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Objective: To investigate the effects of chronic iodine excess on thyroid function, thyroid peroxidase (TPO) activity, and expression of sodium-iodide symporter (NIS)., Methods: 500 Wistar rats were randomly exposed to 4 doses of iodine 4 microg/d (G0, control), 6 microg/d (G1), 12 microg/d (G2), and 24 microg/d (G3) for 1, 2, 4 and 8 months. The urine iodine and tissue iodine was determined by arsenic/cerium catalyzing spectrophotograph. Radioimmunoassays were used to detect thyrotropin (TSH), free thyroxin (FT4), free triiodothyronine (FT3), total thyroxin (TT4), and total triiodothyronine (TT3). Guaiacol reaction method and potassium iodide oxygenation method were used to determine the activity of TPO. Suspension of single cells from thyroid tissue was made and the positive rate of NIS was determined by flow cytometry. The expression of NIS protein was assayed by immunohistochemistry., Results: The urine iodine levels of G1, G2, and G3 were 1.5, 3, and 6 times of G0 respectively. FT4, FT3, and total iodine were found progressively accumulated in thyroid tissue with the elevation of iodine intake. The TPO activities of G2 and G3 at the 8th month were 0.17 +/- 0.04 and 0.15 +/- 0.03 respectively, both significantly lower than that of G0 (0.4 +/- 0.23, P < 0.05). The levels of iodine intake at different time points of G1-3 were significantly reduced in a iodine-dose dependent manner (r = -0.63 to -0.78, P < 0.01). The 131I intake at month 8 of G1, G2, and G3 were 56%, 49%, and 39% that of G0 respectively. At month 8 the NIS positive rates of G2 and G3 were significantly lower than that of G0 (both P < 0.05). The NIS protein positive rate was positively correlated with NIS protein expression intensity (r = 0.7-0.72, P < 0.01). The iodine content of thyroid tissue was negatively correlated with TPO activity, iodine intake rate, NIS protein positive rate and expression intensity (r = -0.62 to -0.88, P < 0.05)., Conclusion: Moderate iodine excess continuously suppresses the thyroid iodine uptake and organification, which presents a mechanism for iodine-induced thyroid failure.

Objective: To observe the effect of testosterone or estradiol on iodine absorption in rat intestine., Method: 50 male adult Wistar rats were divided into 5 groups randomly. 50 females were divided into another 5 groups. Among them, 4 groups were bilaterally testectomized or ovariectomized, 1 group was sham-operated. 7 days after operation, the castrated rats received testosterone (male rats) or estradiol (female rats) at different dosages by intramuscular injection for three days. Then the kinetics of iodine absorption in jejunum and ileum were observed by perfusion in situ. When finished, serum were obtained for detecting TSH, T4 and testosterone or estradiol., Results: In castrated male rats, the value of K12 reduced, K21 increased, K02 reduced, and SP1/2 (the half time of the slow phase) prolonged, implying that the ability of iodine absorption reduced. It reflected that testosterone could promote iodine absorption in intestine in physiological condition. In castrated female rats, the situation was different from that in male rats, the value of K12 increased, K21 reduced, K02 increased, and SP1/2 shortened in jejunum, implying that the ability of iodine absorption increased. It reflected that estradiol could inhibit iodine absorption in intestine in physiological condition. The levels of serum TSH and T4 were not changed significantly in this experiment., Conclusion: In physiological condition, testosterone can promote iodine absorption, while estradiol has the inhibiting effect. The results indicate that gonadol hormone maybe one factor which can influence iodine absorption in intestine. It may explain the phenomenon that the incidence of goiter is different between males and females partly.