Ppm Selenium Research Articles

Adaptation of Rats to Selenium Intake

Changes of liver selenium after intake of organic selenium at different levels and for various lengths of time were studied in 236 young rats. In litters born to mothers fed a diet containing 4.5 ppm selenium (in seleniferous sesame press cake) and kept on this diet after weaning, the liver levels decreased steadily; these levels increased in stock rats fed the same diet. The graphical presentation of these changes resulted in two straight lines, crossing each other. When the selenium diet was fed to dams 5 to 7 days prior to parturition and thereafter, the liver levels of the litters rose rapidly; liver levels increased at a slower rate in rats born to females fed the diet 15 to 19 days prior to birth and decreased in litters from mothers kept on the diet prior to mating. When litters from stock females were nursed by dams fed the seleniferous diet during pregnancy and changed to the stock ration after the birth of their litters, the liver selenium levels rose rapidly for about 3 weeks after weaning and then decreased. On a diet containing 10 ppm selenium, liver values in rats from the stock colony rose for 2 to 3 weeks to high levels and then decreased. Animals bred on the diet containing 4.5 ppm selenium exhibited a slower, more continuous rise of liver selenium when the high selenium diet was fed. The results suggest the existence of an adaptation mechanism which allows rats exposed to chronic selenium ingestion to store less of this element than previously unexposed controls.

Role of Selenium in the Nutrition of the Chick

In an attempt to establish that selenium is an essential trace element for chicks and not merely a substitute for vitamin E, the effects of feeding various diets low in selenium have been investigated. Chicks were protected against exudative diathesis by supplements to semipurified diets of either 10 ppm d-a-tocopheryl acetate or 0.04 ppm selenium. In contrast, chicks given diets prepared with crystalline amino acids and containing less than 0.005 ppm selenium had poor growth and high mortality even when the diet contained up to 200 ppm d-a-tocopheryl acetate. Higher levels of vitamin E prevented mortality but even with 1000 ppm growth was inferior to that obtained with supplements of selenium and no added vitamin E. A relationship was demonstrated between the selenium requirement and the level of vitamin E in the diet. Using diets containing 100 ppm vitamin E, the selenium requirement was less than 0.01 ppm, whereas with 10 ppm vitamin E it was more than 0.02 ppm and with no added vitamin E, approximately 0.05 ppm.

Serum Selenium and Related Parameters of Naturally and Experimentally Fed Horses

A survey was made of serum selenium levels and some related parameters of naturally and experimentally fed horses as part of a study to determine the significance of selenium in light-horse nutrition. Serum selenium levels of suckling foals and naturally fed weanlings, yearlings, trainees, adult mares and stallions were 7.00, 14.7, 13.1, 12.4, 12.7 and 12.1 μg Se/100 ml serum, respectively. Orphaned foals fed a commercial milk replacer had 16.25 μg Se/100 ml. Foals fed a selenium, vitamin A- and vitamin E-deficient semipurified ration containing 33% Torula yeast had serum selenium values (μg/100 ml) of 3.68 in unbedded concrete floor stalls, 7.40 in straw-bedded stalls, and 17.33 in tobacco stem-bedded stalls. Foals fed the semipurified ration supplemented with 0.5, 1 and 2 ppm selenium (as sodium selenite) had serum selenium values of 14.68, 15.30 and 16.67 μg/100 ml, respectively. By selenium repletion-depletion techniques using parenterally administered selenium, an equine selenium requirement was estimated at 2.4 μg/kg body weight/day. The SGOT reducing effects of a single intramuscular injection of selenium occurred over a 45-day period.

Selenium-responsive Myopathies of Myocardium and of Smooth Muscle in the Young Poult

Poor growth, mortality and myopathies of the heart and gizzard have been produced experimentally in young poults fed a practical-type diet containing all nutrients previously shown to be required by the poult except for supplemental vitamin E and methionine. The corn and soybean meal used in this diet were obtained from geographical areas where the soil is known to be low in selenium. Addition of vitamin E and methionine to the diet improved growth but gizzard myopathy was not prevented and maximal growth was not achieved until the diet also was supplemented with at least 0.1 ppm of selenium as sodium selenite. Under the conditions of these experiments, therefore, the selenium requirement in a practical-type diet depended to some extent upon the amount of vitamin E or methionine supplementation; it ranged from approximately 0.18 ppm in the presence of vitamin E to approximately 0.28 ppm of selenium in the absence of added vitamin E. Although myopathy of the skeletal (pectoral) muscle was not observed grossly, necropsy studies revealed histological changes in skeletal muscle typical of Zenker's degeneration. The order of prominence of the “selenium-responsive” diseases of the young poult appear to be: myopathy, first of the smooth muscle (gizzard); second, of the myocardium; and third, of the skeletal muscle. Selenium appears to be the primary nutritional factor required. Vitamin E is of less importance and sulfur amino acids are completely ineffective in prevention of these myopathies in poults.

Toxicity of selenium to post-weanling rats

Dietary selenium, as sodium selenite and as seleniferous wheat, was fed to young rats in 6-week experiments. The selenium additions were at levels of 1.6, 3.2, 4.8, 6.4, 8.0, 9.6, and 11.2 ppm in a wheat-type diet. Except for a slight growth reduction with the diet containing 4.8 ppm of selenium as sodium selenite, growth retardation did not occur unless the diets contained 6.4 ppm or more of the additive from either source. Mortality occurred after the fourth week when the additive was at 8.0 ppm or more. In observations with seleniferous-wheat selenium at growth inhibitory levels, voluntary feed intake reduction accounted for growth reduction, since equal amounts of control diet gave similar or somewhat less weight gain. Diets containing seleniferous-wheat selenium at 1.6–8.0 ppm did not affect water consumption in 4-week observations. However, 6.4 ppm in the diet increased spleen weight and altered liver appearance; and 8.0 ppm or more caused further effects such as enlargement of the pancreas, reduction in hemoglobin content of blood, and elevation of bilirubin content of serum. Selenium from seleniferous wheat was deposited in tissues such as liver, thigh muscle, and hair to a greater extent than was selenium from sodium selenite.

Distribution of Microgram Quantities of Selenium in the Tissues of the Rat, and Effects of Previous Selenium Intake

Small doses of radioselenium were injected as selenite into rats previously fed one of 3 types of low selenium diets for 2 weeks, or into rats fed these diets supplemented with graded levels of selenite up to 5 ppm of selenium. The rats fed the low selenium diets retained over 50% of such doses in their carcasses after 24 hours, and they excreted only 10 to 20% of the dose in the urine. Urinary excretion of the labeled dose increased progressively with previous selenium intake to 47% by rats fed the most selenite, and retention of the labeled dose decreased correspondingly in the carcass. Neither the general character of the basal diet, nor the presence of vitamin E altered this inverse relationship. But in contrast with the rest of the carcass, the liver tended to retain a relatively constant percentage of the labeled single dose, despite previous selenium intake.

Fluorometric Selenium Determinations in the Liver of Normal Pigs and in Pigs Affected with Nutritional Muscular Dystrophy and Liver Dystrophy

The selenium concentration of livers and kidneys in normal pigs and in pigs affected with nutritional muscular dystrophy (NMD) and liver dystrophy (LD) was determined. The kidney values showed great variation in normal pigs. The young pigs generally had the lowest levels. The liver values were less scattered. In NMD and LD the liver contained about 0.2 ppm of selenium on the average, whereas normal livers contained about 1.2 ppm. Kidneys showed corresponding differences. This is in good agreement with the favourable results obtained with selenium therapy.

EFFECT OF DIETARY SELENIUM ON INCIDENCE OF NUTRITIONAL ENCEPHALOMALACIA IN CHICKS.

Addition of 0.13 ppm of selenium as sodium selenite to a semisynthetic diet containing 4% corn oil freed of tocopherol reduced the incidence of encephalomalacia. On the other hand, when 8% corn oil was fed, selenium in levels up to 1.56 ppm had no effect on the proportion of chicks with encephalomalacia. Growth was not affected by addition of selenium.

Gross and Microscopic Pathology of Tocopherol-deficient Mink

Experimental tocopherol deficiency was produced in young male mink to study the subsequent gross and microscopic lesions and the extent to which they were altered or prevented by the addition of cod liver oil, selenium or α-tocopherol to the basal ration. The major gross lesions consisted of internal intercostal, adductor and cardiac myopathy, hepatic peripherolobular fatty infiltration and, in the cod liver oil-supplemented mink, yellow fat. Histologically, the tocopherol-deficiency myopathy was characterized by swollen, differentially stained fibers, vacuolar degeneration, sarcolemmal and myoblastic proliferation and calcification of the nonphagocytized myofibrillae. The myocarditis was focal calcified necrotic and the fatty hepatic infiltration was accompanied by centrolobular hepatic hemorrhage. Yellow, acid-fast pig-ment was deposited at the interstices of the adipose tissue from the cod liver oil-supplemented mink which also had coagulation necrosis and calcification of the renal tubules. Adipose tissue from chronically tocopherol-deficient mink had adipocyte-like, non-acid-fast spheres in its interstices. The basal tocopherol-deficient ration with 0.1 ppm of selenium as sodium selenite prevented all lesions except minor accumulations of amorphous non-acid-fast material at the adipose interstices. The basal mink ration with 25 ppm α-tocopherol prevented all the tocopherol deficiency lesions.

Influence of dietary vitamin E and selenium on distribution of Se75 in the chick.

SummaryThree-week-old chicks fed either a Vit. E deficient or supplemented diet were intraperitoneally injected with Se75, and distribution of the isotope was determined in various tissues at 24, 48, and 168 hours after injection. Similarly, 2-week-old chicks fed a selenium deficient or supplemented diet were given an oral dose of Se75 and the distribution of the isotope in several tissues was determined at 24 and 168 hours after administration. Vitamin E had no effect on distribution of selenium, but selenium itself had a marked effect on the uptake and retention of radioselenium. One-half of the dose was retained by selenium-deficient chicks at 7 days, whereas only 1/5 of the dose was retained by chicks fed 1 ppm selenium from day-of-age. Considerable selenium was deposited and retained in the cerebellum of chicks even though this element cannot prevent encephalomalacia.

Relation of selenium, vitamin E and other factors to muscular dystrophy in the rabbit.

SummaryRabbits maintained on a torula yeast, Vit. E deficient diet developed a severe and rapidly progressing muscular dystrophy. This condition was not prevented by addition to the diet of 1 ppm selenium or of supplements of dl-alpha tocopheryl acetate alone or in combination. Additions of natural feedstuffs (wheat bran, linseed oil meal or kidney beans) to the semi-purified diet did not fully prevent the condition, although they did lessen the severity of the lesion and increase the average number of days of survival indicating deficiencies other than selenium and Vit. E were involved in the particular experimental diets used. A marked alopecia was observed in all animals fed diets not containing a natural feedstuff.

Selenium and Torula yeast in production of exudative diathesis in chicks.

SummaryYit. E. dried brewers yeast, and 0.05 ppm selenium promoted growth and prevented symptoms of exudative diathesis in chicks fed a purified soybean protein diet. Any of the supplements completely replaced the others and maintained normal values for serum protein, A G ratio and blood hemoglobin. Chicks fed Vit E-free diet, containing purified soybean protein as source of protein, developed symptoms of exudative diathesis in 30 days, manifested by mild edema and exudation with subcutaneous hemorrhage in the abdomen. The affected birds had a reduced serum protein level, A G ratio, and blood hemoglobin level. Addition of 0.7% sodium, 0.5 ppm arsenic or a mixture of 1% potassium and 0.07% magnesium, to above Vit. E-free, soybean-protein diet failed to reduce the time needed for development of exudative diathesis. Addition of Torula yeast (20 or 30% of the diet) to Vit. E-free soybean protein diet hastened and increased incidence of exudative diathesis in chicks fed this diet. Thus it appears that some com...

Effect of selenium on reproduction in rats.

SummaryLow concentration (1.5 and 2.5 ppm) selenium in drinking water for two generations had no effect on the reproduction in rats. 2.5 ppm of Se reduced the number of young reared by the second generation of mothers. 7.5 ppm selenium prevented reproduction in females but fertility of the males was not affected.