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Query: UMLS:C0026850 (muscular dystrophy)
 5,870 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The early interest in selenium related primarily to its toxicity, but since 1957 the element has been recognized as a dietary essential. The dietary requirement for selenium by most species is about .1 ppm. Deficiencies of selenium in cattle and sheep have been confirmed under natural grazing conditions in many countries of the world. Overt signs of inadequacy such as white muscle disease (nutritional muscular dystrophy) occur primarily in young calves or lambs born to selenium deficient dams. Infertility has increased in ewes grazing pastures low in selenium. In general, signs of deficiency have not occurred in older animals such as finishing beef cattle and lactating dairy cows. Subclinical deficiencies of selenium are not determined easily, however, and thus an inadequacy of the element may be limiting maximum animal performance under certain circumstances of drylot feeding. The current nutritional status of ruminant animals in many geographical areas and involving various feeding programs with this element has not been established. The recent widespread deficiency problems with nonruminants suggest that such an assessment should be made. Concentration of selenium in tissue, particularly in the liver, has been used in establishing selenium status of the animal. With lambs glutathione peroxidase activity in certain tissues may be a more accurate indicator of selenium adequacy than is selenium content of the tissue. Supplemental sodium selenite and sodium selenate by either oral administration or parenteral injection have prevented clinical signs of selenium deficiency and animal losses in both ruminant and nonruminant animals. Heavy pellets containing elemental selenium for placement in the rumen have proved effective. In general, organic forms of selenium are absorbed more readily by animals than are inorganic compounds. The dietary requirements for selenium and its metabolism are influenced by many nutrient interrelationships, including its interactions with sulfur, lipids, vitamin E, proteins, amino acids, and several microelements. The Food and Drug Administration gave approval in 1974 for the oral administration of supplemental selenium as either sodium selenite or sodium selenate to certain classes of swine and poultry. Similar approval in the United States for ruminants will require additional information, particularly with regard to the influence of dietary intake on concentrations of selenium in tissue and milk in beef and dairy animals.
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PMID:Selenium in ruminant nutrition: a review. 110 75

High mortality and a high incidence of exudative diathesis and muscular dystrophy were observed in chicks fed a diet supplemented with either 800 or 1600 ppm copper. Adding 0.5 ppm selenium to a basal diet containing 0.2 ppm prevented mortality and selenium deficiency signs. Dietary zinc levels of 2100 to 4100 ppm also resulted in high mortality, exudative diathesis, and muscular dystrophy. A selenium supplement of 0.5 ppm completely prevented the deficiency signs and markedly reduced mortality. The results demonstrate that both copper and zinc can induce a selenium deficiency in chicks when a diet relatively low in this element is fed.
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PMID:Precipitation of a selenium deficiency by high dietary levels of copper and zinc. 114 13

A syndrome characterised by bilateral paralysis and associated with degenerative changes in skeletal musculature, has been noted in adult breeder hens, and their progeny broilers, in a commercial poultry organisation in Queensland. Paralysis occurred between the ages of 24 to 63 weeks in broiler breeder hens and at approximately 6 weeks in the broiler chickens. Onset is slow, taking up to 2-3 days from the time leg weakness if first noticed until paralysis was complete. Other than the paralysis the birds appeared normal. Histopathological and experimental observations indicate that the muscular dystrophy is caused by a selenium deficiency. Supplementation of the diet with selenium at a level of 0.1 ppm completely alleviated the symptoms such that the birds may be returned to the mating pens.
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PMID:Selenium-responsive myopathy in broiler breeder hens in Queensland. 116 86

Finland is poor in selenium. Selenium deficit leads to muscular dystrophy in animals. Since 1962, selenium has been added in Finland to some animal foodstuffs, since 1968 to all animal foodstuffs. Addition of selenium to fertilizers started in 1984. Intake of selenium by man and cattle today is roughly 1.0 times higher than it was before selenium supplementation. Collagen is the most important component of the organic matrix of the tooth. Selenium can replace sulphur in bonds of collagen. The resulting bond is stronger than a sulphur bond. Since selenium supplementation, the conditions of the teeth of children and young people has improved considerably. The author believes that selenium supplementation has reduced the incidence of caries in young Finns.
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PMID:Has the increase in selenium intake led to a decrease in caries among children and the young in Finland. 133 51

Selenium is a vestigial element indispensable for man and animal, having adverse effects when in bigger quantities. Among the diseases resulting from selenium deficiency in animals the most important are nutritional muscular dystrophy, exudative disthesis (most common in poultry), and nutritional hepatic dystrophy. In the man chronic intoxication occurs most of all, which is observed in selenium bearing regions. Taking into consideration geographic distribution on some of the diseases beneficial influence of selenium is observed in cardiac and vascular diseases, and hypertension. The correlation between selenium deficiency and mortality caused by neoplasm is also notable. It is unquestionable that selenium inhibits the activity of enzymes, especially those containing sulfohydryl groups. The stabilization of lysosomal membranes leads to the presumption that selenium prevents peroxidation processes in tissues and cell membranes. The influence of selenium on reproduction is also worth noticing. Its supply turns out to be effective in cases of infertility of sheep, and partly in rats, pigs, and poultry. The embryo dies in pigs fed on fodder poor in selenium and vitamin E. The degeneration of the ovaries and placenta accretion occur in cows in cases of selenium deficiency. The excess of selenium can affect negatively the reproductive system. The element is thought to be a teratogenic agent. Since it permeates through the placenta and lactic gland easily, the symptoms of selenosis appear in new-born animals; many of them have developmental anomalies occurring at the same time. In birds the decrease in laying eggs and their incubation occur in case of selenium deficiency.
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PMID:The influence of selenium on the reproduction of rats. 136 82

A 33-day feeding experiment was conducted with 3-day-old broiler chicks to assess the efficacy of various flavonoid and simple phenolic antioxidants in preventing nutritional muscular dystrophy (NMD) resulting from vitamin E deficiency. None of the flavonoids or simple phenolics at a dietary concentration of 1,000 ppm completely prevented NMD but quercetin reduced (P less than .05) its incidence and quercetin, morin, and ferulic acid reduced (P less than .05) the severity of the disorder. The low-selenium, low-vitamin E diet also promoted the development of a mild exudative diathesis (ED) in many of the birds, which was inhibited (P less than .05) by the rutin and silymarin treatments, but exacerbated (P less than .05) by quercetin, morin, and ferulic acid. Changes in concentrations of vitamin E in plasma, liver, or muscle, caused by the various treatments (other than vitamin E), were not related to protection against NMD or ED.
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PMID:Research note: efficacy of various flavonoids and simple phenolics in prevention of nutritional myopathy in the chick. 140 42

Selenium deficiency is responsible for Zenker type muscle degeneration in calves, lambs, and foals in the prenatal and postnatal stages of development. Investigations have shown that the selenium GSH Px, and vitamin E content of the maternal and fetal parts of the placenta in cattle are different. Similarly, low concentrations of selenium are present in milk from cows and sheep. In addition to an inadequate supply of selenium and vitamin E as a contributory cause of fetal nutritive muscular dystrophy (FNMD), it is assumed that a placental transport block and/or impaired selenium metabolism in the placenta are also responsible. Postnatal nutritive muscular dystrophy, however, is attributed to either acute selenium and vitamin E deficiency in basic feed or impaired plant absorption of selenium as a result of antagonistic elements, such as sulphur.
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PMID:The importance of selenium in the prenatal and postnatal development of calves and lambs. 170 68

A time lag factor of about five days has been identified in an increased incidence of SIDS in relation to a cold day. Sudden exposure to chilling appeared to trigger skeletal muscle weakness and renal failure about five days later in a man found to have only 25% of normal carnitine palmitoyl transferase (CPT) activity in biopsied skeletal muscle. White Muscle Disease is a muscular dystrophy in young ruminants which appears about five days after turnout to pasture in the weaned ruminant raised on a diet deficient in vitamin E and selenium (VESD). Pasture has high levels of linoleic and linolenic acid (high PUFA diet) which are modified by developing rumen bacteria. Corbucci investigated the effects of circulatory shock (cardiogenic) on skeletal muscle mitochondrial activity in humans. Cytochrome oxidase activity fell markedly and, in particular, the capacity to oxidase palmitoyl carnitine was greatly reduced. He considered a consequence of this disorder was sequestration of carnitine as acyl carnitine which could not be recycled. Unusual acyl carnitines have been identified in six out of 13 SIDS victims in a USA group. In Finland, researchers identified a rise in SIDS incidence (mostly found in the prone position) after great and rapid temperature changes. Foster found a relationship between 1984 SIDS incidence and the incidence of goitre in World War I troops.
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PMID:Sudden infant death syndrome (SIDS): a time lag factor. 204 96

Oral and parenteral preparations of Se are used worldwide to prevent and treat nutritional muscular dystrophy and other Se deficiency syndromes. There are extensive published data on the effects of oral supplementation on Se residues in food animal products. Very little published data exist on the effects of parenteral administration on Se residues, even for cattle and swine in which parenteral preparations are used extensively. The distribution of Se into kidney and liver appears to be equivalent for both forms of supplementation. Elimination of Se in milk is greater after parenteral administration and correlates with high plasma Se levels, however the milk excretion drops quickly and after 4 d returns to control levels (Little et al. 1979). Of particular interest is the finding that up to 18% of Se in an oral diet may be excreted in milk (Maus et al. 1980). Use of Se supplements in poultry results in increased levels of Se in liver, kidney, and eggs. Distribution of Se into liver and kidney is much greater than into breast muscle indicating a greater capacity of these organs to accumulate Se. Excretion of Se into eggs results in Se levels equivalent to those in liver and kidney, indicating that eggs are an important route of Se excretion in laying hens (Ort and Latshaw 1978). When Se supplementation stops, the liver, kidney, and egg white and yolk residues decline quickly to control values within 1-2 wk. Breast muscle Se content changes little during supplementation and after withdrawal of supplementation. Oral and parenteral selenium supplementation in swine result in greater accumulation of Se in liver and kidney than in muscle. Oral selenium supplementation also increases the excretion of Se into milk. This method has been used to prevent Se deficiency disease in piglets (Mahan et al. 1975). Oral supplementation with 0.1 ppm Se, as sodium selenate, did not result in levels of Se in blood, meat, or viscera at slaughter (Jenkins and Winter 1973). Despite the large amount of data available on Se residues in food animals, additional information on the pharmacokinetics of parenterally administered Se preparations is needed, especially in sheep and goats which receive parenteral Se supplements. Information on the disappearance kinetics of Se residues in meat and milk is needed for all ruminants. The data currently available in the literature does not allow the calculation of pharmacokinetic parameters of Se in any species. Properly performed pharmacokinetic studies would contribute a great deal towards a better understanding of how food animals utilize supplemental selenium.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Effects of oral and parenteral selenium supplements on residues in meat, milk and eggs. 218 65

For the investigation of the cause of white muscle disease (WMD), tocopherol (Toc) and selenium (Se) levels and blood glutathione peroxidase (GSH-Px) activities were examined using lambs with WMD and their ewes. Serum Se levels of 4 lambs with WMD were low under 30 ppb, lambs showing very low levels below 15 ppb. The serum Se level was correlated with blood GSH-Px activity showing remarkably low activities in the lambs with WMD. Se contents in the organs of lambs with WMD were lower than those of control lambs, and particularly liver Se contents were deficient levels below 50 ppb. Serum Toc levels were normal, but alpha-Toc contents in organs showed very low levels, especially in the liver. The serum Toc and Se levels and blood GSH-Px activities of their ewes and other sheep kept in the same farm revealed similar results to those of lambs with WMD. Feedstuffs supplied on the farm showed the deficient level of the Se content below 50 ppb and a very low level of alpha-Toc. It was concluded that WMD of lambs in Hokkaido was nutritional muscular dystrophy resulted from deficiencies of Toc and Se to their ewes.
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PMID:Studies on serum tocopherol and selenium levels and blood glutathione peroxidase activities in lambs with white muscle disease. 239 72


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