Coenzyme Q10 is an oil soluble vitamin-like substance which is present mainly in the mitochondria of almost all cells of humans (Bank et al., 2011). Coenzyme Q10 is also known as ubiquinone, ubidecarnenone, vitamin Q and CoQ10. The amount and intracellular distribution of CoQ10 are correlated with aerobic respiratory activity. Tissues with high energy requirements like heart, brain and liver contain higher amounts of CoQ10.
Most of the activities of CoQ10 are a result of its role in bioenergetics and its antioxidant action. The levels of CoQ10 have been reported to be lowered in many diseases like heart diseases, muscular dystrophies, neurodegenerative diseases, cancer, diabetes and HIV/AIDS. Drug treatments like statin therapy were also identified as reasons for lowered CoQ10 (Mas and Mori, 2010). CoQ10 is mainly responsible for the electron transport in the inner membrane of mitochondria. Mitochondria are responsible for the production of energy from food via respiration. Apart from its bioenergetic role, CoQ10 and its reduced form ubiquinol also act as potent antioxidants.
The supplementation of CoQ10 is an effective treatment in CoQ10 deficiencies and in hypertension (Wyman et al., 2010, Kumar et al., 2009, Rosenfeldt et al., 2007). There is some scientific evidence that CoQ10 supplementation might be useful in muscular dystrophies, Parkinson’s disease, periodontal disease and in migraine. Other uses of CoQ10 include age related macular degeneration, Alzheimer’s disease, cancer, AIDS, angina, asthma and diabetes (Shults et al., 2002). CoQ10 can also improve physical performance and can rejuvenate the wrinkled skin (Littarru and Tiano, 2007).
b. Background of the problem that the drug treats
CoQ10 is endogenously synthesised in the body via the mevalonate pathway. Formation of mevalonate from 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG CoA) by HMG CoA reductase is the rate limiting step in the mevalonate pathway. Cholesterol is also synthesised via the same pathway. Thus, statin treatment which is intended to inhibit the HMG CoA reductase to reduce cholesterol synthesis also inhibits the synthesis of CoQ10. Due to this reason statin treatment results in rhabdomyolysis and other muscular ailments. CoQ10 can also be received from diet apart from endogenous synthesis, however the dietary source does not provide sufficient levels to replace the deficient amount with aging, disease or drug treatment (Bank et al., 2011).
Another important role of CoQ10 is its antioxidant activity i.e. its ability to counteract oxidative stress. Oxidative stress is known to be the cause of many diseases. The human body is equipped with an effective antioxidant defence system which comprises antioxidant enzymes and molecules. Antioxidant enzymes include superoxide dismutase, catalase, glutathione peroxidise etc. Antioxidant molecules are water-soluble or fat-soluble molecules which can scavenge free radicals. Glutathione and vitamin C are examples of water-soluble antioxidants. Fat-soluble antioxidants include vitamin E, carotenoids, CoQ10, etc. However, in some disease conditions, the balance between the production of reactive oxygen species and the antioxidant defence system is altered leading to oxidative stress. Oxidative stress can lead to a chain reaction that produces free radicals which might eventually result in the damage of cellular components and even cell death. Excessive oxidative stress leads to the damage of various cellular components affecting their functions which in turn can lead to pathogenesis or progression of diseases. Antioxidants are the agents which can help prevent and reduce the production of oxidative stress and by doing this they help in the prevention and treatment of diseases. Oxidative stress is also known to be responsible for the aging process.
c. The drug’s mechanisms of action
The possible mechanisms of CoQ10 in cardiac diseases are improvement in cardiac bioenergetics, free radical scavenging and antioxidant effects, correction of CoQ10 deficiency, vasodilatory effect, membrane stabilizing activity, antiviscosity effect and ability to alter immune responses (Kumar et al., 2009).
CoQ10 exists in three different forms; namely ubiquinone, ubisemiquinone and ubiquinol. The antioxidant activity of endogenous or exogenous CoQ10 could be due to direct action of CoQ10 on superoxide radicals, or due to the scavenging activity of ubiquinol on oxygen- or carbon- centered radicals and the recycling of another lipophilic antioxidant, ?-tocopherol (which is a form of vitamin E).
d. Clinical Trials
More than 200 clinical trials have been conducted using CoQ10 in various disease conditions and many trials are being conducted presently. The trials have shown that CoQ10 is beneficial in neurodegenerative disorders, cardiovascular diseases, statin therapy, reproductive health, cancer and periodontal disease. The trials reported that CoQ10 was safe and well tolerated at the tested doses (Bank et al., 2011). Clinical efficacy of CoQ10 is sometimes limited because of the poor absorption of CoQ10 from the gut. High lipophilicity and high molecular weight contribute to the poor bioavailability of CoQ10. Formulations which can enhance the bioavailability of CoQ10 are beneficial for effective response.
CoQ10 is available as oral capsules or tablets. The dose range for CoQ10 supplementation varies from 30 mg – 200 mg per day.
f. Interactions with other drugs, foods, alcohol
CoQ10 is fat soluble and thus the absorption can be enhanced when taken along with food rich in fat content. CoQ10 may be helpful in reducing the toxic effects caused by doxorubicin and daunorubicin. CoQ10 acts as an antihypertensive agent and scientific studies show that supplementation of CoQ10 in patients taking antihypertensive medication allowed to lower the required doses of these antihypertensives.
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LITTARRU, G. & TIANO, L. 2007. Bioenergetic and antioxidant properties of coenzyme Q10: recent developments. Molecular biotechnology, 37, 31-38.
MAS, E. & MORI, T. 2010. Coenzyme Q(10) and statin myalgia: what is the evidence? Current atherosclerosis reports, 12, 407-420.
ROSENFELDT, F., HAAS, S., KRUM, H., HADJ, A., NG, K., LEONG, J. Y. & WATTS, G. 2007. Coenzyme Q10 in the treatment of hypertension: a meta-analysis of the clinical trials. Journal of human hypertension, 21, 297-603.
SHULTS, C. W., OAKES, D., KIEBURTZ, K., BEAL, M. F., HAAS, R., PLUMB, S., JUNCOS, J. L., NUTT, J., SHOULSON, I. & CARTER, J. 2002. Effects of coenzyme Q10 in early Parkinson disease: evidence of slowing of the functional decline. Archives of Neurology, 59, 1541.
WYMAN, M., LEONARD, M. & MORLEDGE, T. 2010. Coenzyme Q10: a therapy for hypertension and statin-induced myalgia? Cleveland Clinic journal of medicine, 77, 435-477.