Pharmacodynamics. Coenzyme Q10 serves as the electron acceptor for complexes I and II of the mitochondrial electron transport chain and also acts as an antioxidant and is neuroprotective. Water-soluble coenzyme Q10 acts by stabilizing the mitochondrial membrane when neuronal cells are subjected to oxidative stress (Somayajulu et al 2005). It would be an effective plasma antioxidant because it can regenerate plasma vitamin E.
Coenzyme Q10 has the potential to be a beneficial agent in neurodegenerative diseases in which there is impaired mitochondrial function and excessive oxidative damage. The following are some of the effects that have been demonstrated in experimental studies:
Coenzyme Q10 was shown to have neuroprotective effect in the 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine model of parkinsonism (Cleren et al 2008). In animal models of Parkinson disease, amyotrophic lateral sclerosis, and Huntington disease, coenzyme Q10 can protect against striatal lesions produced by the mitochondrial toxins malonate and 3-nitropropionic acid. These toxins have been utilized to model the striatal pathology, which occurs in Huntington disease.
It also protects against 1-methyl-1, 2, 3, 6-tetrahydropyridine toxicity in mice. Coenzyme Q10 significantly extended survival in a transgenic mouse model of amyotrophic lateral sclerosis.
Coenzyme Q10 has a neuroprotective effect on the brain in infarction induced by ischemic injury in aged and susceptible transgenic mice (Li et al 2007). Coenzyme Q10 has been shown to ameliorate most of the biochemical changes induced by ischemia/reperfusion in irradiated rat brain (Abd-El-Fattah et al 2010).
Pharmacokinetics. Because of its hydrophobicity and large molecular weight, absorption of dietary coenzyme Q10 is slow and limited. Solubilized coenzyme Q10 formulations show enhanced bioavailability with Tmax of approximately 6 hours and an elimination half-life of approximately 33 hours (Bhagavan and Chopra 2006).
Oral preparations of coenzyme Q10 are used in human therapeutics. A randomized crossover study investigated the absorptive properties of 4 different coenzyme Q10 preparations: fast-melting, effervescent, soft gelatin, and powder-filled hard shell (Joshi et al 2003). Area under the curve for various formulations was not significantly different. Maximum drug concentration for the various formulations ranged between 0.70 and 0.86 µg/mL. Tmax for the fast-melting and effervescent formulations was 1.3 and 2 hours, respectively. This was significantly shorter compared with the Tmax of soft gel and powder-filled forms which was 3.7 and 4.1 hours, respectively. Q-Gel, a solubilized form of coenzyme Q10, is superior to tablets and capsules regarding bioavailability. Therefore, lower doses of Q-Gel are required to rapidly reach and maintain adequate blood coenzyme Q10 levels. A colloidal-Q10 preparation has been shown to improve the intestinal absorption and the bioavailability of coenzyme Q10 in humans (Liu and Artmann 2009).
Clinical laboratory monitoring is available for measurement of total coenzyme Q10 in plasma and tissue and for measurement of redox status, ie, the ratio of reduced and oxidized forms of coenzyme Q10. It is recommended that laboratory monitoring should be correlated with effects of treatment (Steele et al 2004).