Selenium is an essential trace mineral for dogs and cats. Due to wide variation in selenium content among ingredients used to make petfoods, most manufacturers will include a supplemental source in their trace mineral premix. The predominant form used in petfood is sodium selenite, which has been used for decades without much issue.
However, seeds of doubt and confusion have been planted by a few critics of the industry suggesting that sodium selenite (Na2SeO3 and the oxidized form sodium selenate, Na2SeO4) is unsafe and used by petfood manufacturers only because it is cheap. So, are the critics right or is there more to this selenium supplementation story?
Selenium is a naturally occurring rare earth element that ranks 70th out of 98 elements in the Earth’s crust. It was discovered in 1817 and in the 1930s was implicated as the toxic element associated with “alkali disease” in the plains of North America (McDowell, 1992). The pendulum swung a few decades later when dietary selenium deficiency was associated with exudative diathesis in chicks (Patterson et al., 1957) and white muscle disease in calves (Muth et al., 1958).
In dogs fed selenium-deficient diets, muscular weakness, subcutaneous edema, anorexia, dyspnea and intestinal lipofucinosis occurred (Van Vleet, 1975), whereas those fed a high selenium dosage (5 mg/kg dry matter, or DM) had anemia and liver damage (Levander, 1988). No clinical trials for selenium deficiency or toxicity have been reported for cats, and practical cases in any companion animal species are uncommon.
Metabolically, selenium is a component of the key physiological antioxidant glutathione peroxidase, is part of several selenium-containing deiodenases (as selenocysteine), supports immune function and may be protective against certain cancers (NRC, 2006). The established dog and cat requirement ranges from 0.30 to 0.35 mg/kg DM. An upper limit has been suggested for dogs at 2 mg/kg DM, but none has been established for cats.
Selenium chemistry is very similar to that of sulfur with a wide range of reduction (-2) to oxidation (+6) states. The primary source of selenium in animal diets is derived from plant material. In the plant, absorbed selenium in the inorganic form (selenite or selenate) is converted to organic selenoamino acids (selenomethionine, selenocysteine, Se-methyl-selenomethionine and Se-methyl-selenocysteine). The concentration in the plant is dependent on the soil selenium content, soil pH and tillage practices.
Animals do not make selenomethionine themselves but bio-accumulate appreciable amounts of complexed selenoproteins (such as glutathione peroxidase; Schrauzer, 2000). Food sources rich in selenium include Brazil nuts, black walnuts, seafood such as shrimp, crab meat, salmon and halibut, whole grains like brown rice and meats (especially organ meats like kidney and liver) such as chicken, pork and beef. The predominant form of selenium in animal by-product meals, especially those high in ash, is the inorganic selenite and selenate.
Selenium occurs in sulfide ores of heavy metals. It is commonly refined as a co-product of copper or tellurium extraction to selenious acid, which is reacted with sodium hydroxide to form the sodium selenite salt. Commercial sodium selenite and selenate are sold as a white to off-white powder with a selenium content exceeding 45%. Sodium selenite/selenate is commonly included in the diet by way of a trace mineral premix due to the very small supplemental amounts used. From a manufacturing perspective, this increases the mix consistency and reduces the chance of weighing and handling errors.
As with other minerals, absorption and retention depend on the animal’s mineral status and endocrine controls. With all things equal in the diet, selenate is almost completely absorbed, but excretion before incorporation into proteins can be high. Selenite absorption is much lower (about 50%) but better retained. Upon absorption, both are transported with carrier proteins and metabolized to selenocysteine or incorporated into selenium-containing enzymes.
In Europe, sodium selenite and selenate are considered category 3 ingredients and can be added to petfoods up to 0.5 mg/kg. Significant South American petfood manufacturing countries such as Brazil take no issue with this ingredient. However, in the US, there is no provision in the federal code that states explicitly that sodium selenite is allowed in dog or cat diets.
Though no documentation can be found permitting use in petfoods, the virtual consensus inclusion in petfoods for the past 30 years would suggest the various regulatory bodies have found no reason to object as long as petfood manufacturers stay within the provisions of 21CFR573.920 and not add selenium beyond 0.3 mg/kg diet (~0.67 mg/kg sodium selenite).
Given the small amount required and the relatively small window between deficiency and toxicity, selenium requires special care and attention during the petfood manufacturing process—regardless of the dietary source. Because of the small supplemental inclusion level, costs or savings are not what is really driving the use of sodium selenite over other forms. Rather, other options are not universally available for use in pet diets—e.g., selenomethionine is not approved and no one manufactures it for the petfood market, and selenium yeast is not approved for use in feline diets in the US.
Until these options are fully available, critics should refrain from creating fear in the market or disparaging an ingredient like sodium selenite that has been used safely and effectively for decades.
Find more columns by Dr. Aldrich at
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