Selenoprotein profiling in various tissues of mice fed with selenium‐deficient and high‐selenomethionine diets.

Abstract

Selenium (Se) is a trace essential nonmetal element and its deficiency is known to cause myocardial necrosis leading to the heart weakening (e.g. Keshan disease). Se deficiency may contribute to Kashin‐Beck disease, resulting in atrophy, degeneration, and necrosis of cartilage tissue in the joint, or hypothyroidism including extreme fatigue, goiter, mental retardation, and miscarriages. In contrast, Se excess may cause reversible balding and brittle nails, give a garlic odor to the breath, and cause intestinal distress, weakness and slowed mental functioning. All such clinical symptoms could be attributable to dysregulated expression of twenty‐five selenoproteins in humans; mice also have the corresponding 25 selenoproteins. This study examined expression of the representative 11 selenoproteins (Gpx 1/2/3/4, TrxR1/2, Dio1, Sephs2, SelP, SelS, and SelN) in 8 different organs (brain, heart, liver, lung, kidney, pancreas, spleen, and testis) of mice fed ad libitum selenium‐deficient and high‐selenomethionine (a major dietary source from plants) diets. One week with the diets caused significant decreases and increases in Se contents of each organ, respectively, which became slightly more apparent until 4 weeks. Se deficiency in diet induced significant decreases in Gpx1/2 of liver, kidney, and pancreas; however, neither Se deficiency nor selenomethionine excess caused significant expression changes in other selenoproteins of all organs tested. There results indicate that altered organ Se contents upon Se deficiency or excess in short periods (~4 weeks) do not generally reflect selenoprotein expression levels in these organs.Support or Funding InformationSupported by the Grants‐in‐Aid for Scientific Research (16H05107, 16K15194, 17K08287, and 25220103) from the MEXT of Japan.This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.