Article Index "Selenium...The Facts" Article Index

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By: James Coomer, Ph.D.
Dairy Specialist, MoorMan's 5 Star SMA
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Selenium (Se) was first identified in the early 1800s but it's nutritional importance has only been recognized in the later half of this century. Selenium is a micro nutrient element essential in very small quantities. Chemically, selenium falls between tellurium, which is a metal, and sulfur, which is not a metal. In the past, there was controversy over whether selenium was an essential nutrient or a toxic element. In the early 1930s, selenium was identified as the toxic agent causing lameness and death in livestock grazing certain range plants. It was almost 25 years later when selenium was first identified as an essential nutrient.

Selenium Requirement
Although it is not well defined, the requirement for selenium by ruminants is approximately 0.1 to 0.3 ppm. The actual requirement depends on the following factors:

  • The chemical form of selenium.
  • The previous selenium status of the animal.
  • The amounts of interfering or enhancing factors in the diet, including vitamin E, sulfur, lipids (fats), proteins, amino acids, copper, arsenic, and cadmium.

Tissue selenium and glutathione peroxidase concentrations may be used as indicators of selenium status.

Currently, selenium can be supplied to cattle by two methods:

  • Injection of a selenium solution which usually contains vitamin E.
  • Dietary supplementation of selenium. Sodium selenite and sodium selenate are currently the only selenium sources approved for use in livestock feeds.

The addition of selenium to livestock feeds is restricted to designated levels by Food and Drug Administration (FDA) regulations. An organic selenium source, currently being used in human mineral supplements, is in the process of being evaluated by the FDA for use in livestock feeds.

Deficiency Symptoms
The initial deficiency of selenium in cattle was recognized as the cause of "White Muscle Disease" in calves. The condition acquired its name because postmortem examinations usually revealed white streaks in the striated muscle, which result from the degeneration of muscle fibers.

It has been documented that deficiencies in dietary selenium and vitamin E result in increased incidence of mastitis. Supplemental selenium and vitamin E have been shown to lower the frequency and duration of clinical mastitis.

Retained placentas in dairy cattle can be caused by numerous factors, one of which may be a selenium deficiency. Retained placenta can have adverse economic effects because over half of the animals affected develop uterine infections which increase the incidence of infertility. Injections of selenium during the dry period have been shown to reduce the incidence of retained placenta.

Metabolic Role of Selenium
The main role of selenium is as a component of the enzyme glutathione peroxidase. Glutathione peroxidase is an enzyme found inside body cells and is responsible for detoxifying peroxides. Peroxides are "high energy" oxygen-containing molecules that are produced during the metabolism of fat. These peroxides can be very destructive to body cells and tissues if not captured and detoxified by glutathione peroxidase. Selenium is also a component of other enzymes and is required for the normal development of the pancreas.

Metabolic Role of Selenium
Vitamin E and selenium are closely linked and are both involved in a variety of metabolic processes. Both nutrients are required to protect tissue membranes from damage arising from the end products of oxidative processes. Selenium, as a part of glutathione peroxidase, acts within (inside) the cells to capture and destroy peroxides before they can compromise the integrity of the cell membranes. Vitamin E is located within the cell membrane and acts as a free radical scavenger. Therefore, vitamin E acts to reduce the spread of damage to cell membrane once it occurs.

Because selenium and vitamin E work together to reduce damage to cell membranes, selenium and vitamin E can partially replace one another. If adequate levels of selenium are available to detoxify peroxides before they can cause damage, then less vitamin E is necessary to repair or stop damage. Conversely, if inadequate selenium is available, then more vitamin E is needed to prevent damage caused by the peroxides that do not get detoxified by glutathione peroxidase. However, neither selenium nor vitamin E can fully replace the other.

Selenium Toxicity
Selenium toxicity is associated with high selenium levels in soil, primarily in the Dakotas and Wyoming. Soils containing greater than 0.5 ppm of selenium are potentially dangerous to livestock. A few species of plants, such as Astragalus (milk vetch), Macaeranthera (woody aster), Haplopappus (goldenweed), and Stanleya (Prince's plume), are known to be selenium accumulators. These plants can be very toxic to grazing animals because they may accumulate selenium at levels greater than 1,000 ppm.

Blind staggers or alkali disease is the most common problem associated with selenium toxicity. Symptoms include emaciation, loss of hair, soreness and sloughing of the hooves, excessive salivation, blindness, and death. Restricting access to potentially toxic forage and feeding diets high in protein and sulfur to slow selenium absorption are the most practical means of preventing selenium toxicity. For some livestock producers in the U.S., selenium deficiency is a much greater concern than selenium toxicity.

References available upon request.

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Agricultural Research Service

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