Selenium is a micronutrient that horses require in trace amounts to support cellular function. Selenium levels in equine diets vary widely depending on where their forage is grown; levels of this trace mineral in the soil determine its final concentration in plants.

Selenium imbalances are common in horses. While it is more common for horses to be deficient in selenium than to get too much, consuming excess amounts of selenium is potentially life-threatening.

Acute selenium poisoning is usually caused by accidental over-supplementation with inorganic forms of this mineral. The majority of horses suffering from acute selenium toxicity die suddenly before symptoms are noted.

Horses can also develop chronic selenium toxicity, also referred to as alkali disease, due to prolonged consumption of plants high in selenium. Symptoms include hair loss and hoof abnormalities.

Treatment depends on whether the case is chronic or acute. Options for acute poisoning are limited and generally ineffective. Most horses die within two days of acute poisoning, even with medical intervention.

The treatment for chronic alkali disease is supportive and involves pain management, hoof care, removal of the selenium source, and dietary modification.

Selenium in Equine Diets

Selenium (Se) is a non-metallic element occurring naturally in sedimentary rocks, and is found in trace amounts in all feeds and soil. [1][2]

All natural elements exist in multiple chemical forms. Selenium is usually found in one of the following forms: [1][2]

  • Elemental Selenium: the pure form of selenium is relatively non-toxic and is an essential trace element
  • Selenite and Selenate: are inorganic forms that plants can use to make organic forms such as selenomethionine
  • Selenide: both selenite and selenate are converted into selenide in animals, which can be toxic to cells at high levels
  • Selenomethionine and Selenocysteine: amino acids that contain selenium and are incorporated into plant and animal proteins

Selenium in Soil

The geographical distribution of selenium in soil is uneven, and regions worldwide vary from being deficient to having toxic levels. The plants growing in these regions have varying selenium content; consumption of both selenium-rich and selenium-poor plant products can have harmful effects on humans and animals.

In the United States, the Northern Great Plains (eastern Wyoming, North Dakota, Montana, and Nebraska) and the Intermountain Region (Nevada, Utah, Idaho, western Montana, northern Arizona, western New Mexico, and far west Texas ) are selenium-rich.

The Great Lake region and large sections of the Northwest, Northeast, and Atlantic Coast are deficient in selenium. [3][4][5]

Selenium Map of Canada & the USA | Mad Barn USA

Plant Uptake

Selenium intake in the equine diet is primarily determined by the amount of this mineral in forages and grains consumed by the horse.

Equine ingestion of selenium starts with selenium uptake from the soil by plants, the specifics of which vary depending on the plant species, environmental conditions, and selenium concentration in the soil.

Plants can be categorized according to their selenium uptake as follows: [6]

  • Hyperaccumulators: plants that accumulate more than 1,000 milligrams of selenium per kilogram of dry weight (> 1000 mg/kg dry matter) are hyperaccumulators. These include plants belonging to the Astragalus species, the Prince’s plume (Stanleya), and the Xylorhiza family. While hyperaccumulation can be beneficial to the plants, it can pose a threat to grazing animals. However, these plants are frequently very unpalatable, so grazing animals are unlikely to eat them unless they have no other options available
  • Secondary-accumulators: secondary accumulators are plants that can accumulate selenium in the range of 100–1000 mg/kg dry matter. These include False Flax (Camelina sativa), Sunflower (Helianthus), Broccoli (Brassica oleracea), and Rapeseed (Brassica napus). The amount of selenium uptake in secondary accumulators varies depending on the amount of selenium available in the soil and climatic conditions, with uptake increasing in periods following droughts.
  • Non-accumulators: non-accumulator plants are unable to uptake more than 100 mg/kg dry matter. These plants are unable to live in selenium-rich soils.

Another factor contributing to the amount of selenium contained in plants is age, with younger leaves accumulating more compared to older ones. [6]

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Selenium for Horses

Selenium is essential for cellular function in horses, as it is a component of glutathione peroxidase. This enzyme is an important antioxidant that neutralizes free radicals.

As cells in the body metabolize glucose and other sources of energy, they generate free radicals which are unstable molecules with free electrons available to react with other compounds.

Continuous exposure to free radicals can result in damage to cell membranes, potentially leading to cellular dysfunction and health issues. Antioxidant enzymes neutralize free radicals so cell function is not disrupted.

Selenium is also necessary for proper functioning of the immune system, thyroid, reproductive system, and to support growth and development.

An average adult horse weighing 500 kg (1,100 lb) requires a minimum of 1 mg of selenium daily to avoid developing a deficiency. [7]

Selenium Deficiency in Horses

Horses, especially foals, lacking adequate selenium in their diet can develop Nutritional Myodegeneration (NMD), commonly referred to as white muscle disease.

White muscle disease involves cell death in cardiac and skeletal muscles, resulting in white scar tissue. Affected animals have incoordination, weakness, difficulty eating, cardiovascular collapse and, in severe cases, can experience sudden death. [7]

Causes of Selenium Poisoning

While conditions linked to selenium deficiency are more common in horses than toxicity, consuming excess selenium also poses a significant threat.

The maximum safe dietary concentration of selenium in equine diets is 2 mg/kg dry matter. [7] For a 500 kg (1,100 lb) horse, this is equivalent to consuming 20 mg of selenium per day.

Without prompt veterinary attention, excess selenium intake can result in severe poisoning and death. Selenium toxicity is classified as either acute or chronic: [8]

  • Acute selenium poisoning is a life-threatening condition most commonly caused by accidental over-supplementation with inorganic forms of selenium
  • Chronic selenium poisoning is a long-term condition caused by prolonged exposure to moderately high levels of selenium, generally as the result of ongoing consumption of selenium-rich forages

Dietary Sources

Sources of excessive selenium intake in the equine diet include: [8][9]

  • Supplements: unintentional over-supplementation of inorganic selenium is the most common cause of acute selenium poisoning in horses
  • Forage: ingestion of hay or pasture grass high in selenium
  • Water: mining operations, irrigation, and the use of selenium-rich fertilizers can increase selenium in water sources; water containing selenium in a concentration of over 10 ppb (0.01 ppm) can cause chronic toxicosis

If you suspect your horse is affected by high selenium intake, obtain a forage analysis to assess levels of this mineral in your horse’s hay or pasture.

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The precise mechanism of action for selenium toxicity in horses is not fully understood. Absorption of selenium primarily occurs in the horse’s small intestine. Distribution of this mineral through the body depends on which chemical form the selenium is in. [8]

Acute selenium toxicity is believed to be caused by the interaction of excessive amounts of certain selenium compounds with thiols (sulfur compounds), resulting in selenium replacing sulfur on the thiol molecules. [10]

Research suggests this change in thiol chemistry releases abundant free radicals that cause oxidative tissue damage and disrupts healthy cell function. [10]

Chronic selenium poisoning is thought to be caused by oxidative damage and gradual incorporation of selenium in place of sulfur throughout the horse’s body. In particular, sulfur-containing amino acids, namely cysteine and methionine, are converted to selenium-containing versions, called selenocysteine and selenomethionine.

These selenium variants can be incorporated into proteins, resulting in proteins with abnormally low sulfur. Sulfur-containing amino acids in proteins form disulfide bridges with each other which help form the correct shape of the protein and support its normal function.

The sulfur-containing amino acid methionine plays a crucial role in the formation of keratin – a protein that is abundant in hoof and hair. When methionine is replaced by selenomethionine in keratin, the structure is changed which impacts the quality of hair and hooves. [8][10]

Symptoms of Chronic Selenium Toxicosis

Chronic selenium toxicosis, also known as alkali disease or chronic selenosis in horses, is most commonly caused by long-term exposure (generally between 30 to 90 days) to forages containing elevated amounts of selenium. [11]

Horses with chronic selenosis display a range of symptoms affecting different organ systems, including: [8][12][13][14]

  • Bilateral alopecia and rough coat: presents as hair loss on both sides of the body and most commonly affects the mane and tail
  • Abnormal growth of the hooves: in high quantities, selenium replaces the sulfur contained in proteins. Sulfur is a common element in the body that plays various fundamental roles in maintaining health, including production of keratin, which is what horse hooves are made of. Replacing sulfur with selenium leads to abnormal hoof growth that can cause swelling and reddening of the coronary bands, hoof cracking, and hoof separation, and lameness
  • Anorexia (loss of appetite) and unplanned weight loss
  • Reproductive abnormalities: alkali disease can be linked to a number of reproductive abnormalities such as decreased conception rate, increased fetal resorption rate (early death of the embryo), abortions, and stillbirths

Symptoms of Acute Selenium Toxicosis

Horses suffering from severe cases of acute selenium poisoning can present few to no clinical signs and often die suddenly as a result of the toxicosis.

In symptomatic cases, clinical signs progress rapidly and include: [8][11][15]

  • Weakness
  • Dyspnea (difficulty breathing)
  • Colic (abdominal pain)
  • Diarrhea
  • Weak pulse
  • Cyanosis (blue or grey gums)
  • Sweating
  • Hyperexcitability

Horses poisoned with a lethal dose of selenium generally die within one to two days from exposure. [11]

All of the symptoms listed above are medical emergencies. Contact your veterinarian immediately to give your horse the best chance of surviving.


Diagnosis of selenium toxicosis is usually based on the known history of exposure, presence of clinical signs, and diagnostic tests.

Diagnostic testing may include: [4][11][16]

  • Blood tests and urinalysis
  • Physical examination
  • Tissue and hair sample tests
  • Feed and forage analysis
  • Diagnostic imaging

Measuring selenium concentrations in blood and urine is a primary diagnostic tool. However, blood selenium levels in horses do not provide definitive proof of toxicosis as excess selenium accumulates in organs such as the liver and kidneys, not in blood. Blood levels below 1.0 ppm generally rules out selenosis in animals but higher levels do not prove selenosis. [11]

Differential Diagnosis

Signs of toxicosis without a known history of exposure can lead to suspicion of either acute or chronic selenium poisoning, depending on the horse’s symptoms. However, a number of other toxins and conditions can cause similar symptoms, including: [11]

These conditions should be ruled out when your veterinarian is assessing your horse for selenium toxicosis.

Post-Mortem Examination

Unfortunately, especially in cases of severe acute poisoning, horses can die prior to diagnosis.

Horses that die suddenly due to toxic over-supplementation may not develop recognizable symptoms in time to identify the cause of death. In these cases, the horse’s body may be submitted for necropsy (post-mortem examination) to confirm the cause of death.

Common findings in horses that succumb to acute selenium poisoning include: [8]

  • Pale or spotted heart
  • Fluid in the chest cavity (hydrothorax)
  • Pinpoint hemorrhaging of the myocardium
  • Hemorrhage of the gastrointestinal tract
  • Hepatic necrosis (liver death)

Treatment and Management

Once a horse is diagnosed with selenium poisoning, treatment depends on whether poisoning is acute or chronic.

To date, there are no effective treatment options for acute selenosis. Instead, horses are provided supportive care and pain management; supplementation with antioxidants such as Vitamin E may be indicated.

However, while supportive care is essential, its success is limited due to the high risk of rapid cardiovascular collapse.

Treatment of Chronic Selenosis

The first step in the treatment of chronic selenosis is the removal of the selenium source from the horse’s diet.

Further treatment options include: [4][8][10]


The outlook for horses with selenium poisoning varies depending on the type of toxicosis and severity. The prognosis for horses diagnosed with acute selenosis is extremely poor, as supportive care is rarely successful.

With proper care, horses diagnosed with chronic selenosis can recover but require prolonged dietary management, rest, and long-term supportive care. [8][10]


Since there is no antidote for acute selenium toxicosis and treatment options are limited, implementing effective prevention is the only way to protect your horse from alkali disease.

Prevention is somewhat complex, as selenium deficiency in horses also poses a health risk. [7]

It is important for horse owners and caretakers to know if their forage is grown in a high-selenium area and to balance appropriate supplementation with existing dietary exposure to avoid toxicity. If your forages are grown in an area known to have selenium-deficient soils, your horse likely requires selenium supplementation to avoid deficiency.

Prevention strategies include: [8][12][17][18]

  • Feeding organic selenium supplements that supply selenomethionine which the body metabolizes without producing selenide and therefore poses less of a risk of toxicity
  • Grazing management to ensure pastures have sufficient palatable forages so horses do not turn to risky plants as a food source
  • Frequent monitoring of pasture soil in regions where selenium concentrations are high
  • Testing forage, especially after drought, when selenium uptake in plants is highest
  • Avoiding excess supplementation of inorganic sources, especially for horses in regions where soil selenium levels are high

If you are unsure how much selenium your horse is getting, consult with an equine nutritionist for an evaluation of their entire diet. Work with a veterinarian if your horse is showing any symptoms of chronic toxicity.


In trace amounts, selenium is an essential micronutrient required in the horse’s diet for proper cellular function and antioxidant protection.

  • Selenium toxicosis is a potentially life-threatening condition
  • To date, there is no antidote for acute selenium intoxication
  • The leading cause of acute toxicosis is accidental overdose of inorganic selenium supplements
  • The leading cause of chronic selenosis is long-term exposure to high selenium levels in forage
  • Prognosis of acute selenium poisoning is very poor, with most affected horses dying within days
  • Prognosis of chronic selenium poisoning varies depending on the severity of the symptoms and requires long-term management
  • Appropriate selenium supplementation from organic sources is required to prevent selenium deficiency or toxicity in horses

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  1. Barceloux, D.G. Selenium. Journal of Toxicology: Clinical Toxicology. 1999.
  2. Perrone, D. et al. The Chemistry of Selenium. Selenium: Chemistry, Analysis, Function and Effects, First edition. Royal Society of Chemistry. 2015.
  3. Distribution. Selenium in Nutrition: Revised Edition, National Academies Press (US). 1983.
  4. Wilson, D.A., Ed. Clinical veterinary advisor: The horse. St. Louis, Mo: Elsevier Saunders. 2012.
  5. Sharpe, P. Horse pasture management. London: Academic press. 2019.
  6. Gupta, M. and Gupta, S. An Overview of Selenium Uptake, Metabolism, and Toxicity in Plants. Front. Plant Sci. 2017.
  7. National Research Council. Nutrient Requirements of Horses: Sixth Revised Edition. The National Academies Press, Washington, DC.
  8. Hovda, L.R. Blackwell’s Five-Minute Veterinary Consult Clinical Companion Equine Toxicology. Wiley Blackwell. 2022.
  9. Aitken, P. et al. Toxicity: Selenium in Horses (Equis). Vetlexicon.
  10. Bischoff, K. Selenium Toxicosis in Animals – Toxicology. MSD Veterinary Manual. 2022.
  11. Lavoie, J.-P. and Hinchcliff, K.W. Blackwell’s Five-Minute Veterinary Consult Equine, Second Edition. Wiley-Blackwell. 2009.
  12. Gupta, R.C., Ed. Veterinary toxicology: basic and clinical principles, 2nd ed. Elsevier: Academic Press. 2012.
  13. Stegelmeier, B.L. et al. Plant-Induced Reproductive Disease, Abortion, and Teratology in Livestock. Veterinary Clinics of North America: Food Animal Practice. 2020.
  14. Witte, S.T. et al. Chronic selenosis in horses fed locally produced alfalfa hay. J Am Vet Med Assoc. 1993. View Summary
  15. Desta, B. et al. Acute Selenium Toxicosis in Polo Ponies. J Vet Diagn Invest. 2011.View Summary
  16. Plumlee, K.H., Ed. Clinical veterinary toxicology. Mosby. 2004.
  17. Tiwary, A.K. et al. Comparative toxicosis of sodium selenite and selenomethionine in lambs. J Vet Diagn Invest. 2006.
  18. Schrauzer, G.N. Selenomethionine: A Review of Its Nutritional Significance, Metabolism and Toxicity. J Nutr. 2000.