Allen E M
University of Maryland Medical School, Baltimore.
J Endocrinol Invest. 1992 Jul-Aug;15(7):519-23. doi: 10.1007/BF03348796.
There has been recent data suggesting that iodine potentiates lymphocytic thyroiditis (LT) by inciting oxidative stress. However, the mechanism by which iodine induces LT in genetically predisposed animals is unknown. This study was undertaken to examine LT-prone BB/Wor (LT-P) rat thyroids for signs of acute iodine toxicity and oxidative damage before the onset of spontaneous LT. Lipid peroxidation was assessed by the measurement of malonyldialdehyde (MDA) in thyroid homogenates after randomization to a treatment group receiving 0.05% iodide in the drinking water or tap water for 24 hours. Basal MDA levels were higher in LT-prone rat thyroids than Wistar rat thyroids, but iodine treatment did not influence intrathyroidal MDA levels. Electronmicroscopy demonstrated that prolonged treatment with excess iodine, increased the number of apical lysosomes. But there were no ultrastructural changes unique to LT-P rat thyroids. These data suggest that although LT-P rat thyroids may experience subclinical oxidative damage before the onset of histologically demonstrable LT, this activity is not affected by iodine.
最近有数据表明，碘通过引发氧化应激增强淋巴细胞性甲状腺炎（LT）。然而，碘在具有遗传易感性的动物中诱发LT的机制尚不清楚。本研究旨在检查易患LT的BB/Wor（LT-P）大鼠甲状腺，以寻找自发性LT发作前急性碘中毒和氧化损伤的迹象。将大鼠随机分为饮用含0.05%碘化物的饮用水或自来水的治疗组24小时后，通过测量甲状腺匀浆中的丙二醛（MDA）来评估脂质过氧化。易患LT的大鼠甲状腺中的基础MDA水平高于Wistar大鼠甲状腺，但碘治疗并未影响甲状腺内MDA水平。电子显微镜显示，长期用过量碘治疗会增加顶端溶酶体的数量。但LT-P大鼠甲状腺没有独特的超微结构变化。这些数据表明，尽管LT-P大鼠甲状腺在组织学上可证实的LT发作前可能经历亚临床氧化损伤，但这种活性不受碘的影响。
