HMG-CoA reductase inhibitors and CoQ10 because the coenzyme is a byproduct of the cholesterol biosynthetic pathway. Use of HMG-CoA reductase inhibitors (statins i.e. simvastatin, pravastatin, lovastatin) may result in the diminution of CoQ10 blood levels due to interruption of synthesis.38-41 Other antilipidaemic agents such as cholestyramine of fibrate derivatives do not appear to affect CoQ10 concentrations.40

The oral antidiabetic agents (i.e., acetohexamide, glyburide, phenformin, and tolazamide) may inhibit enzymes (e.g., NADH and succinate dehydrogenase) resulting in reductions in serum CoQ10 levels.42

CoQ10 is structurally related to vitamin-K and subsequently possesses procoagulant effects. The potentially critical interaction can result as a diminished response to warfarin therapy. Several reports describe decreases in international normalized ratio (INR) after the addition of CoQ10 in patients previously stabilized with warfarin therapy.43 The concomitant use of warfarin and CoQ10 should be avoided due to the risk of thrombotic complications.

Also, reduced insulin requirements were observed in patients with diabetes who were taking CoQ10 because it exerts favourable effects on ATP, which in turn acts as a chemical energy carrier in the biosynthesis of insulin.42

CoQ10 supplementation in patients with hepatic insufficiency or biliary obstruction may increase serum CoQ10 levels because this molecule is metabolized in liver and excreted primarily through the biliary tract.35

Safety profile of CoQ10 during pregnancy and lactation has not been established, and interactions between CoQ10 and food, herbs, or other dietary supplements are not known.

CoQ10 administered orally has favourable actions in various cardiovascular conditions and appears to be safe and well tolerated in the adult population. A conservative approach to CoQ10 therapy is to support its use as adjuvant treatment for CHF, angina or hypertension. Its favourable effects on ejection fraction, exercise tolerance, cardiac output, and stroke volume were demonstrated in CHF. These clinically significant effects may benefit patients with NYHA class II, III and IV CHF who are using CoQ10 as an adjuvant to traditional heart failure therapy. Patients with angina may see prolonged exercise duration and reduced exercise-induced ST-segment depression with CoQ10. CoQ10 may possibly find a place in the therapy of parkinsonism, dyslipidaemia, migraine, male infertility, and atherosclerosis in near future.
The authors wish to thank the Dean, Dr. ME Yeolekar, for granting us permission to publish this report.
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In a Swedish population with non-bloody diarrhoea, nearly 10% had microscopic colitis found on colonoscopy, a diagnosis missed in the first histological examination. The incidence of micro-scopic colitis almost matched that of Crohn’s disease. The cause of microscopic colitis is unknown. Budesonide and bismuth subsalicylate may work as initial therapy.

BMJ, 2004; 2055.

*Lecturer in Pharmacology, **Lucturer in Biochemistry,
***Trainee Intern, Grant Medical College and Sir JJ Group of Hospitals, Mumbai;
#Lecturer in Pharmacology, TN Medical College and BLY Nair Hospital, Mumbai.