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Bentonites in feeds cause error in the analysis for Se by the AOAC (3.097-3.101) fluorometric method for Se in plants. The error apparently results from the binding of the piazselenol by insoluble residue from the bentonite. This effect is avoided by diluting digests to volume after reduction with HCl, centrifuging or allowing to stand, and analyzing a portion of the clear supernatant liquid. Insoluble residues present after digestion of plant materials do not appear to cause a similar error.

Selenium intake by adults consuming self-selected levels of four different diets averaged 209 micrograms. per day and correlated well with caloric and protein intake. Urinary selenium concentration averaged 0.108 microgram. per milliliter, and 24-hour excretion for the various diets averaged 58.0% to 88.6% of the intake. The data suggest that the RDA upper limit of 200 micrograms. of selenium per day and the suggested maximum urine selenium concentration may be too restrictive. The data further indicate that even though there are differences in the absorption of selenium from different sources, the average is about 70% for foods purchased in the Northern Great Plains area.

There are conflicting reports in the literature concerning the synthesis of selenoamino acids from inorganic selenium in animals, and this work was undertaken to further investigate this. Pronase digests of acetone powders of liver and kidney tissue from rats administered 75SeO3= were subjected to fractionation by cation exchange chromatography using current methods for separating the various amino acids. Very little, if any, selenocystine was found in the digests. However, good evidence was obtained for the occurrence of 2,7-diamino-4-thia-5-selenaoctanedioic acid. It is suggested that the selenocysteine portion of this compound was formed by the reduction of the selenite to selenide with its subsequent incorporation into the amino acid by the action of serine hydrolase (E C 4.2.1.22). No selenomethionine was found under the conditions of this study.

Two experiments were conducted to determine the effect of varying dietary selenium (Se) levels and Se source on growing swine. In Exp. 1, seleniferous wheat and oats were used to formulate diets containing .47, 2.58, 5.60 or 8.40 micrograms/g organic Se. Dietary Se level had no effect on pig performance during the 6-wk experiment as measured by daily gain, daily feed intake or feed/gain. Blood composition and enzyme activity were not affected by dietary treatment. Selenium concentrations of blood, hair, liver, kidney, heart, spleen and diaphragm muscle were increased linearly (P less than .01) as dietary Se increased. In addition, liver weight as a percentage of body weight was increased linearly (P less than .01) as dietary Se level increased. No signs of chronic Se poisoning were observed. Dietary treatments in Exp. 2 were similar to Exp. 1 with the exception that sodium selenite was utilized as the Se source and the diets were fed for 17 wk. Inorganic Se levels of .54, 2.63, 5.69 or 8.33 micrograms/g had no effect on pig performance as measured by daily gain, daily feed intake or feed/gain. Selenium concentrations of blood, hair, liver, kidney, spleen and diaphragm muscle were significantly increased as dietary Se level increased. Liver weight as a percentage of body weight was increased at the two highest dietary Se levels. Blood glutathione peroxidase activity was significantly increased by dietary treatment, while other blood variables were not affected. No signs of chronic Se poisoning were observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Two new cyanogenic glycosides, linustatin and neolinustatin, were isolated from linseed oil meal. Each of the compounds was fed to rats in a corn-based diet at levels of 0.1 and 0.2%. At the 0.2% level, both substances gave significant protection against growth depression caused by 9 ppm selenium as sodium selenite. Both compounds also promoted a significant increase in liver and kidney weight over the selenium control animals. Linustatin and neolinustatin are closely related in structure to linamarin and lotaustralin and were found to be present in linseed oil meal at levels of 0.17 and 0.19%, respectively. Linamarin fed at the level of 0.2% also gave significant protection against growth depression and liver damage. A related cyanogenic glycoside, amygdalin, appeared to give a small but nonsignificant protective response. The isolation of the two new glycosides provides a probable explanation for the protective activity of linseed oil meal against selenium toxicity.

A total of 96 crossbred pigs received various levels of sodium selenite to determine the effect of dietary selenium (Se) on growing swine fed corn-soybean meal diets. Levels of supplemental Se were 0, 4, 8, 12, 16 and 20 micrograms/g. There were linear decreases (P less than .01) in both gain and feed intake with increasing levels of dietary Se. Feed/gain increased numerically as dietary Se increased. Hair Se increased quadratically (P less than .01) and blood Se increased linearly (P less than .01) with increasing level of dietary Se. Cell volume and hemoglobin were not affected by dietary treatment. Increasing dietary Se significantly increased glutathione peroxidase (GSH-Px), glutamic-oxalacetic transaminase (GOT). and glutamic-pyruvic transaminase (GPT). External signs of selenosis were noted in some pigs fed 12 or 20 micrograms/g of Se. The toxic level of Se in a corn-soybean meal diet for crossbred pigs appears to be between 4 and 8 micrograms/g. Of variables studied, growth rate was the most sensitive indicator of chronic selenosis in swine.