The Biology of the Goat

Selenium - the Essential Trace Mineral

Selenium was originally identified as a potentially toxic element long before it was recognized to be an essential trace mineral. Plants absorb selenium from the soil if it is available and incorporates it into several amino acids replacing sulfur as part of the normal structure. Plants can survive just fine without selenium since the amino acids function normally as building blocks of protein whether they contain sulfur or selenium. The most common amino acid that incorporates selenium in plants is methionine. When the sulfur atom is replaced by selenium the amino acid is called selenomethionine.

Absorption

When selenium is incorporated into an amino acid it is considered to be in the organic form. This form is more readily absorbed by animals through the digestive tract. It has been estimated that lactating dairy goats absorb about 65% of ingested selenomethionine. Selenium in its elemental state as selenate or selenite is in an inorganic state. Ruminants absorb inorganic selenium less efficiently than monogastric animals because the rumen microbes reduce it to a less soluble form before it reaches the intestinal tract. High levels of sulfur in the diet interfere with selenium absorption whereas adequate levels of calcium assists in selenium uptake.

Once absorbed through the intestine selenium is taken up by the liver and combined to form the amino acid selenocysteine which is similar to cysteine except that again, sulfur is replaced by selenium. This is the form of selenium that appears in muscle and is a source of selenium for carnivores.

Selenocysteine is then combined with other amino acids to create proteins called selenoproteins. Released into the blood, the selenium in a selenoprotein is transported to tissues throughout the body in a safe yet functional form. Humans have genes for about 25 different selenoproteins. Little is known about the basic functions of many of them, but modern research is actively focused on this field of study. Selenium is stored in the kidney and liver and can be measured in blood and serum. The fetus is born with twice as much selenium in the liver as the adult.

Selenium and the brain

Selenoproteins play an essential role in the normal development and protection of brain cells. The brain is resistant to deficiencies in dietary selenium and levels of selenium in the brain are independent of serum selenium levels. This may be explained by recent studies which suggest that the brain synthesizes its own unique selenoproteins which may serve as a storage for selenium for use by brain cells. Blood delivers selenoproteins to the cells of the blood-brain barrier where the selenium is used to make specialized forms of selenoprotein which are then transferred to brain cells.

Cell Membrane Protection

Approximately 50% of selenium in the blood exists in the form of selenoproteins which have many important functions including thyroid hormone metabolism and in formation of immune cells. In humans a deficiency in selenium can lead to neurodegenerative diseases such as Parkinson's or possibly Alzheimer's disease. Selenium has been shown to prevent certain cancers such as prostate or colorectal.

The most important role for selenium is as an anti-oxidant because it is an essential component of the selenoprotein glutathione peroxidase. The level of blood selenium is determined by measuring the amount of this enzyme.

Glutathione peroxidase protects cell membranes from damage from free radicals released from hydrogen peroxide formed during normal metabolism in the cells' mitochondria. Stress can cause excess hydrogen peroxide to be created which causes an imbalance of free radicals inside the cell. Free radicals have an extra electron allowing them to "steal" electrons from the chemical structures that make up cell membranes. Those structures then become reactive and will steal an electron from a neighbouring structure. This chain reaction serves to damage the membrane causing the cell to die. Glutathione peroxidase converts hydrogen peroxide into water before it can produce damaging free radicals.

Vitamin E works in a similar way to stop the chain reaction of damage by binding up free radicals within the cell membrane. In this respect, selenium and vitamin E work together to prevent damage to cell membranes, DNA and other cellular structures from damage by free radicals.

Selenium deficiency

When livestock animals are deficient in selenium, glutathione peroxidase cannot be formed. If the animal is also deficient in vitamin E they develop nutritional muscular dystrophy due to the damage of the cell membranes of the skeletal and heart muscles. Calcium salts accumulate in the defective and dying membranes resulting in the appearance of white areas in the muscles giving this disease the name "white muscle disease."

White muscle disease occurs in all farm animals including fast growing goat kids. Newborns usually are not affected because selenium readily crosses the placenta to be stored in the fetal liver and kidney. Milk is generally very low in selenium so the newborn requires this store until it is able to begin feeding on plants that contain selenium. If the mother is deficient in selenium her kids will be born deficient and will be weak, unable to stand and suck. The heart and respiratory rates are often elevated due to the damaged heart muscle.

Additional problems encountered from selenium deficiency in adult animals are impaired immune and thyroid function and retained placentas. Mild deficiencies can result in chronic health problems.

The signs of selenium deficiency diseases often do not appear until animals have been raised through several generations. First generation deficient animals are more sensitive to stresses, especially when also deficient in vitamin E, and more sensitive to toxicity of certain chemicals and heavy metals such as mercury. On the other hand, selenium deficiency protects against aflatoxin and acetaminophen poisoning in the laboratory rat.

If animals receive an adequate amount of vitamin E but are deficient in selenium signs include hair loss, slow growth, and reproductive failure.

Selenium Toxicity

Livestock that feed on plants with high levels of selenium develop alkali disease so-called because plants more easily take up selenium when grown in alkali soils. Selenium toxicity is characterized by lameness, hoof malformation, hair loss, emaciation and liver damage. The mechanism behind selenium toxicity is not well understood.

Supplementation

Selenium can be supplemented in the form of selenite by injection along with vitamin E, in a loose or block mineral mix provided free choice, or through boluses.

In some countries selenium is mixed with fertilizer and spread on pastures that are known to be selenium deficient. Canadian farmers have found that selenium-fertilized alfalfa increases the selenium content of milk in dairy cows.

Growing numbers of studies show that selenium supplied in yeast which have been fermented in the presence of selenium is more effective at raising blood and milk selenium levels in animals than when selenium is provided in the inorganic form. In selenized yeast selenium is present as selenomethionine, the form that naturally exists in plants. Calves born to cows that were supplemented with selenomethionine had higher selenium serum levels. Milk casein protein normally incorporates methionine. If there is an ample supply of selenomethionine in the blood this amino acid will be taken up by the milk protein in place of methionine increasing the percent of selenium in the milk. This has health benefits for the nursing kid as well as the humans that drink the milk.