Concentrations of selenium are higher in the thyroid than in any other tissues other than liver and kidney, indicating that it has important functions within the gland.
In 1987, it became apparent that selenium could exert marked effects on thyroid hormone metabolism in tissues other than the thyroid. It, therefore, differs in its action from iodine whose effects on thyroid status are largely confined to the thyroid.
Selenium is an essential component of many selenoproteins that regulate thyroid hormone synthesis, preserve thyroid integrity in conditions of marked oxidative stress, and control hormone metabolism in nonthyroidal tissues where the prohormone Thyroxine (T4), is converted to biologically active T3 or its inactive isomer rT3.
The discovery of increased T4 and decreased T3 concentrations in plasma from selenium deficient rats and cattle provided the first demonstration that selenium could affect thyroid hormone metabolism. These changes were associated with considerable decreases in hepatic and renal type I iodothyronine de-iodinase (IDI) activity which converts T4 to T3.