Coenzyme Q10 (Co Q10, or coenzyme Q) or ubiquinone (because of its wide spread occurrence) is a naturally occurring substance that is found in virtually all cells of the human body. It is important to emphasize that coenzyme Q has several biochemical functions. The most known functions are in mitochondrial energy coupling and its function as a primary regenerating antioxidant. Less commonly known functions include oxidant action in the generation of signals and control of redox state. Through its participation in transmembrane electron transport, Co Q10 can carry reducing equivalents to the inside of vesicles or the outside of cells. Evidence also suggests a role in the control of membrane structure and phospholipids status. Structurally, coenzyme Q is 2,3-dimethoxy,5-methyl, 6-polyisoprene parabenzoquinone. The functional group is the quinone ring through reduction of quinone to quinol, a carrier of protons and electrons is produced (1). Coenzyme Q is distributed in all membranes throughout the cell. There are well defined protein binding sites on the enzymes involved in coenzyme Q oxidation reduction. Coenzyme Q10 or simply just Q is a vitamin-like substance that resembles vitamin E, but which may be an even more powerful antioxidant.

Genetic mutation, aging, cancer and statin type drugs can cause a decrease of Co Q in serum or tissue. Deficiencies can be found in mitochondria of some cells and not others. The amount of coenzyme Q in the diet is not sufficient to increase serum coenzyme Q significantly, and thus, supplementation (~100 mg/day) is required to significantly increase coenzyme Q in the serum.

Coenzyme Q is a vital component of oxidative phosphorylation in mitochondria that converts energy in carbohydrates and fatty acids into ATP to drive cellular machinery and synthesis. Recall that oxidative phosphorylation usually refers to the enzymatic transfer of a phosphate group from ADP to ATP coupled to electron transfer from some substrate to oxygen. The major part of ATP production occurs in the inner membrane of mitochondria, where coenzyme Q is found. Co Q10 is unique in that it transfers electrons from primary substrates to the oxidase system at the same time that it transfers protons to the outer mitochondrial membrane (generating a proton gradient across the membrane). As the protons return to the interior through enzymatic processes for making ATP, they drive ATP formation. The coenzyme Q is bound to the enzymatic protein complexes and as it is oxidized it releases protons to the outside and picks up electrons and protons on the inside of the mitochondrial membrane. The role of antioxidant for Co Q10 is in part due to its location in membranes near unsaturated lipid chains to act as a primary scavenger of free radicals. Interestingly, the amount of Co Q10 in membranes ranges from 3-30 times the tocopherol content (cf. 1).

New roles for coenzyme Q in other cellular functions are only becoming recognized. The new aspects have developed from the recognition that coenzyme Q can undergo oxidation/reduction reactions in other cell membranes such as lysosomes, Golgi or plasma membranes. In mitochondria and lysosomes, coenzyme Q undergoes reduction/oxidation cycles during which it transfers protons across the membrane to form a proton gradient. The presence of high concentrations of quinol in all membranes provides a basis for antioxidant action either by direct reaction with radicals or by regeneration of tocopherol and ascorbate. Evidence for a function in redox control of cell signaling and gene expression is developing from studies on coenzyme Q stimulation of cell growth, inhibition of apoptosis, control of thiol groups, formation of hydrogen peroxide and control of membrane channels. Deficiency of coenzyme Q has been described based on failure of biosynthesis caused by gene mutation, inhibition of biosynthesis by HMG coA reductase inhibitors (statins) or for unknown reasons in ageing and cancer. Correction of deficiency requires supplementation with higher levels of coenzyme Q than are available in the diet.

In normal healthy individuals, coenzyme Q is synthesized in all cells from tyrosine (or phenylalanine) and mevalonate. Low levels of coenzyme Q are found in disease and aging. At this point it is not clear how Co Q10 is distributed in tissue. In normal functioning tissue, there appears to be a saturation level of Co Q10 in membranes. Therefore, supplementation with coenzyme Q10 does not increase tissue levels above normal (except liver and spleen). This is particularly true for young, healthy animals.

The usual average daily intake is approximately ten milligrams per day (2). The biosynthesis of CoQ10 involves a complex process requiring the amino acid tyrosine and at least eight vitamins and some trace elements. The quinone ring of Co10 is synthesized from tyrosine. The polyisoprenoid side-chain is formed from acetyl-CoA. The structure of CoQ10 includes a chemical compound containing a six carbon benzene ring. In humans, there are ten isoprene units, hence the name Coenzyme Q10.

CoQ10 acts as a respiratory chain electron carrier in the electron transport system. Ubiquinone can accept one electron to become a semiquinone radical (UQH) or two electrons to form ubiquinol (UQH2) and like flavoprotein carriers, it is therefore able to act at the junction between a two-electron donor and a one-electron acceptor. Because ubiquinone is both small and hydrophobic, it is freely diffusible within the lipid bilayer of the inner mitochondrial membrane and can shuttle reducing equivalents between other, less mobile, electron carriers in the membrane (3).

All cellular function depends on an adequate supply of ATP. CoQ10’s role as a mobile electron carrier in the mitochondrial electron transport system makes it the crucial nutrient for the production of aerobic energy. Therefore, CoQ10 supports every cell in our bodies by generating an electrical charge on the mitochondrial membrane which is necessary for ATP synthesis.