COENZYME Q10
Coenzyme Q10 belongs to a family of compounds known as ubiquinones. All animals, including humans, can synthesize ubiquinones, so coenzyme Q10 cannot be considered a vitamin (1). The name ubiquinone refers to the ubiquitous presence of these compounds in living organisms and their chemical structure, which contains a functional group known as a benzoquinone. Ubiquinones are fat-soluble molecules with anywhere from 1 to 12 isoprene (5-carbon) units. The ubiquinone found in humans, ubidecaquinone or coenzyme Q10, has a "tail" of 10 isoprene units (a total of 50 carbons) attached to its benzoquinone "head" (diagram) (2).
FUNCTION
Coenzyme Q is highly soluble in lipids (fats) and is found in virtually all cell membranes, as well as lipoproteins (2). The ability of the benzoquinone head group of coenzyme Q to accept and donate electrons is a critical feature in its physiological functions. Coenzyme Q can exist in three oxidation states (diagram): 1) the fully reduced ubiquinol form (CoQH2), 2) the radical semiquinone intermediate (CoQH·), and 3) the fully oxidized ubiquinone form (CoQ).
Mitochondrial ATP synthesis
The conversion of energy from carbohydrates and fats to adenosine triposphate (ATP), the form of energy used by cells, requires the presence of coenzyme Q in the inner mitochondrial membrane. As part of the mitochondrial electron transport chain, coenzyme Q accepts electrons from reducing equivalents generated during fatty acid and glucose metabolism and transfers them to electron acceptors. At the same time, coenzyme Q transfers protons outside the inner mitochondrial membrane, creating a proton gradient across that membrane. The energy released when the protons flow back into the mitochondrial interior is used to form ATP (2).
Lysosomal function
Lysosomes are organelles within cells that are specialized for the digestion of cellular debris. The digestive enzymes within lysosomes function optimally at an acid pH, meaning they require a permanent supply of protons. The lysosomal membranes that separate those digestive enzymes from the rest of the cell contain relatively high concentrations of coenzyme Q. Recent research suggests that coenzyme Q plays an important role in the transport of protons across lysosomal membranes to maintain the optimal pH for cellular recycling (2, 3).
Antioxidant functions
In its reduced form, CoQH2 is an effective fat-soluble antioxidant. The presence of a significant amount of CoQH2 in cell membranes, along with enzymes that are capable of reducing oxidized CoQ back to CoQH2, supports the idea that CoQH2 is an important cellular antioxidant (2). CoQH2 has been found to inhibit lipid peroxidation when cell membranes and low-density lipoproteins (LDL) are exposed to oxidizing conditions outside the body (ex vivo). When LDL is oxidized ex vivo, CoQH2 is the first antioxidant consumed. Moreover, the formation of oxidized lipids and the consumption of a-tocopherol (vitamin E) are suppressed while CoQH2 is present (4). In isolated mitochondria, coenzyme Q can protect membrane proteins and DNA from oxidative damage that accompanies lipid peroxidation (1). In addition to neutralizing free radicals directly, CoQH2 is capable of regenerating a-tocopherol.
Nutrient Interactions
Vitamin E: Alpha-tocopherol and coenzyme Q are the principal fat-soluble antioxidants in membranes and lipoproteins. When alpha-tocopherol (a-TOH) neutralizes a free radical, such as a lipid hydroperoxyl radical (LOO·), it becomes oxidized itself, forming the a-tocopheroxyl radical (a-TO·), which can promote the oxidation of lipoproteins under certain conditions in the test tube. When the reduced form of coenzyme Q (CoQH2) reacts with a-TO·, a-TOH is regenerated and the semiquinone radical (CoQH·) is formed. It is possible for CoQH· to react with oxygen (O2) to produce superoxide (O2·-), which is a much less oxidizing radical than LOO·. However, CoQH· can also reduce a-TO· back to a-TOH, resulting in the formation of fully oxidized coenzyme Q (CoQ), which does not react with O2 to form O2·- (See Reaction Scheme) (4, 5).
Vitamin B6: The first step in coenzyme Q10 biosynthesis (the conversion of tyrosine to 4-hydroxyphenylpyruvic acid) requires vitamin B6 in the form of pyridoxal 5'-phospate. Thus, adequate vitamin B6 is essential for coenzyme Q biosynthesis. A pilot study in 29 patients and healthy volunteers found significant positive correlations between blood levels of coenzyme Q10 and measures of vitamin B6 nutritional status (6). However, further research is required to determine the clinical significance of this association.
SOURCES
Biosynthesis
Coenzyme Q10 is synthesized in most human tissues. The biosynthesis of coenzyme Q10 involves three major steps: 1) synthesis of the benzoquinone structure from the amino acids, tyrosine or phenylalanine, 2) synthesis of the isoprene side chain from acetyl-coenzyme A (CoA) via the mevalonate pathway, and 3) the joining or condensation of these two structures. The enzyme hydroxymethylglutaryl (HMG)-CoA reductase plays a critical role in the regulation of coenzyme Q10 synthesis as well as the regulation of cholesterol synthesis (1, 7).
Food Sources
Based on food frequency studies the average dietary intake of coenzyme Q10 in Denmark was estimated to be 3-5 mg/d (7, 8). Most people probably have a dietary intake of less than 10 mg/d of coenzyme Q10. Rich sources of dietary coenzyme Q10 include mainly meat, poultry, and fish. Other relatively rich sources include soybean and canola oils, and nuts. Fruits, vegetables, eggs, and dairy products are moderate sources of coenzyme Q10. Approximately 14-32% of coenzyme Q10 was lost during frying, but the coenzyme Q10 content of vegetables and eggs did not change when boiled. Some relatively rich dietary sources and their coenzyme Q10 content in milligrams (mg) are listed in the table below (9-11).
Summary
Coenzyme Q10 is a fat-soluble compound primarily synthesized by the body and also consumed in the diet.
Coenzyme Q10 is required for mitochondrial ATP synthesis and functions as an antioxidant in cell membranes and lipoproteins.
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Endogenous synthesis and dietary intake appear to provide sufficient coenzyme Q10 to prevent deficiency in healthy people.
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Oral supplementation of coenzyme Q10 increases plasma, lipoprotein, and blood vessel levels, but it is unclear whether tissue coenzyme Q10 levels are increased, especially in healthy individuals.
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Coenzyme Q10 supplementation has resulted in clinical and metabolic improvement in some patients with hereditary mitochondrial disorders.
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Although coenzyme Q10 supplementation may be a useful adjunct to conventional medical therapy for congestive heart failure, additional research is needed.
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Roles for coenzyme Q10 supplementation in other cardiovascular diseases, neurodegenerative diseases, cancer, and diabetes require further research.
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Coenzyme Q10 supplementation does not appear to improve athletic performance.
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Although coenzyme Q10 supplements are relatively safe, they may decrease the anticoagulant efficacy of warfarin (Coumadin).
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Presently, it is unclear whether individuals taking cholesterol-lowering medications, known as HMG-CoA reductase inhibitors (statins), would benefit from coenzyme Q10 supplementation. More information
By The Linus Pauling Institute
http://lpi.oregonstate.edu/infocenter
