Coenzyme Q10: Benefits, Side Effects, Uses, Dosage, Warnings?


COENZYME Q10: Benefits, Side Effects, Uses, Dosage, Warnings?

Ubiquinone-10 (also UQ of English. ubiquinone or Q-10 or coenzyme Q 10 [2] ) is a quinone derivative with lipophilic isoprenoid side chain, structurally related to vitamin K and vitamin E . Reduced phenolic form is Ubihydrochinon or ubiquinol (QH short 2 ) called. Ubiquinone-10 is one of the ubiquinones .

Q-10 is an electron - and protons -Überträger between the complex I or complex II and the complex III of the respiratory chain .
Q-10 as a component of cosmetic creams as well as dietary supplements offered for sale.

Contents [ Hide ]
1 properties
2 Biological Function
2.1 Biochemistry
2.2 Prooxidante and antioxidant properties
2.3 Lack
2.4 Biosynthesis
3 Nutritional Supplements
4 Cosmetics
5 occurrences
6 production
7 history
8 sources
9 Literature
10 See also
11 Web Links
Properties [ Edit ]
Q-10 is a yellow-orange crystalline powder without smell and taste.

The hydrophobic isoprenoid side chain allows the anchoring of the molecule also in the hydrophobic region of biological membranes , the mitochondria build.

Biological Function [ Edit ]
Q-10 is an endogenous substance. It is partly about the food taken, but also produced in the body itself. In each human cell , the energy is from food into body's energy ( ATP converted). Q-10 is a coenzyme in the oxidative phosphorylation involved, over 95% of total body energy (ATP) is produced. [3] [4] The organs with the highest energy requirements - such as heart , lung and liver - have therefore also the highest Q-10 concentration. [5]

Biochemistry [ Edit ]
The respiratory chain in the mitochondria of the cell allows the gradual transfer of electrons and protons on oxygen with simultaneous production of ATP as a biochemical energy equivalent. This sequence of reactions, sometimes referred to as "controlled oxyhydrogen reaction is called "place at localized membrane proteins, the complexes I to V, and mobile components, ubiquinone and cytochrome c , instead. The latter serve as shuttle systems between the complexes: ubiquinone mediates between complexes I / II and III, cytochrome c between complexes III and IV.

The electrons for the reduction of ubiquinone come from the oxidation of NADH at the complex I of the respiratory chain , the NADH dehydrogenase , or from the oxidation of succinate at complex II, wherein the succinate dehydrogenase of the citric acid cycle is identical. A ubiquinone molecule can accommodate two electrons gradually. In the first step, forming QH • , a fairly stable semiquinone - radical . Receiving the second electron can after protonation the hydroquinone ubiquinol created, that is the reduced form. In addition to the electron transport, this allows also the binding of two protons - ubiquinone may thus also serve as a proton carrier. These operations are within the respiratory chain in the Q cycle at complex III of importance.

Prooxidante and antioxidant properties [ Edit ]
Ubiquinone is also involved in the formation of reactive oxygen species (ROS) by the formation of superoxide by Ubi semiquinone - radicals which cause oxidative damage, which is based on many degenerative diseases. Paradoxically, the ubiquinone pool is also an important mitochondrial antioxidant . [6]

Deficiency [ Edit ]
A permanent Q-10 deficiency is rare. It is found more frequently in patients with myopathies . Since the enzymes involved in the biosynthesis of Q-10 are not all known, it is readily possible that mutations in one of the genes involved have not yet been identified. [7] [8] [9]

A way for temporary Q 10 deficiency, the medication with statins is where the inhibition of HMG-CoA reductase , the starting materials for the biosynthesis of Q-10 is reduced, leading to a decrease in the plasma levels. About the availability of Q-10 in the muscle on the other hand nothing is known, as little as a efficacy of increased supply. [10]

Biosynthesis [ Edit ]
The biosynthesis of Q-10 in the eukaryote involves both of 4-hydroxybenzoic acid from that of the amino acid tyrosine in five steps, including on Hydroxyphenylbernsteinsäure and 4-coumaric acid is obtained to form the quinone moiety; on the other side is the side chain of general trans required -Decaprenylphosphat consisting Geranylgeranylphosphat (GGP, from the mevalonate pathway is built up) in six steps. Both starting materials using the p-hydroxybenzoate Polyprenyltransferase ( EC together) to 3-decaprenyl-4-hydroxybenzoate. In seven further steps arises ubiquinol-10 , which is to ubiquinone-10 by electron transfer. [11]

Nutritional Supplements [ Edit ]
About the food takes a person a day about three to five milligrams of coenzyme on what is not absolutely necessary. [12] In rare elevated Q-10 may need a dietary supplement to help avoid a deficiency or balance. For adults, the recommended by most scientists in such a case dose of Q-10 is a dietary supplement 30-200 mg per day. [13] [14] The Federal Office of Consumer Protection and Food Safety has decreed that in Germany with food supplements in capsule form Q-10 may be marketed only if "the daily intake of 100 mg of coenzyme Q10 at a Recommended dosage of one capsule per day is not exceeded" and warns the labeling prior to consumption by pregnant women, nursing mothers, children under 18 years . [2]

Cosmetics [ Edit ]
Q-10 is also propagated active ingredient often offered skin creams . They are intended to offset the allegedly increasing the age lack of Q-10 and ensure z. B. the elimination of harmful radicals. [15]

Occurrence [ Edit ]
Q-10 is found rich in meat organs ( liver ), oily fish ( sardines , mackerel , etc.), nuts (eg. B. pistachios), legumes , sesame seeds, sunflower seeds, vegetable oils , cabbage, onions, potatoes, spinach, Brussels sprouts and broccoli. But can cook the coenzyme destroy.

Production [ Edit ]
For the production of Q-10, three methods are used: fermentation of yeast , the fermentation of bacteria , and chemical synthesis.

When Hefefermentationsverfahren arises Q-10 in the so-called trans configuration, which means that it is identical to the naturally occurring CoQ 10 , as found in meat, fish or other foods.

The security of yeast fermentation was confirmed by several safety studies of one of the world's leading research laboratories ( Covance Laboratories Inc. ) [16] were performed. In addition, in a double-blind, randomized, placebo-controlled study demonstrated that CoQ 10 is of yeast fermentation in doses up to 900 milligrams per day absolutely safe and well tolerated. [17]

The produced by chemical synthesis Q-10 contains the cis-isomer (a naturally occurring in Q-10 is not known molecular structure), have so far been carried out on its safety no intensive studies.

History [ edit ]
Ubiquinone-10 was discovered in 1957 and first used by Fred L. Crane from bovine isolated hearts. [18] The chemical structure was 1958 Karl August Folkers be elucidated. [19] For the evidence on the role of Q 10 in the Q cycle of complex III of the respiratory chain was the British scientist Peter D. Mitchell 1978 Nobel Prize in Chemistry .

Coenzyme Q10
Definition, synthesis, absorption, transport and distribution
Coenzyme Q10 (synonym: ubiquinone) is a vitaminoid (vitamin-like substance), which was discovered in 1957 at the University of Wisconsin. The Enlightenment whose chemical structure was a year later by the Working Group to the natural product chemist Prof. K. Folkers [24].

At the coenzymes Q is compounds selected from oxygen (O 2 ), hydrogen (H) and carbon (C) atoms, a so-called annular structure quinone form. At the benzoquinone ring is a lipophilic (fat-soluble) isoprenoid side chain bound [9, 10, 20, 25]. The chemical name of coenzyme Q is 2,3-dimethoxy-5-methyl-6-polyisoprene parabenzoquinone [4]. Depending on the number of isoprene units which are coenzymes Q1-Q10 to distinguish which all occur in nature. For example, the coenzyme Q9 of plants for photosynthesis is required. For man is the only Coenzyme Q10 is essential [4, 9, 10, 17, 20, 25].

Since the Coenzyme Q in all cells - human, animal, plant, bacteria - are represented, they are also called ubiquinone ("ubique" lat = "everywhere."), [24]. Animal foods such as lean meat, liver, fish and eggs, mainly contain coenzyme Q10 , while foods of plant origin predominantly ubiquinones with a smaller number of isoprene units have - for example, found in whole grains, a high amount of coenzyme Q9 [10, 17, 20, 25].

Ubiquinones have structural similarities to vitamin E and vitamin K [10, 17, 20, 25].


The human organism is capable of producing coenzyme Q10 in almost all tissues and organs themselves. Main synthesis places are the membranes of the mitochondria ("power plants" of eukaryotic cells) in the liver [3, 9, 20]. Precursor of the benzoquinone moiety, the amino acid tyrosine , which (in the body) from the essential (vital) amino acid endogenous phenylalanine is synthesized. The bound on the quinone ring methyl (CH 3 ) groups derived from the universal methyl group donor (emission of CH 3 groups) S-adenosylmethionine (SAM) . The synthesis of the isoprenoid side chain follows the general biosynthesis pathway of isoprenoid compounds via mevalonic acid (branched-chain, saturated hydroxy) - a so-called mevalonate pathway (formation of isoprenoids from acetyl coenzyme A (acetyl-CoA)) [3, 4, 9, 17, 20, 24, 25]. For coenzyme Q10 own synthesis in addition various vitamins of the B group, as are niacin ( vitamin B3 ) , pantothenic acid ( vitamin B5 ) , pyridoxine ( vitamin B6 ) , folic acid ( vitamin B9 ) and cobalamin ( vitamin B12 ) required [3, 13, 25]. Thus, for example pantothenic acid in the provision of acetyl-CoA, pyridoxine in the biosynthesis of tyrosine of the benzoquinone and folic acid and cobalamin in the remethylation (transmission of a CH 3 group) of homocysteine ​​to methionine (SAM → synthesis) involved [12, 28 ].

An insufficient supply with the Ubichinonvorstufen tyrosine, SAM and mevalonic acid and vitamins B3, B5, B6, B9 and B12, the body's own Q10 synthesis significantly reduced and the risk of coenzyme Q10 deficiency increase [3, 24]. Similarly, a deficit (inadequate) supply of vitamin E reduce the endogenous synthesis of Q10 and lead to a significant waste of Ubichinongehaltes of organs [3].

Patients with long-term total parenteral nutrition (parenteral nutrition, bypassing the gastrointestinal tract) have due to insufficient endogenous (body's own) synthesis often a coenzyme Q10 deficiency on. Cause of the lack of self-Q10 synthesis is the absence of first-pass metabolism (conversion of a substance during its first passage through the liver) of phenylalanine to tyrosine and the preferred use of tyrosine for protein biosynthesis (endogenous production of proteins). The first-pass effect of methionine to SAM is dispensed with, so that methionine primarily outside the liver to sulfate transamination (movement or delivery of an amino (NH 2 ) group) is [24].

In the course of diseases such as phenylketonuria , Q10 synthesis rate can be also reduced. This disease is the most common inborn error of metabolism with an incidence (number of new cases) of about 1: 8000th Affected patients have a lack or decreased activity of the enzyme phenylalanine hydroxylase (PAH) in which the degradation of phenylalanine to tyrosine is responsible. The result is an accumulation (accumulation) of phenylalanine in the body, leading to impaired brain development. By the absence of the tyrosine metabolic pathway occurs a relative deficiency of this amino acid on, in addition to the biosynthesis of the neurotransmitter dopamine, and thyroid hormone thyroxine of the pigment melanin pigment synthesis of Coenzyme Q10 decreased [10].

A therapy with statins (drugs to lower cholesterol) in the hypercholesterolemia is (elevated cholesterol serum levels) are used, is associated with an increased coenzyme Q10 needed. Statins, such as simvastatin, pravastatin, lovastatin, and atorvastatin, are of the pharmacological substance class of 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMG-CoA reductase) inhibitors , which by enzyme blocking the conversion of HMG-CoA to mevalonic acid - the rate-limiting step in cholesterol synthesis - inhibit (inhibit). Statins are therefore also called cholesterol synthesis enzyme (CSE) inhibitor called. On the blockade of the HMG-CoA reductase to a reduced supply of mevalonic acid leads to prevent addition to the statin cholesterol biosynthesis endogenous Ubichinonsynthese [6, 9, 10, 11, 19, 20, 25]. In patients treated with statins, is often a reduced Q10 serum concentration observed [4, 8, 14, 18, ​​22, 26]. However, it is unclear whether the reduced Q10 content in the serum is due to the reduced endogenous synthesis or the statin-induced reduction in the lipid-serum level, or of both, for the serum concentration of ubiquinone-10, which is transported by lipoproteins in the blood correlate with the of circulating blood lipids [11, 14].
, the limited endogenous synthesis of Q10 using statins increased with simultaneously low alimentary (food) Regulations Q10 supply the risk of coenzyme Q10 deficiency [6, 9, 8, 15, 19 , 20, 25, 26]. For this reason, patients who need to take HMG-CoA reductase inhibitor regularly, ensure adequate CoQ10 dietary intake or an additional Q10 supplementation (dietary supplement) obtained [4, 9, 10, 19, 20, 25]. Through the use of coenzyme Q10, the side effects of CSE inhibitors can significantly reduce, as they are partly due to a lack of ubiquinone-10 [25].

With increasing m age can a decreasing Q10 concentration in various organs and tissues are observed [5, 10, 17, 25]. The cause, among other things, a reduced endogenous synthesis is discussed, presumably from an insufficient supply of the Ubichinonvorstufen and / or with various vitamins of the B group results [25]. Thus we find in seniors often hyperhomocysteinemia (elevated homocysteine ​​levels) due to a lack of vitamin B12, folic acid or vitamin B6 , with a reduced supply of SAM is associated [10, 12, 29].


Similar to the lipid soluble vitamins A, D, E and K and the coenzymes Q can be due to their lipophilic isoprenoid side chain as part of the digestion of fats in the upper small intestine absorbed (recorded), that the presence of fats as the transport of lipophilic molecules of bile acids to solubilize ( increase the solubility) and micelle formation (formation of transport beads that fat soluble substances make transportable in aqueous solution) and of Pankreasesterasen (digestive enzymes from the pancreas) for the dissociation of bound ubiquinones is necessary for optimal intestinal absorption (absorption through the intestine).

Food-bound ubiquinones subject in the intestinal lumen of a first hydrolysis (cleavage by reaction with water) by means of esterases (digestive enzymes) from the pancreas (pancreatic). The released thereby Coenzyme Q arrive as part of the mixed micelles (aggregates of bile salts and the amphiphilic lipids) to the brush border of the enterocytes (cells of the small intestinal epithelium) and are internalized (added to the cells). Intracellular (within the cells), the incorporation of (recording) of ubiquinones in chylomicrons (fat lipoproteins), which transport via the lymphatic system, the lipophilic vitaminoids in the peripheral circulation [2, 4, 11, 14, 17].

Due to the high molecular weight and lipid solubility is the bioavailability of the supplied low ubiquinones and is probably from 5-10% . The absorption rate decreases with increasing dose. Concomitant intake of fats and phytochemicals, such as flavonoids, increases the bioavailability of coenzyme Q10 [1, 9, 25, 27].

Transport and distribution in the body

During transport to the liver and free fatty acids, monoglycerides of chylomicrons under the action of lipoprotein lipase (LPL) , which is located on the cell surface cleaves and triglycerides, is output to peripheral tissues, such as adipose tissue and muscle. Through this process, the chylomicrons are degraded to chylomicron remnants (chylomicron remnant low fat particles) that bind to specific receptors in the liver. The inclusion of coenzyme Q in the liver by means of receptor-mediated endocytosis (uptake into the cells by invagination of the biomembrane to form vesicles) [2, 4, 11, 14, 17, 27].

In the liver, alimentary supplied niedrigkettige coenzymes (coenzyme Q1-Q9) are converted into coenzyme Q10 [3, 9, 17, 25]. ubiquinone-10 is following in VLDL (very low density lipoproteins; fat very low density lipoproteins) intercalates. VLDL is secreted by the liver (secreted) and introduced into the bloodstream in order to distribute coenzyme Q10 to extrahepatic (outside the liver) tissue [2, 4, 11, 14].

Coenzyme Q10 is in lipophilic membranes and subcellular structures, particularly in the inner mitochondrial membrane of all body cells localized - primarily those with high energy expenditure [4, 24]. The highest Q10 levels were found in heart, liver and lung, followed by kidney, pancreas (pancreatic) and spleen [13, 24, 25]. Depending on the respective redox ratios (reduction / oxidation conditions) is the vitaminoid in oxidized (ubiquinone-10 in short, CoQ10) and reduced form (ubiquinol-10, Ubihydrochinon-10, short CoQ10H 2 ) before and thus influences both the structure and the enzymatic equipment of the cell membrane [4, 10]. For example, the activity of the transmembrane phospholipases (enzymes which cleave phospholipids and other lipophilic substances) by the redox control [4].

The absorption of coenzyme Q10 by the target cells is closely related to the Lipoproteinkatabolismus coupled (catabolism of lipoproteins). VLDL by binding to peripheral cells, through the action of lipoprotein lipase, a part of the Q10, free fatty acids and monoglycerides are internalized by passive diffusion (recorded in the cells). This results in the catabolism of VLDL to IDL (intermediate density lipoproteins) and then to LDL (low density lipoproteins, cholesterol-rich low density lipoproteins). Bound to LDL ubiquinone-10 is received on the one hand on receptor-mediated endocytosis in liver and extrahepatic tissues and on the other hand, HDL (high density lipoproteins, protein-rich high density lipoproteins) transferred. HDL is important in the transport of lipophilic substances from peripheral cells to the liver involved [2, 4, 11, 14, 17, 27].

The entire ubiquinone-10 inventory in the human body is dependent on supply and is probably 0.5-1.5 g [24].

In various diseases or processes , such as heart muscle and tumor diseases, diabetes mellitus, neurodegenerative diseases, radiation exposure, chronic stress and increasing age or risk factors such as smoking and UV rays, the coenzyme Q10 concentration in the blood plasma, in organs and tissues, such as in the skin, reduces his. The cause are free radicals or pathophysiological conditions discussed. It remains unclear whether the decreased Q10 content itself has pathogenic effects or just a side effect is [4, 17, 24].

The reduced ubiquinone-10 Full stock with increasing age is noticeable next to liver and skeletal muscle, especially in the heart muscle. While 40-year-old about 30% less Q10 in heart muscle have a healthy 20-year-old who is Q10 concentration 80-year-old to 50-60% below the healthy 20-year-old [16, 17, 25]. In a Q10 deficit of 25% of malfunctions to be expected with a decrease in Q10 concentration over 75% with life-threatening disorders [25]. The cause of a decrease in the ubiquinone-10 content in age, several factors come into consideration. In addition to a reduced endogenous synthesis and inadequate dietary intake, a decrease in mitochondrial mass and increased consumption by oxidative stress appears to play a role [7, 21, 23, 25].

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