Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply
Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply
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DOI：
10.1042/bj20041973
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发表时间：
2005-03-01
影响因子：
4.1
通讯作者：
Schomburg, L
中科院分区：
文献类型：
--
作者：
Schweizer, U;Streckfuss, F;Schomburg, L
肝脏特异性失活Trsp（硒代半胱氨酸tRNA的基因），从血浆中去除SePP（硒蛋白P），导致血清硒水平从298 μ g/l下降到50 μ g/l，肾脏硒下降到野生型水平的36%。同样，血浆和肾脏中的谷胱甘肽过氧化物酶活性分别降低至野生型水平的43%和18%。这与SePP敲除小鼠的数据非常一致，支持肝脏表达的SePP的硒转运作用。然而，脑硒水平保持不受影响，并且在肝脏特异性Trsp敲除小鼠中不发生神经缺陷，而SePP敲除小鼠患有神经缺陷。这表明，血浆中的运输功能是由肝脏来源的SePP发挥的，而在大脑中，SePP发挥了第二个迄今为止意想不到的重要作用。
Liver-specific inactivation of Trsp, the gene for selenocysteine tRNA, removes SePP (selenoprotein P) from plasma, causing serum selenium levels to fall from 298 mu g/l to 50 mu g/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.