Field J B, Larsen P R, Yamashita K, Mashiter K, Dekker A
J Clin Invest. 1973 Oct;52(10):2404-10. doi: 10.1172/JCI107430.
Benign and malignant nodules in human thyroid glands, which did not concentrate iodide in vivo, were also unable to accumulate iodide in vitro. The mean thyroid-to-medium ratio (T/M) in seven benign nodules was 0.8+/-0.2 compared with 7+/-2 in adjacent normal thyroid tissue. In four malignant thyroid nodules, the mean T/M was 0.5+/-0.1 compared with 11+/-4 in adjacent normal thyroid. Despite the inability of such nodules to concentrate iodide, iodide organification was present but was only one-half to one-third as active as in surrounding normal thyroid. Thyroid-stimulating hormone (TSH) increased iodide organification equally in both benign nodules and normal thyroid although it had no effect in three of the four malignant lesions. The reduction in organification is probably related to the absence of iodide transport, since incubation of normal thyroid slices with perchlorate caused similar diminution in iodide incorporation but no change in the response to TSH. Monoiodotyrosine (MIT) and di-iodotyrosine (DIT) accounted for most of the organic iodide in both the nodules and normal tissue. The MIT/DIT ratio was similar in normal and nodule tissue. The normal tissue contained much more inorganic iodide than the nodules, consistent with the absence of the iodide trap in the latter tissue. The thyroxine content of normal thyroid was 149+/-17 mug/g wet wt and 18+/-4 mug/g wet wt in the nodules. The transport defect in the nodules was not associated with any reduction in total, Na(+)-K(+)- or Mg(++)-activated ATPase activities or the concentration of ATP. Basal adenylate cyclase was higher in nodules than normal tissue. Although there was no difference between benign and malignant nodules, the response of adenylate cyclase to TSH was greater in the benign lesions. These studies demonstrate that nonfunctioning thyroid nodules, both benign and malignant, have a specific defect in iodide transport that accounts for their failure to accumulate radioactive iodide in vivo. In benign nodules, iodide organification was increased by TSH while no such effect was found in three of four malignant lesions, suggesting additional biochemical defects in thyroid carcinomas.
人体甲状腺中的良性和恶性结节在体内不能摄取碘化物，在体外也无法积累碘化物。7个良性结节的平均甲状腺与培养基比值（T/M）为0.8±0.2，而相邻正常甲状腺组织的该比值为7±2。在4个恶性甲状腺结节中，平均T/M为0.5±0.1，而相邻正常甲状腺组织的该比值为11±4。尽管这些结节无法摄取碘化物，但碘的有机化过程存在，但其活性仅为周围正常甲状腺的二分之一到三分之一。促甲状腺激素（TSH）在良性结节和正常甲状腺中均能同等程度地增加碘的有机化，尽管在4个恶性病变中有3个对TSH无反应。有机化的降低可能与碘转运的缺失有关，因为用高氯酸盐孵育正常甲状腺切片会导致碘摄取的类似减少，但对TSH的反应无变化。一碘酪氨酸（MIT）和二碘酪氨酸（DIT）占结节和正常组织中大部分有机碘。正常组织和结节组织中的MIT/DIT比值相似。正常组织中的无机碘比结节中的多得多，这与后者组织中碘捕获机制的缺失一致。正常甲状腺的甲状腺素含量为149±17μg/g湿重，结节中的含量为18±4μg/g湿重。结节中的转运缺陷与总ATP酶、Na(+)-K(+)-或Mg(++)-激活的ATP酶活性或ATP浓度的降低无关。结节中的基础腺苷酸环化酶高于正常组织。尽管良性和恶性结节之间没有差异，但腺苷酸环化酶对TSH的反应在良性病变中更大。这些研究表明，无功能的甲状腺结节，无论是良性还是恶性，在碘转运方面都有特定缺陷，这解释了它们在体内无法积累放射性碘化物的原因。在良性结节中，TSH可增加碘的有机化，而在4个恶性病变中有3个未发现这种作用，这表明甲状腺癌存在其他生化缺陷。
