By Dr. Aimee Hafla, Ph.D., P.A.S.
Selenium is a necessary mineral for both humans and animals, and naturally occurs in varying concentrations within the soil in all parts of the world. Available selenium in the soil is taken up by many plants, including some cereal grains and forages used for livestock feed.
Selenium is an integral component of the glutathione peroxidase enzyme which works as a cellular antioxidant. The major role of this enzyme is to protect cellular membranes from damage by converting hydrogen peroxide to water. Hydrogen peroxide and other intermediates of cellular reduction pathways can damage cellular membranes, disrupt cellular function and may negatively impact animal health (Miller et al., 1998). Tissue concentrations of selenium are associated with glutathione peroxidase activity and are directly related to dietary selenium intake. The liver and glandular tissues have the greatest selenium concentrations of all the bodily tissues (NRC, 2001). Selenium and vitamin E are often discussed together as they are both involved in protecting cells against free radicals that cause cellular damage. Selenium contributes to the destruction of oxidizing components, while vitamin E prevents their formation and often a deficiency in one leads to an increased requirement for the other.
It is important to understand animal requirements for selenium, especially since the range between dietary toxicity and deficiency is rather narrow. It is worth noting that this mineral is regulated by the FDA, and the maximum amount of selenium that can be supplemented in the diets of livestock is 0.30 mg/kg. In nearly all situations, the legal limit of supplemental selenium in the diet in addition to the diet ingredients, will maintain or exceed selenium requirements of all livestock classes. Refer to Table 1 for selenium requirements of various classes of livestock and horses.
|Table 1. Selenium requirements for various classes of livestock and horses.|
|Heifers 6 months||Early lactation||Mid to late lactation||
Stressed receiver calves
|Growing and finishing||Gestating cows||
Early lactation cows
|SE (ppm)||0.10 – 0.20||0.10||0.10||0.10|
7 to 22 lb
|22 to 44 lb||44 to 265 lb||Gestating sow||
|Broilers||Broiler breeders||Turkeys, starter-breeders||
|Adult, not working||Adult, heavy exercise||Stallions||6 month growing||
18 month growing
|Values adapted from Beef NRC and Feedstuffs Vol. 86 # 37. Se requirements for all classes of sheep and goats = 0.30 ppm.|
Deficiency of selenium in animals whose primary diet is composed of pasture or rangeland follows a geological pattern, and there are regions of the United States where selenium supplementation is necessary. The Pacific Northwest, the Great Lakes states, the Northeast, the Atlantic Seaboard, and Florida are regions where selenium tends to be deficient in forages (NRC, 2000). When dietary supplies of selenium do not meet animal requirements, cells have a diminished capacity to detoxify peroxides and signs of deficiency may occur (NRC, 2001).
Selenium has been identified as an essential part of normal reproductive and immune function (Gerloff, 1992). Some general indicators of selenium deficiency in ruminants include: reproductive failure, retained placenta in dairy cows, increased calf mortality, decreased calf weaning weights, and immune suppression. Selenium deficiency and its relationship to embryonic loss and reduced fertility appear to be more prominent in sheep compared to cattle (Miller et al., 1998). Supplementing dairy cows that are deficient in selenium has been shown to reduce the incidence of retained placentas (Julien et al., 1979). It is hypothesized that selenium deficiency resulting in reduced glutathione peroxidase enzyme activity combined with a deficiency of vitamin E could allow for the buildup of free radicals, causing damage to cells and tissues and subsequent retention of placenta. Furthermore, selenium readily passes through the placenta therefore the selenium status of the gestating dam will be directly related to the selenium status of the calf at birth. Little data exists to indicate that dietary intake exceeding the 0.30 ppm requirement for dairy cows will result in a reduction of mastitis (Smith et al., 1997), however, deficiencies of selenium have been associated with decreased intracellular kill of pathogens by neutrophils, and subsequently decreased immune function (Gerloff, 1992). White muscle disease is the most severe clinical sign of selenium deficiency in ruminants and other animals. Some indicators of white muscle disease as most often seen in young calves (or lambs) include:
- Leg weakness and stiffness
- Flexion of the hock joints
- Muscular tremors
- Chalky striations and necrosis of cardiac and skeletal muscles
- Death from cardiac failure
Several other nutrients can affect the absorption and metabolism of selenium and impact the requirement for selenium. High levels of sulfur and lead, as well as high or low levels of calcium in the diet can negatively impact selenium absorption in ruminants (NRC, 2005). Organic sources of selenium, which include Se-enriched yeasts, are a more effective way to increase selenium status and the activity of the glutathione peroxidase enzyme in livestock, compared to feeding inorganic selenium sources (NRC, 2001).
Selenium was originally recognized as a nutritional factor due to its toxicity, and was not given credit as an essential dietary element for livestock until 1957. Potentially toxic dietary concentrations in ruminant feeds are considered to be 2 to 5 ppm, which is only about 10 to 20 fold greater than dietary levels considered to be adequate. Often, acute selenium toxicity results when a grazing animal consumes a sufficient amount of selenium accumulating weeds. Death from acute selenium toxicity usually occurs due to respiratory failure.
Signs of acute selenium toxicity include:
- Uncertain gate
- Lowered head
- Elevated body temperature
- Weak, rapid pulse
- Labored respiration
Alkali disease results from a chronic form of selenium intoxication by ruminants or horses, usually from the consumption of forages containing 5 to 50 ppm selenium over a period of weeks or months.
Signs of chronic selenium toxicity include:
- Loss of hair (loss of tail switch)
- Malformation and sloughing of hooves
- Reduced fertility
- Stiffness of joints
- Malformed legs (lambs born to ewes with selenium toxicity)
- Kneeling while grazing (painful feet)
In conclusion, selenium is a necessary mineral for all classes of livestock and horses; however care must be taken to ensure the supplementation of selenium follows FDA guidelines to not exceed 0.30 mg/kg selenium in the diet. The range between dietary toxicity and deficiency is narrow, therefore understanding selenium concentrations in your feeds and forages is important when considering supplementation. Agri-King’s beef and dairy ration program works to balance selenium levels around the values found in your own feedstuffs and forages and therefore optimize livestock performance. For more information about Agri-King nutrition, contact a representative near you or visit the website at www.agriking.com. AK
Gerloff, B. 1992. Effect of selenium supplementation on dairy cattle. Journal of Animal Science. 70:3934-3940.
Julien, W.E., H.R. Conrad, J.E. Jones, and A.L. Moxon. 1979, Selenium and vitamin E and incidence of retained placenta in parturient dairy cows. Journal of Dairy Science. 59:1954-1959.
Miller, J.K., N. Ramsey, and F.C. Madsen. 1998. The Trace Elements. In D.C. Church (Ed.), The Ruminant Animal: Digestive Physiology and Nutrition (pp. 373-383). Prospect Heights, IL.
National Research Council, 2005. Mineral Tolerance of Animals. 2nd Revised Edition
National Research Council, 2001. Nutrient Requirements of Dairy Cattle. 7th Revised Edition
National Research Council, 2000. Nutrient Requirements of Beef Cattle. Update 2000
Smith, K.L., J.S. Hogan, and W.P. Weiss. 1997. Dietary vitamin E and selenium affect mastitis and milk quality. Journal of Animal Science. 75:1659-1665.