- 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.

References:

– 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]