Wang K, Sun Y N, Liu J Y, Zhang L, Ye Y, Lin L X, Yan Y Q, Chen Z P
Department of Biochemistry, Tianjin Medical University, Tianjin, China.
Biol Trace Elem Res. 2009 Jul;130(1):72-85. doi: 10.1007/s12011-009-8315-z. Epub 2009 Feb 12.
Thyroid function ultimately depends on appropriate iodine supply to the gland. There is a complex series of checks and balances that the thyroid uses to control the orderly utilization of iodine for hormone synthesis. The aim of our study is to evaluate the mechanism underlying the effect of iodine excess on thyroid hormone metabolism. Based on the successful establishment of animal models of normal-iodine (NI) and different degrees of high-iodine (HI) intake in Wistar rats, the content of monoiodotyrosine (MIT), diiodotyrosine (DIT), T(4), and T(3) in thyroid tissues, the activity of thyroidal type 1 deiodinase (D1) and its (Dio1) mRNA expression level were measured. Results showed that, in the case of iodine excess, the biosynthesis of both MIT and DIT, especially DIT, was increased. There was an obvious tendency of decreasing in MIT/DIT ratio with increased doses of iodine intake. In addition, iodine excess greatly inhibited thyroidal D1 activity and mRNA expression. T(3) was greatly lower in the HI group, while there was no significant difference of T(4) compared with NI group. The T(3)/T(4) ratio was decreased in HI groups, antiparalleled with increased doses of iodine intakes. In conclusion, the increased biosyntheses of DIT relative to MIT and the inhibition of thyroidal Dio1 mRNA expression and D1 activity may be taken as an effective way to protect an organism from impairment caused by too much T(3). These observations provide new insights into the cellular regulation mechanism of thyroid hormones under physiological and pathological conditions.
甲状腺功能最终取决于甲状腺获得适当的碘供应。甲状腺利用一系列复杂的制衡机制来控制碘用于激素合成的有序利用。我们研究的目的是评估碘过量对甲状腺激素代谢影响的潜在机制。基于成功建立Wistar大鼠正常碘（NI）和不同程度高碘（HI）摄入的动物模型，测定了甲状腺组织中单碘酪氨酸（MIT）、二碘酪氨酸（DIT）、T4和T3的含量、甲状腺1型脱碘酶（D1）的活性及其（Dio1）mRNA表达水平。结果表明，在碘过量的情况下，MIT和DIT的生物合成，尤其是DIT的生物合成增加。随着碘摄入量增加，MIT/DIT比值有明显下降趋势。此外，碘过量极大地抑制了甲状腺D1活性和mRNA表达。HI组T3水平显著降低，而与NI组相比，T4无显著差异。HI组T3/T4比值降低，与碘摄入量增加呈反相关。总之，相对于MIT，DIT生物合成增加以及甲状腺Dio1 mRNA表达和D1活性受到抑制，可能是保护机体免受过多T3损害的有效方式。这些观察结果为生理和病理条件下甲状腺激素的细胞调节机制提供了新见解。
