title: Selenium metabolism and excretion in mice after injection of (82)Se-enriched selenomethionine.
abstract: 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.
authors.affiliation: Faculty of Science and Engineering, Department of Applied Chemistry, Chuo University, 1-13-27, Kasuga, Bunkyo-ku, Tokyo 112-8551, Japan.
authors.forename: Yoshinari
authors.initials: Y
authors.lastname: Suzuki
authors.forename: Yoshiteru
authors.initials: Y
authors.lastname: Hashiura
authors.forename: Tatsuya
authors.initials: T
authors.lastname: Sakai
authors.forename: Takao
authors.initials: T
authors.lastname: Yamamoto
authors.forename: Takehisa
authors.initials: T
authors.lastname: Matsukawa
authors.forename: Atsuko
authors.initials: A
authors.lastname: Shinohara
authors.forename: Naoki
authors.initials: N
authors.lastname: Furuta
mesh_terms: D000818:Animals; D002850:Chromatography, Gel; D056148:Chromatography, Reverse-Phase; D003600:Cytosol / Q000187:drug effects / Q000201:enzymology; D004912:Erythrocytes / Q000187:drug effects / Q000378:metabolism; D005243:Feces / Q000737:chemistry; D005979:Glutathione Peroxidase / Q000378:metabolism; D007275:Injections, Intravenous; D007554:Isotopes; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D051379:Mice; D009752:Nutritional Status / Q000187:drug effects; D012643:Selenium / Q000097:blood / Q000378:metabolism* / Q000652:urine; D012645:Selenomethionine / Q000008:administration & dosage* / Q000097:blood / Q000494:pharmacology*; D013997:Time Factors; D014018:Tissue Distribution / Q000187:drug effects; D000094765:Glutathione Peroxidase GPX1
chemical_list: D007554:Isotopes; D012645:Selenomethionine; D005979:Glutathione Peroxidase; D012643:Selenium; D000094765:Glutathione Peroxidase GPX1; C000722068:Gpx1 protein, mouse