Stimulation of Lipid Peroxidation in Vivo by Injected Selenite and Lack of Stimulation by Selenate 1

Abstract

Abstract

Male weanling rats were raised on diets based on torula yeast which were deficient in vitamin E and selenium, or supplemented with these substances. They were injected intraperitoneally with sodium selenite at 2 mg Se/kg or with sodium sulfite to give the same level of sodium. Following injection, lipid peroxidation in vivo was estimated by monitoring the production of ethane, a volatile product formed on the peroxidation of ω-3-unsaturated fatty acids. In the hour following injection, vitamin E- and selenium-deficient rats injected with selenite produced 15 times as much ethane as did controls injected with sulfite. All rats in this group died from 1 to 4 hr after injection. Rats fed diets supplemented with selenite showed only a two- to threefold stimulation of ethane production by selenite and 3/4 survived. Rats fed diets supplemented with vitamin E did not produce more ethane in response to selenite injection and 3/4 survived. All four rats supplemented with both vitamin E and selenium survived without showing increased ethane production. Thus, the increased vulnerability of vitamin E- and selenium-deficient rats to acute selenite toxicity may involve peroxidation in vivo. Rats fed diets supplemented with vitamin E could survive at least twice as much selenite as rats deficient in selenium and vitamin E. Seven-day survival figures for rats fed the basal diet and injected with selenite were: 1 mg Se/kg, 7/8; 2 mg Se/kg, 0/8. For rats supplemented with vitamin E the figures were 2 mg Se/kg, 7/8; 4 mg Se/kg, 2/8. When sodium selenate was injected into rats deficient in vitamin E and selenium at 3 mg Se/kg it caused acute mortality without increasing peroxidation in vivo.