Abstract

Selenium is a chemical element participating in the synthesis of selenocysteine residues that play a pivotal role in the enzymatic activity efficiency of selenoproteines. The methionine sulfoxide reductase (Msr) system that reduces methionine sulfoxide (MetO) to methionine comprises the selenoprotein MsrB (MsrB1) and the non-selenoprotein MsrA, which reduce the R- and the S- forms of MetO, respectively. The effects of a selenium deficient (SD) diet, which was administrated to wild type (WT) and MsrA knockout mice (MsrA-/-), on the expression and function of Msr-related proteins are examined and discussed. Additionally, new data about the levels of selenium in brain, liver, and kidneys of WT and MsrA-/- mice are presented and discussed.

Highlights

  • Selenium is a chemical element participating in the synthesis of selenocysteine residues that play a pivotal role in the enzymatic activity efficiency of selenoproteines

  • Limited information is available regarding the importance of selenium to the methionine sulfoxide reductase (Msr) system components that require selenium to their activity, namely Trr and MsrB1

  • Lack of the MsrA gene exacerbates the accumulations of proteinmethionine sulfoxides and protein-carbonyls when prolonged administration of a selenium deficient (SD) diet occurs

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Summary

Introduction

Selenium is a chemical element participating in the synthesis of selenocysteine residues that play a pivotal role in the enzymatic activity efficiency of selenoproteines. A major biological role of the Msr system is suggested by the fact that the MsrA knockout mouse (MsrA-/-) is more sensitive to oxidative stress, accumulates higher levels of carbonylated protein and has a shorter life span than wild type mice [5]. Weaned pups of first mouse generation (F1) of wild type (WT) and MsrA-/- mice, fed with a selenium deficient (SD) diet, exhibited higher protein-MetO and carbonyl levels detected as early as six months of age [9].

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