The Importance Of Sulfation In Thyroid Hormone Metabolism

The role of sulfation in thyroid hormone metabolism is intriguing. Sulfated iodo-thyronines do not bind to the thyroid hormone receptors nor are they substrates for D2 and D3, but their deiodination by D1 is strongly augmented. Figure 7.2 shows the effects of sulfation on the deiodination of different iodothyronines by D1 (Visser, 1996b). IRD (inactivation) of T4 sulfate (T4S) and T3 sulfate (T3S) is markedly facilitated, whereas outer ring deiodination (activation) of T4S is blocked (Visser, 1994, 1996b; Visser et al., 1988). However, outer ring deiodination of other substrates is not inhibited by sulfation; in fact, deiodination of rT3 sulfate (rT3S) is not affected and that of 3,3'-T2 sulfate (T2S) is even greatly stimulated (Visser, 1994; Visser et al., 1988). Under normal conditions, therefore, the main function of sulfation is to induce the irreversible degradation of thyroid hormone.

Normally, as a result of the very rapid IRD of T4S and T3S and outer ring deiodination of rT3S and T2S, the plasma concentrations of these sulfated iodothyronines are low (Chopra et al., 1992, 1993; Eelkman Rooda et al., 1989; Wu et al., 1993). However, in conditions in which D1 activity is low, e.g., in selenium deficiency and after administration of iopanoic acid or propylthiouracil, iodothyronine sulfate levels are increased (Chopra et al., 1992; Rooda et al., 1989; Wu et al., 1995). Elevated serum T3S/T3 ratios have also been reported in patients with nonthyroidal illness and in hypothyroid patients, in whom D1 activity is known to be decreased (Chopra et al., 1992).

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