White muscle disease, selenium deficiency

Heart disease and selenium—A review of the effects of selenium deficiency reveals a repetitious undercurrent of vascular-type lesions suggesting a heart involvement in selenium disorders. Sudden death associated with selenium deficiency in newborn or rapidly growing lambs and calves apparently results from weakening of the heart muscle, commonly called white muscle disease. Selenium-deficient monkeys also have heart lesions. This disorder is characterized by white streaks in muscles, and in some cases, by abnormal electrocardiograms. Often, the animals affected with this diseeise die suddenly when they are subjected to moderate stresses. 

In 1956 selenium was identified (123) as an essential micronutrient iu nutrition. In conjunction with vitamin E, selenium is effective iu the prevention of muscular dystrophy iu animals. Sodium selenite is adrninistered to prevent exudative diathesis iu chicks, a condition iu which fluid leaks out of the tissues white muscle disease iu sheep and infertility iu ewes (see Eeed ADDITIVES). Selenium lessens the iacidence of pneumonia iu lambs and of premature, weak, and stillborn calves controls hepatosis dietetica iu pigs and decreases muscular inflammation iu horses. White muscle disease, widespread iu sheep and cattle of the selenium-deficient areas of New Zealand and the United States, is insignificant iu high selenium soil areas. The supplementation of animal feeds with selenium was approved by the U.S. EDA iu 1974 (see Eeed additives). Much of selenium s metaboHc activity results from its involvement iu the selenoproteia enzyme, glutathione peroxidase. 

In 1957, Schwartz and associates showed that the toxic element selenium was also a nutritional factor essential for prevention of the death of liver cells in rats.527 Liver necrosis would be prevented by as little as 0.1 ppm of selenium in the diet. Similar amounts of selenium were shown to prevent a muscular dystrophy called "white muscle disease" in cattle and sheep grazing on selenium-deficient soil. Sodium selenite and other inorganic selenium compounds were more effective than organic compounds in which Se had replaced sulfur. Keshan disease, an often fatal heart condition that is prevalent among childen in Se-deficient regions of China, can be prevented by supplementation of the diet with NaSe03.528 Even the little crustacean "water flea" Daphnia needs 0.1 part per billion of Se in its water.529... 

Adsorption of anions at mineral surfaces is important in soils because of the limit this process imposes on the availability of plant nutrients such as P, S, and Mo which occur naturally as anions and are added in anionic form in fertilizers. Anion adsorption is also relevant in geochemistry, ore processing, and other fields where minerals with high surface areas are brought into contact with aqueous solutions of anions. Selenite and goethite were chosen for this study because in Western Australia a selenium deficiency in pastures has been shown to be related to the incidence of white muscle disease in sheep (3), and according to workers quoted by Rosenfeld and Beath (9) selenium in soils of higher... 

Gross necropsy lesions of a selenium deficiency are identical to those of a vitamin E deficiency (NRC, 1994) and include exudative diathesis and myopathy of the gizzard. Paleness and dystrophy of the skeletal muscles (white muscle disease) are also common. The incidence and degree of selenium deficiency may be increased by environmental stress. Selenium is generally included in trace mineral premixes. Common sources for supplementation of poultry diets are sodium selenite and sodium selenate. Selenium yeast is also used in conventional diets. 

Livestfick grown on soils high in selenium are poisoned by eating Anrogolus ( ioco-weed ). which concentrates it stie grown on land deficient in selenium develop "white muscle disease." Deficiency of seleiuiun involved in Key-shan disease in China. ... 

Ishihara H, Kanda F, Matsushita T, Chihara K, Itoh K. White muscle disease in humans myopathy caused by selenium deficiency in anorexia nervosa under long term total parenteral nutrition. J Neurol Neurosurg Psychiatry 1999 67(6) 829-30. 

A combined deficiency in Se and vitamin E has occurred naturally in farm animals (sheep, cattle) in regions of the world where the soil is low in selenium, such as in western Oregon in the United States and m New Zealand, where forages low in vitamin E were used. This deficiency results in muscular dystrophy. The heart and skeletal muscle appear white. The disease has been called white muscle disease. Death may occur. The disease can be prevented by supplementing the animals with either Se or vitamin E. 

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. 

The role of selenium in human medicine has been reviewed. Animal studies in the 1950s demonstrated the nutritionally beneficial, effects of selenium by showing that there was a selenium-responsive liver necrosis in vitamin E-deficient rats. There are important selenium-dependent diseases in farm animals, such as white muscle disease in sheep and cattle, and myopathy of cardiac and skeletal muscle in lambs and calves. In these animals, some cause of oxidative stress, such as increased physical activity or vitamin E deficiency—together witli dietary selenium deficiency—is required to elicit the disease. 

Schwarz observed that rats maintained on yeast diets developed a fatal necrosis of the liver, which could be prevented either by vitamin E and cysteine, as well as by a third factor ( Factor 3 ), which was recognized to be an organic selenium compound (Schwarz and Foltz 1957). Sodium selenite and other inorganic and organic selenium compounds were generally found to have lower Factor 3 activity. Other selenium-responsive disorders are White Muscle disease in sheep, calves, and horses, hepatosis dietetica and mulberry heart disease in swine, and exudative diathesis and pancreatic fibrosis in chickens. In goats, selenium deficiency adversely affected growth, reproduction and milk performance (Anke et al. 

With regard to the nutritional aspects of selenium metabolism, the essentiality of this element was established in studies which demonstrated that a number of deficiency diseases " such as exudative diathesis in chicks and turkeys, necrotic liver degeneration in rats and swine and white muscle disease which is a nutritional type of muscular dystrophy often affecting young lambs and calves, could be overcome or prevented by administering small doses of selenium. 

TTiis selenoprotein is not nearly so well characterized as glutathione peroxidase and its biochemical role is still unknown. This is a small molecular weight selenoprotein (10,000 daltons) which was reported in 1972. It was isolated from heart and muscle homogenates of normal lambs. This protein is missing in animals which suffer from white muscle disease, which is a type of muscular dystrophy resulting from a deficiency of selenium in the diet . Further work on this selenoprotein has been reported and recently the form of selenium present was identified as selenocysteine . ... 

Clinical selenium deficiency in mminants is expressed as white muscle disease, lethargy, impaired reproduction, weight loss and reduced growth, shedding, decreased immune response, decreased erythrocyte glutathione peroxidase, and sudden death. Selenium deficiency - as judged by blood concentrations <0.1 mg Se/L - has been documented in California among domestic cattle, mule... 

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... 

In contrast to arsenic, trace concentrations of selenium are essential for human and animal health. Until the late 1980s, the only known metabohc role for selenium in mammals was as a component of the enzyme glutathione peroxidase (GSH-Px), an anti-oxidant that prevents ceU degeneration. There is now growing evidence, however, that a seleno-enzyme is involved in the synthesis of thyroid hormones (Arthur and Beckett, 1989 G. F. Combs and S. B. Combs, 1986). Selenium deficiency has been linked to cancer, AIDS, heart disease, muscular dystrophy, multiple sclerosis, osteoarthropathy, immune system and reproductive disorders in humans, and white muscle disease in animals (Levander,... 

The realization that selenium (Se) may be an essential micronutrient for human diets has arisen only recently, in the second half of the twentieth century. Selenium deficiency, attributable to low soil selenium levels in farm animals, especially sheep that are afflicted by selenium-responsive white muscle disease, has been recognized for at least half a century. However, the more recent identification of Keshan and Kashin-Beck diseases as endemic selenium-responsive conditions, occurring in a central 4000-1— km-wide belt of central China and in areas of Russia, demonstrated conclusively that not only is selenium an essential element for man but also deficiencies occur naturally and require public health measures to alleviate them. Selenium incorporation into plants is affected by the acidity of the soil and by the concentrations of iron and aluminum present so that selenium content of human diets is modulated by these components of the environment. The very recent discovery that these diseases probably arise through the interaction of selenium deficiency with enhanced viral virulence has added a further layer of complexity, but it does not alter the fact that selenium is an essential dietary component that cannot be substituted by any other element. Another complicating factor is that moderately increased soil selenium concentrations result in the opposite condition of seleno-sis, or selenium overload, with equally debilitating consequences. Of all elements, selenium has a very narrow safe intake range, and unlike some other potentially toxic elements, it is absorbed efficiently by the intestine over a wide range of concentrations and across a variety of different molecular forms. 

The precise functional roles of selenoproteins P and W are not well understood. Selenoprotein P contains more selenium (up to 10 atoms per molecule) than any other mammalian selenoprotein, and it can form equimolar selenium-mercury complexes, thereby probably helping to detoxify mercury. It is the major selenoprotein fovmd in plasma and may also act as a selenium transport protein and selenium reserve. Selenoprotein W is found in muscle, and its decline may help explain the molecular basis of white muscle disease in selenium-deficient sheep. 

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