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碘化物诱导BB/W大鼠发生淋巴细胞性甲状腺炎:碘化物对甲状腺亚细胞结构直接毒性作用的证据。

Iodide induced lymphocytic thyroiditis in the BB/W rat: evidence of direct toxic effects of iodide on thyroid subcellular structure.

作者信息

Li M, Boyages S C

机构信息

Department of Clinical Endocrinology, Westmead Hospital, NSW, Australia.

出版信息

Autoimmunity. 1994;18(1):31-40. doi: 10.3109/08916939409014677.

DOI:10.3109/08916939409014677
PMID:7999954
Abstract

A high dietary iodine intake accelerates the development of lymphocytic thyroiditis (LT) in the BB/W rat. Our previous studies have defined the temporal sequence of the immunological events triggered by excess iodide intake in these animals. It was still not clear, however, whether these observed immunological changes were a direct effect on immune effector cells, or whether they represented a secondary response to a toxic effect of iodine on thyroid tissue. In the present study, the effect of excessive iodine intake on the subcellular structure of the BB/W rat thyroid gland, particularly, whether iodide had a toxic effect independent of its immune response has been examined. BB/W rats were exposed, prenatally through maternal drinking water, to excessive iodide at two doses (Moderate 3 x 10(-6) M iodide/l; High 3 x 10(-3) M iodide/l); a third group of BB/W rats was given tap water; till 12 weeks postnatal age. Two groups of Wistar rats received high dose iodide water or tap water for the same period of time and served as controls. Thyroid gland ultrastructure was determined by electron microscopic (EM) examination. Thyroid 125I uptake and perchlorate discharge tests were also performed in separate experiments. We found that thyroid glands of non-iodine supplemented Wistar rats were morphlogically normal under EM. There were no overt changes in the iodide treated Wistar rats. By contrast, iodide treated BB/W rats exhibited marked accumulation of secondary lysosomes and lipid droplets; markedly swollen and disrupted mitochondria and extreme dilatation of rough endoplasmic reticulum (RER).(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

高膳食碘摄入量会加速BB/W大鼠淋巴细胞性甲状腺炎(LT)的发展。我们之前的研究已经确定了这些动物因摄入过量碘化物而引发的免疫事件的时间顺序。然而,尚不清楚这些观察到的免疫变化是对免疫效应细胞的直接影响,还是代表了碘对甲状腺组织毒性作用的继发反应。在本研究中,研究了过量碘摄入对BB/W大鼠甲状腺亚细胞结构的影响,特别是碘化物是否具有独立于其免疫反应的毒性作用。通过母体饮用水,在产前将BB/W大鼠暴露于两种剂量的过量碘化物(中等剂量3×10⁻⁶ M碘化物/升;高剂量3×10⁻³ M碘化物/升);第三组BB/W大鼠给予自来水;直至出生后12周龄。两组Wistar大鼠在相同时间段内接受高剂量碘化物水或自来水,并作为对照。通过电子显微镜(EM)检查确定甲状腺超微结构。在单独的实验中还进行了甲状腺¹²⁵I摄取和高氯酸盐释放试验。我们发现,在电子显微镜下,未补充碘的Wistar大鼠的甲状腺形态正常。碘化物处理的Wistar大鼠没有明显变化。相比之下,碘化物处理的BB/W大鼠表现出次级溶酶体和脂滴明显积累;线粒体明显肿胀和破裂,粗面内质网(RER)极度扩张。(摘要截取自250字)

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Iodide induced lymphocytic thyroiditis in the BB/W rat: evidence of direct toxic effects of iodide on thyroid subcellular structure.碘化物诱导BB/W大鼠发生淋巴细胞性甲状腺炎:碘化物对甲状腺亚细胞结构直接毒性作用的证据。
Autoimmunity. 1994;18(1):31-40. doi: 10.3109/08916939409014677.
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[Studies on the iodide metabolism and the expression of thyroglobulin and thyroid peroxidase mRNA in the thyroid of BB/W rats].[BB/W大鼠甲状腺中碘代谢及甲状腺球蛋白和甲状腺过氧化物酶mRNA表达的研究]
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Clin Exp Immunol. 2006 Jun;144(3):467-74. doi: 10.1111/j.1365-2249.2006.03080.x.
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