- CoEnzyme Q10 acts as an antioxidant.
- CoEnzyme Q10 is needed for basic cell functions in energy production.
CoEnzyme Q10’s primary function is to transfer electrons through the electron transport chain in the mitochondrial inner membrane. The electrons are received directly from succinate, or indirectly from several other substrates such as pyruvate, acyl-CoA, and alpha–ketoglutarate in the form of NADH (=Nicotinamide adenine dinucleotide). CoEnzyme Q10 moves from one electron carrier complex to the next, ultimately delivering electrons, one at a time. While the electrons are delivered one at a time, they leave in pairs to form ATP and H20.
If CoEnzyme Q10 availability is not adequate the electrons will not be able to travel in pairs and single electrons will take another, less desirable, pathway that can lead to the generation of superoxide radicals. Optimal functioning of this pathway is critical for the fundamental energy generation that powers all cell functions. CoQ10 is also an antioxidant. Therapeutic approaches targeting mitochondrial disfunction and oxidative damage using CoEnzyme Q10 hold great promise. [L]Since your body can make coenzyme Q10, it is not called a vitamin. If you are making enough to meet the demands of your tissues, you do not need to take any extra. However, many people do not make enough coenzyme Q10. Certain drugs have been shown to block coenzyme Q10 production. Elevated lipid peroxides may indicate a need for coenzyme Q10. High hydroxymethylglutarate can reveal a block in your body’s synthesis of coenzyme Q10. Other functional markers, such as lactate, succinate, fumarate, and malate, indicate whether your body is able to produce energy efficiently by utilizing coenzyme Q10.
– Mitochondrial approaches for neuroprotection. [L]
– Anti-atherogenic effect of coenzyme Q10 in apolipoprotein E gene knockout mice. [L]
– Dietary cosupplementation with vitamin E and coenzyme Q(10) inhibits atherosclerosis in apolipoprotein E gene knockout mice. [L]
Inadequate amounts of CoQ10 lead to a failure of mitochondria to produce cellular energy.
CoEnzyme Q10 synthesis is dependent on the availability of hydroxymethylglutarate(HMG), if HMG is low it will slow the rate of CoEnzyme Q10 synthesis. Statin drugs block the conversion of HMG to cholesterol and to CoEnzyme Q10. A functional impairment at the level of mitochondrial CoEnzyme Q10 electron transfer can also lead to elevations of succinate, malate, fumarate, and pyruvate, which are the energy pathway intermediates. The direct transfer of electrons from succinate in the electron transport system is slowed when the electron shuttle action of CoEnzyme Q10 is inadequate to meet the demands. CoEnzyme Q10 has been found to inhibit LDL-oxidation and atherosclerosis in research studies, the effect was increased with co-supplementation of vitamin E. [L, L]
Coenzyme Q 10 deficiency may occur in three ways: primary coenzyme Q10 deficiency, secondary coenzyme Q10 deficiency, or related to another drug or disease.
Primary coenzyme Q10 deficiency is rare and caused by genetic disorder that affects the CoQ10 molecule. Secondary coenzyme Q 10 deficiency, on the other hand, is caused by a problem in the mitochondria. Mitochondrial diseases cause a variety of symptoms but most are related to muscle weakness and neurological symptoms. This can lead to breathing problems, heart muscle problems, seizures, and cognitive problems.
Some specific causes of low coenzyme Q10 levels are:
– Mitochondrial diseases
– Primary CoQ10 deficiency (rare)
– Secondary CoQ10 deficiency
– Cerebellar ataxia
– Severe infantile multisystem disease
– Isolated myopathy
– Statin us
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Abnormally high levels of coenzyme Q10 are only practically possible through the use of supplements. It is unclear whether moderately excessive amounts of coenzyme Q10 are harmful to humans. While it is fat soluble, CoQ10 does not accumulate after supplementation has stopped.
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