Selenoprotein P as an <i>in vivo</i> redox regulator: disorders related to its deficiency and excess

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  • Saito Yoshiro
    Laboratory of Molecular Biology and Metabolism, Graduate School of Pharmaceutical Sciences, Tohoku University

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  • Selenoprotein P as an in vivo redox regulator: disorders related to its deficiency and excess

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Abstract

<p>Selenoprotein P (encoded by SELENOP) contains the essential trace element selenium in the form of selenocysteine, which is an analog of cysteine that contains selenium instead of sulfur. Selenoprotein P is a major selenium-containing protein in human plasma and is mainly synthesized in the liver. It functions as a selenium-transporter to maintain antioxidative selenoenzymes in several tissues, such as the brain and testis, and plays a pivotal role in selenium-metabolism and antioxidative defense. A decrease of selenoprotein P and selenoproteins causes various dysfunctions related to oxidative stress. On the other hand, recent studies indicate that excess selenoprotein P exacerbates glucose metabolism and promotes type 2 diabetes. This review focuses on the biological functions of selenoprotein P, particularly its role in selenium-metabolism and antioxidative defense. Furthermore, the effects of excess selenoprotein P on glucose metabolism, and resulting diseases are described. The development of a therapeutic agent that targets excess selenoprotein P is discussed.</p>

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