Coenzyme Q₁₀ (CoQ₁₀)

R.A.S HEMAT, MB;BCh, FRCSI, DUL.

CoQ₁₀ is a lipid soluble benzoquinone, which has properties potentially useful in preventing or attenuating the damage, associated with ischaemia reperfusion. CoQ₁₀ is directly involved in energy transduction and aerobic ATP production as it transports electrons in the respiratory chain, as well as couples the respiratory chain to oxidative phosphorylation.

An extremely basic function of CoQ₁₀ in medication and preservation of antioxidant function in cells acts to remove oxygen radicals, and reduce tocopheryl radicals and semihydroascorbate back to tocopherol and ascorbate, respectively. CoQ₁₀ acts as antioxidant because it can be reduced by metabolic supply of NADH or NADPH in the cell to form the hydroquinone.

The reduced CoQ₁₀ can reduce tocopheryl radical. CoQ₁₀ acts to reduce extracellular ascorbate free radical back to ascorbate.
NADH cytochrome b5 (Nb5R) is located on the cytosolic side of all endomembranes including the plasma membrane and is known primarily for its function in reduction of the non-heme iron fatty acid desaturase. Nb5R can reduce CoQ₁₀.

Increased demand for CoQ may be: a- bioenergentics (decreased activity of the respiratory chain, or increased affinity for CoQ of respiratory enzymes); b- oxidant (oxidative stress, aging). Changes in the characteristics of CoQ₁₀, flavoproteins and iron-sulfur centers in mitochondrial membranes, produced by prolonged ischaemia, are the underlying pathology in the reperfusion or re-oxygenation damage of cells. The interaction between ubiquinol, vitamin E and vitamin C play an important protective role against oxidative stress.

About 60% of plasma CoQ₁₀ is found associated with LDL. LDL is drastically involved in the onset of atherosclerosis. The redox status of CoQ₁₀ in plasma may change in acute or chronic pathological conditions, where a certain degree of peroxidative insult is present.
CoQ₁₀ or ubiquinone is a redox component of the respiratory chain, which may be involved in the pathogenesis of cancer. Since prooxidants may promote tumourigenesis, ubiquinone supplementation in cancer could be relevant.

CoQ₁₀ can provide rapid protective effects in patients with acute myocardial infarction (AMI) when administered within 3 days of the onset of symptoms. Definite levels of CoQ₁₀ are also found in white and red blood cell components, as well as in platelets.

Between the ages of 20-30 and 60-90, there are large and significant decreases in the activities of Complexes I (NADH) and IV (CoQ₁₀) of oxidative phosphorylation by 59% and 47% respectively. As CoQ₁₀ levels decrease dolichol levels increase, indicating a shift in the regulation of the related pathways of dolichol, CoQ₁₀, and cholesterol synthesis. Statin lowers both LDL-C and apo-B plasma levels together with the plasma and platelet levels of CoQ₁₀, Statins inhibit synthesis of mevalonate, a precursor of ubiquinone that is a central compound of the mitochondrial respiratory chain. The main adverse effect of statins is a toxic myopathy possibly related to mitochondrial dysfunction.

Oral antidiabetic agents (i.e., acetohexamide, glyburide, phenformin, and tolazamide) inhibit CoQ₁₀ enzymes (e.g., NADH and succinate dehydrogenase), thus reducing serum CoQ₁₀ levels.

CoQ₁₀ may result in improvement in sperm functions in selective patients. There is a correspondence between a low CoQ₁₀ level and spontaneous abortion.

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Dr. R.A.S HEMAT declares no conflicts of interest or financial interests in any product or service mentioned in this article, including grants, employment, stock holdings, gifts, or honoraria.