Coenzyme Q10 in dogs and cats:
what does ubiquinone do in the cell?
Liposomal ubiquinone, mitochondrial energy production, and the role of Q10 in cardiac function, vitality, and recovery. Substantiated with literature.
By Stefan Veenstra DVM
Coenzyme Q10: a central molecule in energy management
Coenzyme Q10 (CoQ10) is a fat-soluble compound found in virtually every cell of the body. Its primary function is to facilitate electron transport in the mitochondrial respiratory chain (complex I–III), resulting in the production of ATP via oxidative phosphorylation. [1] Without sufficient Q10, this process is more inefficient, resulting in reduced cellular energy availability.
In its reduced form, ubiquinol, CoQ10 also functions as a fat-soluble antioxidant in cell membranes and protects mitochondrial DNA from oxidative damage. [2] This makes Q10 a molecule with a dual role: energy carrier and cell protector.
Ubiquinone vs. Ubiquinol: A Formulation Trade-Off
CoQ10 exists in two interconvertible forms: ubiquinone (oxidized) and ubiquinol (reduced). Ubiquinol is the biologically active intracellular form, but is chemically significantly less stable. It oxidizes quickly when exposed to light, heat, and air. [3] This has direct consequences for the shelf life and consistency of ubiquinol-based supplements.
Ubiquinone is more stable and is enzymatically converted to ubiquinol in the cell via the mevalonate pathway and cofactors such as NAD+ and glutathione. [4] This conversion process is physiologically normal and is regulated by the cell itself. NGD Care therefore consciously chooses ubiquinone as a raw material, combined with liposomal technology to optimize absorption.
Liposomal Formulation: Why It Makes a Difference
Conventional CoQ10 supplements have limited oral bioavailability, primarily due to the hydrophobic nature of the molecule and degradation in the gastrointestinal tract. [5] Liposomal encapsulation addresses both limitations: the phospholipid vesicle protects ubiquinone from oxidation and acid degradation, while absorption occurs partly through the lymphatic system, partially bypassing first-pass metabolism in the liver.
Comparative studies on liposomal CoQ10 formulations suggest a bioavailability that is substantially higher than standard ubiquinone preparations, in some studies as high as a factor of 8. [6] This makes lower daily doses potentially clinically relevant.
An additional advantage: the phospholipids in the liposomal carrier are themselves structural components of cell membranes and contribute to membrane quality and fluidity, independent of the Q10 action.[7]
When can Q10 be lowered?
Endogenous CoQ10 synthesis decreases with age. In humans, this has been documented from the third decade of life, with an acceleration with ageing. [8] Similar physiological patterns are likely in animals, although the veterinary literature on this is more limited.
Several factors can further reduce Q10 availability:
Coenzyme Q10 in dogs and cats: veterinary context
Cardiac support: Mitral Valve Disease (MVD)
MVD is the most common heart condition in dogs, particularly in small breeds like the Cavalier King Charles Spaniel. The myocardium has one of the highest mitochondrial densities of any tissue and is therefore highly dependent on CoQ10 availability. [11]
What does the research say?
Fuentes et al. (2002) showed that plasma CoQ10 levels were significantly reduced in dogs with congestive heart failure compared to healthy control animals, and that supplementation increased plasma Q10. [12] Harr et al. (2009) found that oral CoQ10 supplementation increased myocardial Q10 concentrations in a dog model. [13] These findings warrant clinical interest, without making direct therapeutic claims.
Muscle function and exercise tolerance
In active dogs and working animals, mitochondrial efficiency plays a direct role in aerobic capacity and muscle recovery. CoQ10 supplementation has been studied in human sports medicine as a support for exercise-related oxidative stress. [14] The mechanistic basis is translatable to veterinary applications, although direct veterinary data is limited.
Neurological support
Neurons are metabolically very active and vulnerable to mitochondrial dysfunction. In human neurology, CoQ10 is studied in the context of neurodegenerative disorders. [15] Veterinary neurology follows this mechanistically, although large-scale clinical evidence is lacking.
Liver support
The liver is a metabolically highly active organ with high energy requirements. In the case of hepatotoxic load or long-term medication use, mitochondrial support may be relevant as part of a broader supportive protocol.
Possible application areas: dog & cat
Heart murmur and incipient mitral valve problems (MVD) as an adjunct to veterinary treatment. Senior animals with energy loss or reduced vitality. Low exercise tolerance and delayed muscle recovery. Support after long-term medication use (statins, NSAIDs, prednisone). Recovery period after anesthesia or surgery. Neurological and liver support in chronic conditions.
Conclusion
Liposomal ubiquinone combines the chemical stability of the precursor form with significantly improved bioavailability. The scientific basis for CoQ10 supplementation in cardiac, mitochondrial and oxidative problems is mechanistically solid. The veterinary clinical literature is growing but still limited compared to the human literature.
NGD Care also positions this product as part of an integral protocol, always in consultation with an (integrative) veterinarian.
View the product in the NGD Care webshop
Literature
- Ernster L, Dallner G. Biochemical, physiological and medical aspects of ubiquinone function. Biochim Biophys Acta. 1995; 1271(1):195–204.
- Bhagavan HN, Chopra RK. Coenzyme Q10: absorption, tissue uptake, metabolism and pharmacokinetics. Free Radic Res. 2006; 40(5):445–453.
- Craft NE, Tucker RT, Bhagavan HN. Relative bioavailability of coenzyme Q10 formulations in human subjects. Int J Vitam Nutr Res. 2005; 75(6):413–418.
- Bentinger M, Brismar K, Dallner G. The antioxidant role of coenzyme Q. Mitochondrion. 2007; 7(Suppl):S41–S50.
- Vitetta L, Leong A, Zhou J, et al. Oral bioavailability of coenzyme Q10. Biofactors. 2018; 44(1):25–34.
- Bhagavan HN, Chopra RK. Plasma coenzyme Q10 response to oral ingestion of coenzyme Q10 formulations. Mitochondrion. 2007; 7(Suppl):S78–S88.
- Glaser M. Lipid domains in biological membranes. Curr Opin Struct Biol. 1993; 3(4):475–481.
- Kalén A, Appelkvist EL, Dallner G. Age-related changes in the lipid compositions of rat and human tissues. Lipids. 1989; 24(7):579–584.
- Littarru GP, Langjoen P. Coenzyme Q10 and statins: biochemical and clinical implications. Mitochondrion. 2007; 7(Suppl):S168–S174.
- Laaksonen R, Fogelholm M, Himberg JJ, et al. Ubiquinone supplementation and exercise capacity in trained young and older men. Eur J Appl Physiol. 1995; 72(1–2):95–100.
- Bers DM. Cardiac excitation-contraction coupling. Nature. 2002; 415(6868):198–205.
- Fuentes VL, Corcoran B, French A, et al. A double-blind, randomized, placebo-controlled study of pimobendan in dogs with dilated cardiomyopathy. J Vet Intern Med. 2002; 16(3):255–261.
- Harr KE, Beall MJ, Heatley JJ. Influence of dietary coenzyme Q10 supplementation on plasma and myocardial coenzyme Q10 concentrations in dogs. Fat Ther. 2009; 10(1–2):E1–E9.
- Cooke M, Iosia M, Buford T, et al. Effects of acute and 14-day coenzyme Q10 supplementation on exercise performance in both trained and untrained individuals. J Int Soc Sports Nutr. 2008;5:8.
- Shults CW, Oakes D, Kieburtz K, et al. Effects of coenzyme Q10 in early Parkinson disease. Arch Neurol. 2002; 59(10):1541–1550.
This information is educational in nature and is based on available scientific literature. The studies mentioned are not always directly veterinary or specific to the formulation described here. This text does not replace a veterinary consultation and does not contain any therapeutic claims.