[Long-term effects of high iodine intake: inhibition of thyroid iodine uptake and organification in Wistar rats].
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).


CONCLUSIONS
Moderate iodine excess continuously suppresses the thyroid iodine uptake and organification, which presents a mechanism for iodine-induced thyroid failure.
Man
Na
N
Department of Endocrinology, Institute of Endocrinology, First Hospital of China Medical University, Shenyang 110001, China.
Guan
Hai-xia
HX
Shan
Zhong-yan
ZY
Li
Yu-shu
YS
Fan
Chen-ling
CL
Guo
Xiu-juan
XJ
Chen
Wei
W
Tong
Ya-jie
YJ
Chong
Wei
W
Mao
Jin-yuan
JY
Teng
Wei-ping
WP
D000818:Animals; D062787:Drug Overdose; D005260:Female; D007453:Iodide Peroxidase / Q000378:metabolism*; D007455:Iodine / Q000008:administration & dosage* / Q000493:pharmacokinetics / Q000633:toxicity; D017136:Ion Transport / Q000187:drug effects; D008297:Male; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012964:Sodium / Q000378:metabolism; D027981:Symporters / Q000378:metabolism*; D013961:Thyroid Gland / Q000187:drug effects* / Q000378:metabolism; D013997:Time Factors; D000099209:Sodium-Iodide Symporters
D007453:Iodide Peroxidase; D007455:Iodine; D012964:Sodium; D027981:Symporters; D000099209:Sodium-Iodide Symporters