Selenium in Nutrition, Revised Edition (1983) / Chapter Skim
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6 NUTRITIONAL ASPECTS
6 NUTRITIONAL ASPECTS
Pages 77-106
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From page 77... ...
For example, in young swine there may be no measurable differences in weight gain between pigs receiving diets containing 0.04 or 0.14 ppm selenium, but the former may result in mortality of 15 to 20 percent (Ullrey, 1974~. Other criteria may give different answers.
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From page 78... ...
(1973) found the stability of sodium selenite and potassium selenate was satisfactory for poultry when premixed with glucose monohydrate, wheat bran, corn, linseed meal, soybean meal, or soybean protein as a carrier and kept reasonably cool and dry.
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From page 79... ...
(1971) depleted rats of selenium in one of two ways: by feeding a basal purified diet containing amino acids as the only nitrogen source or by feeding females through pregnancy on a torula yeast diet (12 ppb Se)
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From page 80... ...
Selenium-deficient mice treated with paraquat (a broad-spectrum herbicide) had significantly elevated plasma glutamicpyruvic transaminase activity, longer hexobarbital sleeping times, and slower clearance of indocyanine green than paraquat-treated seleniumsupplemented mice (Cagen and Gibson, 1977~.
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From page 81... ...
GUINEA PIG S Myopathy produced in guinea pigs by feeding a diet low in vitamin E was not prevented by supplementing the diet with selenium (Seidel and Harper, 1960; Bonetti and Stirpe, 1963~. The selenium content of the basal diets used in these studies was not indicated.
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From page 82... ...
As expected, blood selenium levels and erythrocyte and plasma GSH-Px activities were significantly higher in the selenium-supplemented than in the seleniumdeficient animals. No differences, however, in the activities of plasma creatine phosphokinase, lactic dehydrogenase, glutamic oxaloacetic transaminase, or ornithine carbamyl transferase, or in plasma tocopherol levels, have been found between selenium-deficient and selenium-supplemented animals.
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From page 83... ...
CHICKENS The chick shows three selenium-deficiency diseases: exudative diathesis, nutritional muscular dystrophy, and nutritional pancreatic dystrophy. Exudative diathesis and nutritional pancreatic dystrophy can be completely prevented by dietary selenium, whereas nutritional muscular dystrophy depends upon adequate dietary levels of vitamin E or sulfur-containing amino acids for its complete prevention.
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From page 84... ...
Chicks with exudative diathesis show low activities of vitamin E and selenium-dependent GSH-Px in most tissues, but increased levels of reduced glutathione, which result from inability to use its reducing equivalents in peroxide metabolism. Nutritional muscular dystrophy occurs in chicks fed diets low in selenium, vitamin E, and sulfur-containing amino acids (Calvert et al., 1962~.
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From page 85... ...
The disease is prevented by adding less than 50 ppb available selenium to low-selenium (less than 15 ppb) purified diets; the selenoamino acid selenomethionine has been shown to be a particularly effective source of selenium for prevention of nutritional pancreatic atrophy (Cantor et al., 1975a)
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From page 86... ...
In contrast to the nutritional muscular dystrophy of the chicken, the nutritional myopathies of the poult are not influenced by the levels of sulfur-containing amino acids in the diet, and they are completely prevented by selenium. Whereas the exudative diathesis of the poult is prevented by either selenium or vitamin E, the nutritional myopathies of the poult appear to be primarily related to selenium deficiency.
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From page 87... ...
These activities respond quickly to dietary supplementation with sodium selenite or vitamin E Supplemental selenium supports optimal growth in the absence of vitamin E when added to the diet to provide 0.10 to 0.15 ppm total selenium.
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From page 88... ...
Mulberry heart disease developed when swine were fed diets containing high levels of unsaturated fats and was accompanied by muscular dystrophy and hepatosis dietetica. The administration of selenium and vitamin E prevented mulberry heart disease and hepatosis dietetica, and vitamin E prevented muscular dystrophy.
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From page 89... ...
(1978a) fed a semipurified diet containing 0.008 ppm selenium and 1.4 mg or-tocopherol/kg.
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From page 90... ...
However, Michigan workers (Miller et al., 1973j were unable to produce mortality or muscle lesions in pigs from sows fed corn-soybean meal diets unsupplemented with selenium and vitamin E when the pigs were fed 600 ppm iron from ferrous sulfate or injected intramuscularly with 1,000 mg of iron from iron-dextran. When 5 percent aerated cod liver oil was incorporated into the gestation diet and offspring were orally dosed with 5 to 10 ml aerated cod liver oil daily, an intraperitoneal injection of 750 mg iron from iron-dextran/kg of body weight produced myopathy in two of eight 8-day-old pigs (Cook, 1974~.
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From page 91... ...
Hepatosis dietetica was the predominant lesion when plasma AspAT and ICD activities were very high and AlaAT activity was only moderately increased. When activities of all three enzymes were significantly elevated, lesions were found in myocardium and/or skeletal muscle, as well as in liver.
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From page 92... ...
(1977a) found that elevated serum creatine phosphokinase activity was a useful indicator of subclinical muscular dystrophy in vitamin E- and/or selenium-deficient swine; and vitamin E deficiency increased red cell lipid peroxide concentration, while selenium deficiency did not (Fontaine and Valli, 1977)
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From page 93... ...
It may be significant that these workers observed hepatosis dietetica, mulberry heart, skeletal muscle degeneration, cutaneous microangiopathy, gastric ulcers, and gastric parakeratosis in pigs fed a diet containing 0.008 ppm selenium and 1.4 mg o`tocopherol/kg supplemented with 15 mg D,L-o`-tocopheryl acetate/kg. Forty-five milligrams of D,L-or-tocopheryl acetate/kg prevented the development of these lesions.
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From page 94... ...
Nutritional muscular dystrophy and other selenium-responsive diseases are widespread in areas where the feeds consumed contain between 20 and 30 ppb selenium in dry matter. Supplements of selenite, selenate, and selenium-rich protein have been used successfully to correct deficiencies.
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From page 95... ...
(1973) concluded that selenium levels below 5 ppm in kidney cortex dry matter and 0.5 ppm in muscles of calves and lambs might be used as an indication of selenium deficiency in ruminants, although lower muscle selenium concentrations
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From page 96... ...
In northern Europe, or-tocopherol has been considered the most effective component of the selenium-vitamin E mixture in preventing nutritional muscular dystrophy. In these countries, the problem is associated with poor curing of lightly fertilized grass forages and with an alteration of the unsaturated fat components in the cured hays.
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From page 97... ...
(1969) first observed higher retention rates for placentas in herds with correspondingly greater problems of nutritional muscular dystrophy and were able to reduce incidence through supplementation of selenium and vitamin E (Trinder et al., 1973~.
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From page 98... ...
(1960) have described a muscular dystrophy in horses that is consistent with selenium deficiency.
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From page 99... ...
Respective serum selenium concentrations were 0.147, 0.131, 0.127, 0.121, and 0.124 ppm. When orphaned foals were fed a semipurified diet unsupplemented with vitamin A, vitamin E, or selenium, serum selenium values after 60 days were 0.037 ppm, compared to 0.142 to 0.167 ppm in serum of foals supplemented with 0.5, 1.0, or 2.0 ppm selenium.
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From page 100... ...
The total glutathione reductase activity increase could have been a response to insufficient absolute concentrations of reduced nicotinamide adenine dinucleotide phosphate (NADPH) or a response to apparent insufficiency induced by declining blood pH, which could increase the glutathione reductase Km for NADPH.
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From page 101... ...
Plasma glutamic-oxaloacetic transaminase and creatine phosphokinase activities were markedly increased and were associated with a severe myopathy and renal mineralization. These signs were prevented by supplements of 1.0 ppm selenium as sodium selenite or by 30 IU o`-tocopherol/kg of diet.
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From page 102... ...
, low birth weights and retarded growth, and transient and shifting lameness in both juveniles and adults. Serum creatine phosphokinase activity was elevated, and necropsy lesions included muscular dystrophy and hepatic necrosis.
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From page 103... ...
The low plasma selenium levels seen in this patient, along with the favorable response to selenium treatment, suggest the essential role of selenium in human nutrition. Another case of apparent selenium deficiency during TPN was described
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From page 104... ...
The disease primarily affects children from 1 to 9 years of age and is characterized by gallop rhythm, heart failure, cardiogenic shock, abnormal electrocardiograms, and heart enlargement. The Chinese workers first showed that the average selenium content of human hair in areas affected by Keshan disease was generally below 0.12 ,ug/g, whereas in areas removed from the affected region, hair selenium content ranged from 0.25 to 0.6 Gig.
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From page 105... ...
Gross (1976) studied a group of premature infants whose vitamin E status was adequate as judged by serum vitamin E levels but whose GSH-Px activities and plasma selenium levels declined from 4.2 units/g hemoglobin and 0.080 ,ug/ml at 1 week of age, respectively, to 2.7 units/g hemoglobin and 0.035 ,ug/ml at 7 weeks of age.
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From page 106... ...
Such comparisons of data from different countries reinforce the original conclusion of the Chinese investigators that selenium may be only one of the agents involved in the etiology of Keshan disease and that other predisposing environmental conditions may be necessary for the disease to occur. The elderly may also be in danger of suboptimal selenium status since this age group in New Zealand had lower blood-selenium levels and erythrocyte GSH-Px activities than young adult controls (Thomson et al., 1977b)
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