Pharmacology: Pharmacodynamics: Mechanism of Action: Coenzyme Q10 is a fat-soluble, vitamin-like compound that is naturally found in most tissue of the human body. It is essential for life and health of every living cell. The highest concentrations are found in the heart, liver, kidney and pancreas. The lowest concentrations are found in the lungs.
The human body produces coenzyme Q10. Humans can replenish co-enzyme Q10 from dietary sources, including meats and sea food. Everything living or once living contains coenzyme Q10.
Within the cell, coenzyme Q10 is mostly present in the mitochondria (40-50%). It is the electron acceptor for the mitochondrial electron transport chain. It is also a co-factor used in processes of aerobic respiration, aerobic metabolism, oxidative metabolism and cell respiration. Coenzyme Q10 primary functions are as an antioxidant, membrane stabilizer and production of adenosine triphosphate (ATP) in the oxidative respiration process. As an antioxidant and its role in ATP, coenzyme Q10 offers many therapeutic benefits. Also, coenzyme Q10 has been shown to help preserve myocardial sodium-potassium ATPase activity and stabilize myocardial calcium-dependent iron channels.
The possible therapeutic mechanisms of action of coenzyme Q10 in cardiovascular diseases are as follows: Improvement of cardiac bioenergetics, direct free radical scavenger and antioxidant effect, correction of coenzyme Q10 deficiency state, improved endothelial function and vasodilatory effect, direct membrane-stabilizing activity due to phospholipid-protein interactions, preservation of myocardial Na-K ATPase activity, stabilization of integrity of Ca2+-dependent slow channels, correction of mitochondrial "leak" of electrons during oxidative respiration, induction of DT diaphorase, possible effects on prostaglandin metabolism, antiviscosity effect, altering the immune response.
EPA and DHA compete with arachidonic acid (AA) for the enzyme cyclooxygenase. EPA is converted by platelet cyclooxygenase to thromboxane A3 (TXA3), which is only a very weak vasoconstrictor, unlike A2 (TXA2), which is formed by the action of cyclooxygenase on AA and is a strong vasoconstrictor. However, prostacyclin I3 (PGI3), formed from EPA in the endothelium, is as potent as vasodilator and inhibitor of platelet aggregation as is prostacyclin I2 (PGI2) formed from AA. The net effect, therefore, of an increased dietary EPA: AA ratio is relative vasodilation and platelet aggregation inhibition. EPA yields the 5-series of leukotrienes, which are only weakly chemotactic. A relative reduction in chemotaxis might be expected to be anti-atherogenic. Fish oil decreases both very low-density lipoproteins (VLDLs) and triglycerides due to inhibition of hepatic triglyceride synthesis. Because VLDL is a precursor to LDL, a reduction in LDL cholesterol is seen in some patients with hypertriglyceridemia; however, fish oil does not appear to lower plasma cholesterol in subjects with hypercholesterolemia.