Selenium deficiency symptoms

It is noteworthy, too, that cataracts are one of the selenium deficiency symptoms noted in rats. " Many other injurious agents and nutrient deficiencies might also be eissociat with the formation of cataracts, so it is uncertain whether selenium deficiency is a frequent cause of this disorder. 

Excess selenium intake can occur in both animals and humans living in areas with elevated selenium in the soil. Most grass and grains do not accumulate selenium, but when an animal consumes plants that do accumulate selenium (some up to 10,000 mg/kg) they can develop a condition called the blind staggers . Symptoms include depressed appetite, impaired vision, and staggering in circles and can ultimately lead to paralysis and death. Humans are susceptible to similar effects as well as additional neurological effects. Selenium deficiency results in heart disorders, skeletal muscle effects, and liver damage. 

In livestock and laboratory animals, a deficiency of vitamin E substances may cause degeneration of reproductive tissues, muscular dystrophy, encephalomalacia, and liver necrosis. Considerable research is required to fully determine supplementation of livestock diets unless typical symptoms of a deficiency appear. Symptoms have appeared where there are selenium deficiencies in the soil and where there are excessive levels of nitrates in the soil. White muscle 1 is the term used to describe a condition of muscular dystrophy in cattle. 

Selenium deficiency in soils occurs in some parts of the world [56] and it is standard practice in such areas to dose animals with selenium in order to correct this deficiency. Selenium-responsive diseases can appear when the level of selenium is lower than 0.03 xg/g in the blood [57]. Levels of selenium in pasture plants associated with deficiency symptoms in animals are in the range 0.01-0.03 xg/g [58]. 

The growing interest in selenium speciation is due to its toxic and/or essential properties that depend on the actual physicochemical form of the element. Strong evidence exists on the adverse health effects related to selenium deficiency. It was also demonstrated that supplementation with different selenium forms might help to remove the symptoms of deficit. Selenium has been found in the active site of different antioxidant enzymes, protecting cells against the action of free radicals. The species-dependent cancer-preventive properties are well documented, yet the specific biological functions have not been ultimately elucidated. The list of small selenium compounds includes inorganic forms (two stable valence states), volatile alkylated species, and... 

Livestock and other animals are particularly affected by either selenium deficiency or excess selenium. In animals with selenium-deficient diets, liver necrosis arises. In areas with deficient selenium concentrations in soil, calves and lambs develop muscle atrophy, which is referred to as either white muscle disease or stiff muscle disease. Selenium supplementation (often injections) prevents these symptoms. 

Selenoprotein W. This is a selenoprotein found in skeletal muscle that is reduced in concentration in white muscle disease in animals. Deficiencies in the production of these selenoproteins, especially the glutathione peroxidases, are likely to be related to signs and symptoms of selenium deficiency disease. 

Selenium is a trace metal, which is part of glutathione peroxidase, which protects cell components from oxidative damage caused by peroxidases produced in cellular metabolism. It is indicated for its use as a supplement to IV total parenteral nutrition (TPN) solutions to prevent depletion of endogenous stores and subsequent deficiency symptoms. 

The toxicological significance of the chemical form does not only derive from the fact that the great majority of the elements in the periodic table are metals and metalloids many metals also make it possible to demonstrate the dose-effect relationship very clearly. Copper, manganese, selenium, cobalt and zinc, for example, are essential trace elements whose absence inevitably results in deficiency symptoms or loss of proper functioning. On the other hand, large doses are cytotoxic or cause cancer. 

Selenium Antioxidant No known deficiency symptoms Seafood, cereals, meat, egg yolk, garlic 0.055... 

Deficiency of T. e. can lead to characteristic deficiency symptoms or diseases, thus indicating the essential nature of these nutritional factors, e g. iodine is a component of the thyroid hormones and essential for thyroid function. Iodine deficiency is responsible for endemic goiter, and certain types of cretinism it can be avoided by addition of iodides to drinking water. Other T. e. are chromium, copper, fluoride, magnesium, manganese, nickel, vanadium, silicon, tin, selenium, zinc (see individual entries). 

Vitamin E deficiency is relatively rare, but occasionally occurs in newborns and adolescents. It manifests with similar symptoms as selenium deficiency, because the specific selenoproteins are also involved in transport of tocopherols and protect the tocopherols against oxidation. Manifestation of vitamin E deficiency is mainly through degenerative nerve and muscle (neuromuscular) changes known as myopathy and encephalomalacia. Consumption of excessive amounts of tocopherols occurs only rarely. 

Selenium deficiency in animals is manifested by hepatic necrosis and a set of symptoms called white muscle disease. Very serious selenium deficiency in humans has been reported in China, in the Keshan region, where there is very low selenium content in the... 

Absorption, Metabolism, Excretion Factors Which May Affect Dietary Selenium Functions of Selenium Interrelationship of Selenium and Vitamin E Deficiency Symptoms Evidence of Selenium Deficiencies Associations Between Certain Diseases and Selenium... 

DEFICIENCY SYMPTOMS. There are no clear-cut signs or symptoms which indicate when people are mildly to moderately deficient in selenium. However, many tests on diverse species of animals and man have shown that blood and tissue levels of selenium are in most cases accurate reflections of the selenium nutritional status. But the interpretation of laboratory findings and the diagnosis of selenium deficiency are strictly jobs for health professionals, even though certain laboratories may analyze specimens for lay persons. Henc e, the information which follows is presented so that the patient and his or her doctor might consider whether such tests are advisable. 

INTERRELATIONSHIP OF VITAMIN E AND SELENIUM. During the 1950s, an interrelationship between vitamin E and the element selenium was established. It was found that selenium prevented exudative diathesis (a hemorrhagic disease) in vitamin E-deficient chicks and liver necrosis in vitamin E-deficient rats. Subsequent research demonstrated that both selenium and vitamin E protect the cell from the detrimental effects of peroxidation, but each takes a distinctly different approach to the problem. Vitamin E is present in the membrane components of the cell and prevents free radical formation, while selenium functions throughout the cyto-pleism to destroy peroxides. This explains why selenium will correct some deficiency symptoms of vitamin E, but not others. 

Erythrocyte fragility, hemolysis, and anemia were described as vitamin E deficiency symptoms in various animals fed diets devoid of vitamin E. Additionally, studies in experimental animals have shown that a deficiency of both selenium (a required component of glutathione peroxidases) and vitamin E causes a more rapid and severe onset of debilitating deficiency symptoms. Hypothetically, a deficiency of both vitamins E and C should also cause more severe antioxidant deficiency symptoms, but most animals make their own vitamin C, so this interaction has not been unequivocally demonstrated in humans or animals. 

Selenium is required, but levels must fall into a narrow window. Both deficiency and toxicity symptoms occur. The element is also used therapeutically in cancer treatment. It is the co-factor of the enzyme glutathione peroxidase which is thought to play an important role in oxygen toxicity. The determination of Se in blood or serum is not easy, as many incorrect, inaccurate and imprecise methods have been published (Magee and James 1994). A suggested procedure for Se in body fluids is based on GF-AAS (Thomassen et al. 1994)- For tissues SS-AAS may be used (Fler-ber 1994a). Recent developments by Turner et al. (1999) show that LC-ICP-MS is sensitive and reproducible at low levels. 

A twelve-month selenium-supplementation trial in children with KBD in Tibet did not show any effect on the main symptoms and signs of the disease (Moreno-Reyes et al., 2003). But, in the same study, correction of iodine deficiency before the administration of selenium supplements induced partial recovery of growth retardation. Selenium had no additional effect on either growth or thyroid function, despite the normalization of serum-selenium levels. 

Dietary intakes of many essential trace elements are being determined by NAA, and results may serve as a basis for improved recommendations of safe and adequate daily average intakes of these elements. As a next step, possibly deficient or toxic intakes, the influence of the environment on dietary intake, correlations with tissue concentrations and clinical symptoms, and so forth may be investigated. A special example of such studies is the correlation of low dietary intakes of selenium with a particular syndrome known as Keshan disease in China. 

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