中文摘要：

目的研究过量碘性甲状腺激素代谢紊乱的机制并寻求合适的硒干预剂量。方法140只Balb/c小鼠分为7组：正常组、过量碘组（饮水含碘3000μg/L）和5个补硒组（饮水含碘3000μg/L,硒分别为0.1、0.2、0.3、0.4和0.5mg/L）,共喂养16周。放射免疫法测定血清甲状腺激素水平,砷铈催化分光光度法测定尿碘和甲状腺碘水平,测定甲状腺谷胱甘肽过氧化物酶（GSH-Px）、超氧化物歧化酶（SOD）和甲状腺过氧化物酶（TPO）活性以及丙二醛（MDA）水平。结果0.1～0.5mg/L补硒组甲状腺激素水平与正常组比较差异无显著性,0.2mg/L补硒组甲状腺内碘含量较过量碘组显著下降（P〈0.05）,0.2～0.3mg/L补硒组甲状腺GSH-Px、SOD活性和MDA水平与正常组比较差异无显著性,0.1～0.3mg/L补硒组TPO活性与正常组比较差异无显著性。结论补充硒对过量碘导致的小鼠甲状腺氧化/抗氧化水平失衡、TPO活性水平下降都有有效的干预作用。

英文摘要：

Objective To study the mechanism of the disorder of thyroid hormone metabolism resulted from iodine excess in order to seek suitable selenium intervention dosage. Methods 140 Balb/c mice were randomly divided into seven groups, the normal control group, the excessive iodine group （drank the water containing potassium iodate 3000 μg/L） and five selenium intervention groups （drank the water containing 3000μg/L of potassium iodate and 0. 1,0.2,0.3, 0.4 and 0.5mg/L of selenium） . All of the miee were cultivated for 16 weeks and the thyroid hormone in plasma were assayed by radioimmunoassay. The iodine in urine and thyroid were analyzed by Cer-Arscnite colormetric method. The activities of glutathione peroxidase, superoxide dismutase and thyroid peroxidase and the level of malondialdehyde in thyroid were analyzed. Results The level of thyroid hormone of selenium intervention groups had no significant difference with that of normal control group（ P 〉 0.05）. Compared with excessive iodine group, the iodine in thyroid of 0.2mg/L selenium intervention group increased significantly（ P 〈 0. 05 ）. Compared with the normal control group, the activities of glutathione peroxidase and superoxide dismutase and the level of malondialdehyde of 0.2 - 0.3mg/L selenium intervention groups in thyroid were not significantly different. Compared with the normal control group, the activity of thyroid peroxidase of 0. 1 - 0.3mg/L selenium intervention groups were not significantly different. Conclusion The results indicated that the optimal dose of selenium could restrain the disorder of thyroid hormone metabolism induced by excessive iodine in mice.