Upregulation of proteolytic pathways and altered protein biosynthesis underlie retinal pathology in a mouse model of Alzheimers disease
Andriole GL, Bostwick DG, Brawley OW, Gomella LG, Marberger M, Montorsi F, Pettaway CA, Tammela TL, Teloken C, Tindall DJ, Somerville MC, Wilson TH, Fowler IL, Rittmaster RS
Key Points Selenium is needed for biosynthesis of selenoproteins, including thyroid hormone metabolizing enzymes (iodothyronine deiodinases), hydrogen peroxide degrading enzymes (glutathione peroxidases) and enzymes affecting endoplasmic reticulum function Endogenous pathways ensure that the thyroid gland and thyroid selenoproteins are exceptionally well supplied with selenium and largely resistant to selenium deficiency Selenium status declines and selenoprotein biosynthesis is impaired in inflammatory diseases, which potentially necessitates supplementation with this trace element Selenium supplementation trials in patients with Hashimoto thyroiditis successfully reduced autoantibody concentrations and improved selenium status and quality of life However, not all selenium supplementation trials have been successful and the underlying mechanisms of the selenium effects and the major parameters controlling trial outcome are unknown Selenium supplementation is hypothesized to improve functioning of both thyrocytes and immune cells, thereby rectifying the derailed interaction of lymphocytes with thyroid autoantigens in selenium-deficient patients This is a preview of subscription content, access via your institution Access options Subscribe to this journal Receive 12 print issues and online access 186,36 per year only 15,53 per issue Buy this article Purchase on SpringerLink Instant access to the full article PDF
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