Induction of lesions of selenium-vitamin E deficiency in weanling swine fed silver, cobalt, tellurium, zinc, cadmium, and vanadium.

Forty-two weanling pigs were allotted to 7 groups and fed (for 10 weeks) a commercial ration that was adequate in selenium and vitamin E (Se-E) content, either alone or with supplements of Ag (3,000 mg/kg of feed, as acetate), Co (500 mg/kg, as chloride), Te (500 mg/kg, as tetrachloride), Zn (3,000 mg/kg, as sulfate), Cd (500 mg/kg, as sulfate), or V (200 mg/kg, as vanadate). The pigs fed the Ag supplement died after 25 to 39 days and had lesions characteristic of Se-E deficiency with accumulations of serous transudates in body cavities and hepatic and cardiac necrosis. In the pigs fed the Ag supplement, there was high hepatic Se content terminally; blood glutathione peroxidase (GSH-Px) activity decreased to low levels several weeks before the pigs died with lesions of Se-E deficiency. Macroscopic lesions of Se-E deficiency were not found in pigs fed Co, Te, Zn, Cd, or V. However, evidence of Se-E deficiency, as indicated by microscopically detected necrosis of cardiac and skeletal muscle, was present in 50% to 65% of the pigs fed Co or Te and occasionally in pigs fed Zn, Cd, and V supplements. The pigs fed Te had marked decrease of blood GSH-Px activity over the last 6 weeks of the feeding period. No consistently abnormal values for blood GSH-Px activity or terminal hepatic Se content were observed in pigs fed Co, Zn, Cd, or V. The pigs fed the Zn supplement grew as rapidly as the control pigs. Evidence of V toxicosis was observed as severe growth suppression, mortality, and marked enteritis and cystitis (with accompanying hydroureter in 1 pig).