Selenium is an essential trace mineral, nutrient of fundamental importance to human biology in 70^s of the last century. It functions in the body as the amino acid selenocysteine at the active sites of seleno-dependent enzyme. The average adult contains about 20 mg of selenium and most of it is in the liver, kidney, heart, spleen and testes.

Physiological role of selenium

Selenium is an integral part of glutathione peroxidase, an enzyme that plays an antioxidant role in cells, and affect the function of vitamin E. It is very important to protect red blood cells and cell membranes from damage by free radicals. Glutathione peroxidase has also a role in protecting the skin from ultraviolet radiation.

Protein thyroxine deiodinase is also seleno-protein. Selenoprotein P is a plasma glycoprotein of unknown function that contains 7-8 selenocysteines per molecule. Under normal conditions, about 65% of plasma selenium is placed in selenoprotein P.

Selenium is important for the growth and health of hair and skin.

Selenium plays a role in maintaining the body's resistance to various diseases. It increases production and efficiency of white blood cells and protects them from the effects of free radicals that are produced during infection. Selenium increases the production of antibodies and participates in strengthening of the body against cancer.

Selenium is involved in maintaining normal liver function, protein synthesis and protect the body from toxic minerals such as arsenic, cadmium, mercury and lead. It plays an important role in the creation of male reproductive capacity and maintain the health of the eyes, hair and skin. Also involved in the metabolism of prostaglandins that control inflammation.

Metabolism

Organic selenium is more thoroughly resorbed and more efficiently metabolized than its inorganic equivalent, which is poorly resorbed and acts more as a pro-oxidant provoking glutathione oxidation and oxidative damage to the DNA.

Selenium may be present in the form of inorganic selenium (selenite SeO₃^2-) or in the form of amino acids selenocysteine and selenomethionine (analogues of amino acids containing sulfur-cysteine and methionine). Plants that grow in soil with large amounts of selenium form methylselenocysteine and selenohomocysteine that can be accumulated in quantities of 5000 ppm thus causing selenium poisoning of humans and animals that consume them.

Inorganic selenium salts and organically bound selenium is probably well absorbed, although there is little information about the mechanism and regulation of resorption. Selenocysteine is decomposed by selenocysteine β-lyase (an enzyme that require vitamin B6 for its functioning) giving selenide (Se²⁺), and alanine. Selenate and selenite are reduced to selenide by an enzyme glutathione reductase.

One part of inorganic selenide is directly excreted, while other forms dimethyl selenide – (CH₃)²Se and trimethylselenium ion – (CH₃)³Se⁺. Trimethylselenium ion is the major selenium metabolite that is expelled in urine. Of the total selenium intake around 55-60% is removed in urine, perspiration around 5%, and less than 1% by breathing. If selenium poisoning occurs, then the percentage of selenium expelled by breath is significantly increased (breath of garlic).

Seleno-enzyme glutathione peroxidase reduces hydrogen peroxide to water and thus reduces the amount of peroxide that can generate free radicals. In the case of vitamin E deficiency selenium plays an important role in decreasing of precursors of lipid alkyl peroxy radicals, as if there is a lack of selenium, vitamin E plays a protective role by eliminating radicals. In this case, membrane lipid peroxidation will be prevented. Selenium plays a very important role in the restoration of vitamin E.

In addition to the liver the largest concentration of selenium in the body is in muscle. Skeletal muscles contain more selenium from the heart.

Creating selenocysteine: The metabolic functions of selenium (as selenocysteine) is in the catalytic site of glutathione peroxidase and thyroxine deiodinase. Selenocysteine is incorporated into proteins in the process of protein synthesis on ribosomes. Less commonly is added to post synthetic modifications of precursor proteins. Codon for selenocysteine is UGA, which usually serves as a STOP codon signaling the end of the translation. The synthesis of proteins that contain selenocysteine codon encodes the amino acid selenocysteine more than ending translation. Such a reading of a codon is the result of a sequence of four nucleotides in untranslation region at the 3' end of the _mRNA. Selenocysteine is formed from serine bound to _tRNA.

Food sources of selenium

The quantity of selenium in the diet depends on the soil on which the food products growth. Good sources of selenium are meat, fish, shellfish, grains, cereals, broccoli, mushrooms, cabbage, celery, pork and beef kidney, tuna, oysters, fish, leaf, beef liver.

The preparation of food may lose significant amounts of selenium. The content of selenium in food products

Recommended daily allowance

The maximum permitted intake of selenium should not exceed 5.7 mmol (450 mg) daily or 6 mg per kilogram of body weight. 

Selenium deficiency

Symptoms of selenium deficiency are present only in people who live in areas where there is little selenium in the soil. Some parts of Europe, U.S., New Zealand and China are places where there is small amount of selenium in the soil.

Selenium deficiency occurs in the critical group of people, such as alcoholics, people who consume processed food and fast food, people with HIV, people with liver disease, people with Down syndrome and diagnosed with fibrocystic breast disease.

Selenium deficiency causes enlargement of the heart, which eventually leads to congestive heart failure, as well as atrophy of the cells of the pancreas. This in turn leads to inadequate secretion of lipase.

Keshan disease is endemic cardiac myopathy that occurs in areas where the soil does not have enough selenium (parts of China). This disease is characterized by heart failure, increasing cardiac arrhythmias, electrocardiographic changes. It affects mainly children and women.

Kashin-Beck disease is endemic osteoatrophy and is characterized by weakness, joint stiffness, pain, degeneration and necrosis of the joints. It also occurs in areas where the soil has small amount of selenium (parts of China).

Selenium deficiency in youth can cause more skin wrinkles in old age.

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