Abstract
Supplementation of selenium as sodium selenite results in an increase in hepatic organic solvent-soluble lipofuscin pigments, the metabolic end products of lipid peroxidation. Weanling mice fed a basal diet containing 0.05 ppm selenium had a significant increase in hepatic organic solvent-soluble lipofuscin pigments and glutathione peroxidase activity following supplementation of an additional 0.1 ppm selenium as sodium selenite from 5 to 9 months of age. Normal levels of vitamin E (30 mg/kg) were insufficient to protect against the oxidative effect of this increased dose of selenite. However, 10 times the normal level of vitamin E markedly suppressed this oxidative effect.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 79-85 |
| Number of pages | 7 |
| Journal | International Journal of Toxicology |
| Volume | 5 |
| Issue number | 1 |
| DOIs | |
| State | Published - 1986 |