Selenium metabolism and excretion in mice after injection of (82)Se-enriched selenomethionine

The organic Se compounds (particularly selenomethionine [SeMet]) in plants and yeasts are very effective chemoprotectants for mammalian cancer. To characterize the dynamics of selenomethionine utilization pathways, we intravenously injected (82)Se-enriched SeMet into mice under different nutritional states (Se-adequate and Se-deficient mice) and then measured their endogenous and exogenous (82)Se levels. Furthermore, we quantified Se compounds and selenoproteins in liver, kidneys, plasma, and urine. The average recoveries of exogenous (82)Se from solid tissues, urine, and feces were 81% for Se-adequate mice and 84% for Se-deficient mice. Exogenous (82)Se was distributed in the hepatic and renal cytosols as cellular glutathione peroxidase (cGPx), selenosugar, and SeMet within 1 h after injection. Synthesis of cGPx was maintained until 72 h after injection, regardless of the Se nutritional status. Whereas plasma levels of exogenous (82)Se as selenoprotein P (Sel-P) peaked at 6 h after injection, those of Se-containing albumin (SeAlb), extracellular GPx, and SeMet peaked at 1 h after injection. These results suggest three Se transport pathways in mice injected with SeMet: SeAlb (within 1 h after injection); SeMet (from 1 to 72 h after injection); and Sel-P (from 6 to 72 h after injection). The amount of Sel-P in Se-deficient mice was 1.5 times that of Se-adequate mice, and this increase was much larger than Se-containing compounds other than Sel-P. Our results indicate that Sel-P has an important role in Se transport when the nutritional supply of Se is insufficient.