SULFATION PATHWAY OF THYROID-HORMONE METABOLISM IN SELENIUM-DEFICIENTMALE-RATS

Male Sprague-Dawley rats were fed a selenium-deficient yeast-based lab oratory diet or a control diet for 6 wk. The tissue type I 5'-monodeio dinase (5'-MDI) activity and the immunoassayable 5'-MDI were significa ntly (P < 0.05) reduced in the liver and the kidney but not in the thy roid of selenium-deficient rats. The mean serum concentrations of thyr oxine sulfate (T4S), 3,3',5'-triiodothyronine sulfate (T3S), and rever se T-3 sulfate (rT(3)S) (ng/dl) were significantly increased in seleni um-deficient rats (15.7, 59.4, and 22.8, respectively, n = 12) compare d with control rats (< 1.0, 18.5, and 9.1, respectively, n = 12, P < 0 .01). Kinetic studies were carried out during a constant infusion of u nlabeled sulfated iodothyronines (T4S, T3S, or rT(3)S, n = 5-6/group) at a rate of 1 mu g/h by Alzet minipump for 48 h. The data showed that elevated serum concentrations of T4S or T3S in the selenium-deficient rat are due both to reduced metabolic clearance rate (MCR, mean, 1 . kg(-1). day(-1), 7.4 for T4S and 4.5 for T3S in selenium deficiency vs . 12 and 9.2, respectively in controls, P < 0.05) and increased produc tion rate (mean, mu g . kg(-1). day(-1), 1.2 for T4S, and 2.7 for T3S in selenium deficiency vs. 0.12 and 1.7, respectively, in the controls , P < 0.05). However, the increased serum rT(3)S concentration in sele nium-deficient rats is due mainly to reduced MCR (mean, 1 . kg(-1). da y(-1), 34 vs. 67 in controls, P < 0.05) and its daily production rate remained unchanged in selenium deficiency (mean, mu g . kg(-1). day(-1 ), 7.6 vs. 6.1 in the control group, P > 0.05). In conclusion, our dat a suggest that reduced activity of MDI in tissues of selenium-deficien t rats is associated with a significant ''shunting'' of T-3 and T-4 in to sulfation pathways. These data are also consistent with the hypothe sis that there may be a hidden pool for sulfated iodothyronines.