PANTER, K. E., HARTLEY, W. J., JAMES, L. F., MAYLAND, H. F., STEGELMEIER, B. L., AND KECHELE, P. O. (1996). Fundam. Appl. Toxicol. 32, 217-223. Selenium is an essential micronutrient, although ingestion in excess in pigs can cause disease conditions including neurological dysfunction and chronic skin and hoof lesions. Controlled feeding trials in growing swine, using the same Se content in feed sources, resulted in higher concentrations (p =£ 0.05) of Se in blood and organs of pigs fed seleno-DL-methionine compared with those receiving Astragalus bisulcatus or sodium selenate. Clinical signs of Se toxicity including neurological signs of paralysis were more severe and occurred sooner in the A. bisulcatus group than in the sodium selenate or seleno-DL-met hionine groups. All five pigs fed A. bisulcatus developed neurological signs of paralysis, and in four the signs occurred within 5 days of the start of treatment. Four of five pigs fed sodium selenate also developed paralysis, but this occurred 4 to 21 days after treatment began. The fifth pig in the group developed signs of chronic selenosis. Two of five pigs fed seleno-DL-methionine developed paralysis on 9 and 24 days, respectively, and the remaining three developed chronic selenosis. Selenium fed to pigs in three forms [plant (A. bisulcatus), sodium selenate, or seleno-DL-methionine] resulted in neurological dysfunction and lesions of symmetrical poliomyelomalacia. These were most severe in the A. bisulcatus group, which also had polioencephalomalacia. Although seleno-DL-methionine caused the greater increase in tissue and blood Se concentrations, this did not correlate with severity of pathological changes, since animals fed A. bisulcatus developed more severe and disseminated lesions. Field observation and experimental trials in the United States have shown a great variety of syndromes and pathology resulting from ingestion of certain species of Astragalus by livestock. The syndromes include disease conditions induced by the nitro-containing Astragalus (A. miser), the swainsonine-containing Astragalus (A. lentiginosus, locoweeds), and the selenium-containing Astragalus (A. bisulcatus). These syndromes have been reviewed by James et al. (1981). Two Se-accumulating plants (A. bisulcatus and A. praelongus) and inorganic Se compounds have been shown to produce neurological signs and microscopic lesions of focal symmetrical polioencephalomalacia and poliomyelomalacia when fed to young pigs (Hartley et al., 1984). Both plant species also contain small amounts of swainsonine, an amannosidase inhibitor that causes the lesions and clinical syndrome known as locoism. This toxin might contribute to the development of lesions when animals are poisoned eating these plants. In previous studies of Se intoxication, organic Se was fed to growing pigs in the form of selenocystine . The animals failed to thrive and had varying degrees of hepatic fibrosis, but neither neurological signs nor histological lesions were seen in the central nervous system (Hartley et al., 1984). The biochemical parameters of some of these pigs have been reported (Baker et al., 1989). This report details additional trials including dosing with seleno-DL-methionine (organic form of Se) and a comparison of the resulting tissue Se and histological lesions with those seen in animals treated with sodium selenate (inorganic form of Se) or A. bisulcatus (nonprotein, water-soluble plant forms of Se) at the same Se dose.