The effect of selenium deficiency on the fatty acid metabolism of rats and lambs Public Deposited

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  • Selenium deficiency in rats results in increased carbon metabolism, approaching twice the rate of selenium supplemented animals (normal). This is also reflected in a 50 percent increase in lysosomal enzyme activity in tissues of selenium deficient animals. Isolation of rat liver lysosomes shows a 17 percent increase in membrane thickness of selenium deficient rats. Lamb muscle lysosomes could not be completely separated from other organelles. The level of arachidonic acid in selenium deficient tissues from both lambs and rats is elevated upwards to 50 percent above normal. Injection of ¹⁴C-acetate into normal and selenium deficient rats shows a rapid uptake of radioactivity into the liver phospholipids by selenium deficient rats which was approximately 100 percent greater than normal. However, no accumulation was evident because of a precipitous drop of radioactivity to normal levels within 36 hours, Phospholipid arachidonate is also synthesized in selenium deficient rats approximately twice as rapidly as in normal but again does not accumulate. Vitamin E is rapidly oxidized and excreted by selenium deficient rats. Nearly 30 percent of a vitamin E dose is excreted within 48 hours by deficient animals as opposed to only 18 percent by normal. This apparently results in aberrations of metabolic pathways requiring vitamin E. For example, heme levels in the liver microsomes of selenium deficient rats are only 50 to 60 percent of normal. These data suggest a direct dependence of vitamin E metabolism on the presence of selenium. Since selenium deficiency has been shown to cause a decrease in glutathione peroxidase activity, fatty acid peroxides would accumulate in these animals. These peroxides apparently oxidize vitamin E which is then rapidly excreted, producing an inadequate vitamin E status.
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