Selenium is an essential
trace element, and its deficiency can cause
cardiomyopathy, arrhythmias and increased susceptibility to
infection. Such clinical symptoms are considered primarily attributed to decreased expression of some of the 25
selenocysteine-containing
selenoproteins in humans. Conversely, a
selenium-excessive diet can cause acute
poisoning and chronic symptoms with unknown mechanisms. To reveal the impact of
selenium deficiency and excess on
selenoprotein expression in vivo, mice (that possess 24
selenoproteins) were fed with
selenium-deficient or
selenomethionine-excessive diets for up to 4 weeks, and the expression levels of nine representative
selenoproteins [
glutathione peroxidase (Gpx) 1/2/3/4,
thioredoxin reductase 1/2,
deiodinase 1, and
selenoprotein P/S] were measured in 10 organs (brain, heart, liver, lung, kidney, pancreas, spleen, testis, skeletal muscle and thymus). We observed a time-dependent decrease in the
selenium content of most organs (except testis) of
selenium-deficient mice but not in the expression levels of the nine
selenoproteins, with the exceptions of Gpx1/2 in the heart/liver/kidney/pancreas/spleen and Gpx3 in the pancreas/spleen. Serum lipid peroxidation levels were up-regulated in response to Se deficiency because of the decreased expression/activity of Gpx3, a plasma-type Gpx. In contrast, a time-dependent increase was observed in the
selenium content of all organs but not the expression levels of the nine
selenoproteins in most organs of
selenomethionine-excessive mice; however, markedly elevated
protein-bound
selenium levels were observed in the liver/kidney. These results suggest that the systemic response to
selenium deficiency and
selenomethionine excess involves the down-regulation of some
selenoproteins such as Gpx1/Gpx3 and up-regulation of
selenium-containing
proteins (not
selenoproteins), respectively.