Remodeling of Selenium Metabolism through Adduct Formation of Selenoprotein P with Epigallocatechin Gallate

Abstract

Selenoprotein P (SeP) is the major selenium transport protein in the blood and plays a central role in selenium metabolism by being involved in selenoprotein synthesis via selenium supply in various tissues. On the other hand, excess selenoprotein P, which is increased in patients with diabetes and other diseases, can be a malignant protein that causes metabolic disorders in various tissues through disruption of redox homeostasis. Therefore, developing methods to control selenium metabolism in physiological and pathological conditions are significant. In this study, we focused on epigallocatechin gallate (EGCg), an electrophilic plant component, and newly found that modification of the cysteine residue in SeP by this molecule inhibits its cellular uptake in SH-SY5Ycells. SeP-EGCg adduct failed to induce the expression of glutathione peroxidase, which is synthesized in cells by selenium supply through SeP. These results suggest that EGCg can be a candidate molecule to induce negative remodeling of selenium metabolism by inhibiting SeP incorporation into the cells.

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