Coenzyme Q10 (CoQ10) has two interconverting forms: its yellow, oxidized state (ubiquinone) and milky-white, reduced counterpart (ubiquinol). CoQ10 is ubiquitously present in mammalian tissues; origins are synthesis in the body and intestinal uptake from ingested foods. CoQ10 plays a significant role in energy production by the mitochondria, the powerhouses of body cells. Some supplements, treats and complete foods for dogs and cats feature CoQ10 as health-promoting ingredient.
Among the various claimed effects of CoQ10, antioxidant capacity and support of heart and gum health are most common. As heart muscle has a high energy requirement, it is believed that extra CoQ10 enhances the organ’s function. Because reduced CoQ10 can donate electrons, it is seen as neutralizer/scavenger of free radicals, thus fighting oxidative DNA damage and aging. As antioxidant and bioenergizer, CoQ10 is thought to suppress bacterial gum inflammation.
For the claimed health effects of supplemental CoQ10 there is no scientific substantiation in the form of controlled experiments with dogs or cats. Moreover, there is no indirect evidence from which the health claims may be inferred. Admittedly, demonstrating that supplemental CoQ10 increases life span of dogs and cats is practically hardly possible, not least due to long duration, but studies in mice (1-3) do not support the anti-aging claim.
CoQ10 is not recognized as an essential nutrient for dogs and cats (4), implying that body synthesis in normal animals is adequate. In addition to their own supply, dogs and cats also ingest CoQ10 with their regular food, but the actual quantities are unknown. In a dog study, supplemental CoQ10 did not increase antioxidant capacity of blood. CoQ10 might enhance canine and feline mitochondrial energy production under specific conditions (cf. 5, 6), but this remains to be shown.
Function and metabolism
CoQ10 is a lipophilic electron carrier, consisting of a quinone/quinol group and 10 isoprene units in the side chain. Successive uptake and release of two reducing equivalents (2 H+ + 2 e-) transfers the quinone portion into quinol and back again. As such, CoQ10 is part of the mitochondrial electron transport chain of redox couples, producing a high energy state that powers ATP synthesis.
All body cells may synthesize CoQ10 (7), inclusive of attaching the side chain to 4-hydroxybenzoate derived from tyrosine. The adjunct consists of isoprene units made from mevalonate as precursor. Inhibition of mevalonate production by statin drugs lowered both myocardial (8) and serum CoQ10 (9) in dogs. CoQ10 disposal likely involves glucuronidation and excretion with bile and urine (10-12).
In mitochondrial electron transport, the CoQ10 redox couple acts as conduit for electrons, not as net electron donor or acceptor. For CoQ10 as free radical scavenger, the quinol form should donate electrons and the quinone generated should be disposed of by conjugation and excretion.
For dog and cats, the CoQ10 sources are body synthesis and ingestion. Daily whole-body synthesis cannot be estimated. Concentrations of CoQ10 in finished petfood are unknown. Complete petfoods featuring CoQ10 do not declare the added amounts. Thus, supplemental CoQ10 cannot be played off quantitatively against endogenous synthesis and supply by the base petfood. In addition, absorption efficiencies of ingested CoQ10 sources may vary.
Food based on 50% corn and 30% poultry meal may contain 30 mg CoQ10/kg (14-16). For commercially manufactured crystalline CoQ10, the recommended maximum inclusion level is 100 mg/kg petfood (17). That dietary CoQ10 level roughly equals the dosage for a dog supplement (18), while some dogs with heart disease are prescribed twice as much (19).
Oral administration of CoQ10 (equivalent to 600 and 90 mg/kg dry food) increased group-mean concentration of CoQ10 in dog’s serum, but left the amounts in myocard (20) and gingiva (21) unchanged. Via daily oral gavage, dogs received capsules with crystalline ubiquinol dissolved in warmed corn oil (22). Administration of 150 mg/kg body weight.day (kg/ bw.d), or 898 mg/kg dry food, raised pre-dosing serum CoQ10 concentration into a new steady state within 7 weeks. No further increase was observed with higher doses of either dissolved (22) or undissolved CoQ10 (23). Ubiquinol and ubiquinone (600 mg/kg bw.d) produced similar serum CoQ10 concentrations (22).
Following single-gavage dosing of dissolved CoQ10, maximum serum concentration responded dose dependently (22). Higher, undissolved amounts provoked a dose-independent response (23). CoQ10 has low water solubility, implying limited intestinal absorption. After oral administration of CoQ10, the area under the plasma concentration time curve was similar for a powder and oil-based preparation (24), but greater when applying an emulsifying carrier (25) or complexation with a cyclodextrin (26).
Cardiac and antioxidant status
In dogs with experimentally-induced congestive heart failure (CHF) or periodontitis, oral CoQ10 therapy did not (meaningfully) reduce end-diastolic volume (20) and gingivitis (21). Dogs with untreated CHF did not have lower serum CoQ10 concentrations and total antioxidant capacity (TAC) than healthy controls (27). A morning meal with CoQ10-cyclodextrin complex raised dogs’ plasma CoQ10 during the day, but did not increase plasma TAC (28).
A 13-week toxicity study in dogs showed that the no-observed adverse-effect level for ubiquinol was more than 600 mg/kg bw.d (22). A follow-up study lasting 39 weeks showed that 1800 mg CoQ10/kg bw.d was safe also (23).
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