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
Summary
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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