Tissue selenium and serum tocopherol concentrations in selenium-vitamin E deficient pigs fed peas (Pisum sativum).

An experiment was conducted to study the effects of feeding growing pigs a diet low in selenium (Se) and vitamin E (E) with and without supplementation of various levels of Se and/or E on tissue Se and serum tocopherol concentrations. Nine of 10 pigs fed the unsupplemented cull pea diet had lesions attributed to a Se-E deficiency and eight of these pigs died during the 135-day experiment. No deaths, clinical signs or lesions attributed to Se-E deficiency were observed among pigs fed any of the supplemented diets. In pigs fed the unsupplemented basal ration, hepatic Se concentrations on a dry matter basis decreased from .50 to .16, renal cortical from 3.27 to 1.86, and blood from .46 to .05 ppm during 135 days. Supplementation of the basal ration with .10 ppm Se as sodium selenite resulted in an eightfold increase in hepatic, nearly a fivefold increase in renal cortical and a 25-fold increase in blood Se concentrations compared to pigs fed the unsupplemented basal ration. Supplementation of the basal ration with 100 ppm E resulted in increased renal cortical (P<.01) and blood (I~.05) Se concentrations. Hepatic, renal cortical, and blood selenium concentrations of .25, 2.5 and .1 ppm, (dry basis) respectively, were determined to be the critical levels below which clinical illness, death or lesions of Se-E deficiency could be expected. Selenium concentration in liver, renal cortex and blood each