Selenium responsive diseases

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]. 

Fordyce F. M., Zhang G., Green K., and Liu X. (2000b) Soil, grain and water chemistry in relation to human selenium-responsive diseases in Enshi District, China. App/. Geochem. 15, 117-132. 

Kubota J, Allaway WH, Carter DL, et al. 1967. Selenium in crops in the United States in relation to selenium responsive diseases of animals. J Agric Food Chem 15 448-453. 

Selenium in Crops in the United States in Relation to Selenium-Responsive Diseases of Animals, J. Agr. Food Chem. (1967) 15, 448. 

Norman, B. B. and Johnson, W. (1976) Selenium responsive disease. Animal Nutritional and Health 31 6. 

In contrast, selenium deficiency has been implicated in several human diseases, most notably Keshan disease (KD) and Kashin-Beck disease (KBD). KD is an endemic selenium-responsive cardiomyopathy that mainly affects children and women of child-bearing age and is named after... 

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. 

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 most common toxic metals in industrial use are cadmium, chromium, lead, silver, and mercury less commonly used are arsenic, selenium (both metalloids), and barium. Cadmium, a metal commonly used in alloys and myriads of other industrial uses, is fairly mobile in the environment and is responsible for many maladies including renal failure and a degenerative bone disease called "ITA ITA" disease. Chromium, most often found in plating wastes, is also environmentally mobile and is most toxic in the Cr valence state. Lead has been historically used as a component of an antiknock compound in gasoline and, along with chromium (as lead chromate), in paint and pigments. 

Larger particles (several micrometers in size) are deposited in the ciliated portion and are cleared from the respiratory system by muco-ciliary action into the gastronomical tract, but may produce systemic toxic effects by absorption in body fluids. Finer particles reach the lower non-ciliated portion of the lungs, are cleared very slowly, and are responsible for diseases such as pneumoconiosis and lung cancer. Metallic lead (Pb), tellurium ( ), selenium (Se), and platinum (Pt) are known to cause both systemic and respiratory toxicity in laboratory animals and several cases of acute and chronic poisoning among metal workers have also been documented. 

Trace metals have been measured in various tissues by ICP-MS to investigate Alzheimer s disease [249-252]. Various sample preparation and processing approaches have been used, including flow injection analysis and extraction. Al, Si, and Sn levels were reported to be higher than in healthy tissue, whereas zinc and selenium concentrations were lower. In the temporal cortex there were also reductions of cesium and cerium concentrations. The mechanisms responsible and the key elements remain incompletely understood. 

Dalton TP, Li Q, Bittel D, Liang L, Andrews GK (1996) Oxidative stress activates metal-responsive transcription factor-1 binding activity. Occupancy in vivo of metal response elements in the metallothionein-I gene promoter. J Biol Chem 271 26233-26241 Danscher G, Howell G, Perez-Clausell J, Hertel N (1985) The dithizone, Timm s sulphide silver and the selenium methods demonstrate a chelatable pool of zinc in CNS. A proton activation (PIXE) analysis of carbon tetrachloride extracts from rat brains and spinal cords intravitally treated with dithizone. Histochemistry 83 419 22 Danscher G, Jensen KB, Frederickson CJ, Kemp K, Andreasen A, Juhl S, Stoltenberg M, Ravid R (1997) Increased amount of zinc in the hippocampus and amygdala of Alzheimer s diseased brains a proton-induced X-ray emission spectroscopic analysis of cryostat sections from autopsy material. J Neurosci Methods 76 53-59... 

Medical surveys have shown that increased selenium intake decreases the risk of breast, colon, lung, and prostate cancer. In order to determine which species could be responsible for disease-preventive effects of selenium, several studies have characterized the selenium compounds in Brazil nut [46,49,53-56]. 

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... 

Although some similarities are observed in the tissues of chicks suffering from these diseases, it appears that no common metabolic defect can be held responsible for all three conditions, since various specific dietary changes unrelated to the vitamin E content of the diet can completely prevent one of the diseases without having any effect upon the other two. The most important of these are the prevention of encephalomalacia with synthetic antioxidants, the effectiveness of inorganic selenium in prevention of exudative diathesis, and the role of cystine in preventing muscular dystrophy. 

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). 

The following discussion of heavy metals in infant foods is based on recent developments in trace element research that suggest that some elements presently recognized only as "toxic" may have essential functions in certain animal species and perhaps in man. The data discussed here are not intended to detract from the concern for the safety of infant foods they are meant to complement the concern for safety with the concern for adequacy of intake. Before the identification of selenium as an essential element in 1957 the presence of certain concentations of selenium in infant foods would have given rise to serious concern, had one been able to analyze them accurately, because selenium was known only as a carcinogen. Twenty-five years later, hundreds of thousands of children in China are protected by selenium supplements against an endemic cardiomyopathy, the Keshan disease (Chen et al., 1980). This example alone should alert us to the need for a comprehensive understanding of the action of trace elements, of their proven or inferred requirements and of their total dose-response curve. 

Among nutritional interactions that may have an influence on the effect of vitamin E on immune responses and disease resistance, vitamin A and poly-unsaturated fatty acids (PUFA) are particularly interesting since they have, themselves, immunoregulatory roles (Mertin and Meade, 1977 Sheffy and Schultz, 1979), Protein malnutrition, and selenium effects are discussed elsewhere in this symposium, thus will not be mentioned here. 

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