| First Author | Schweizer U | Year | 2005 |
| Journal | Biochem J | Volume | 386 |
| Issue | Pt 2 | Pages | 221-6 |
| PubMed ID | 15638810 | Mgi Jnum | J:104447 |
| Mgi Id | MGI:3611989 | Doi | 10.1042/BJ20041973 |
| Citation | Schweizer U, et al. (2005) Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply. Biochem J 386(Pt 2):221-6 |
| abstractText | Liver-specific inactivation of Trsp, the gene for selenocysteine tRNA, removes SePP (selenoprotein P) from plasma, causing serum selenium levels to fall from 298 microg/l to 50 microg/l and kidney selenium to decrease to 36% of wild-type levels. Likewise, glutathione peroxidase activities decreased in plasma and kidney to 43% and 18% respectively of wild-type levels. This agrees nicely with data from SePP knockout mice, supporting a selenium transport role for hepatically expressed SePP. However, brain selenium levels remain unaffected and neurological defects do not occur in the liver-specific Trsp knockout mice, while SePP knockout mice suffer from neurological defects. This indicates that a transport function in plasma is exerted by hepatically derived SePP, while in brain SePP fulfils a second, hitherto unexpected, essential role. |
