Contempre B, Dumont J E, Denef J F, Many M C
IRIBHN, Free University of Brussels, Belgium.
Eur J Endocrinol. 1995 Jul;133(1):99-109. doi: 10.1530/eje.0.1330099.
It has been suggested that selenium deficiency is a co-factor to iodine deficiency in the pathogenesis of myxoedematous cretinism. The mechanism proposed is that the generation of hydrogen peroxide is greatly increased in iodine-deficient thyroid glands, and that selenium is involved in the control of hydrogen peroxide and its derived free radicals. This study was carried out to investigate the effect of the possibly impaired cellular defence mechanism associated with selenium deficiency on thyroid necrosis and tissue repair. For this purpose, we studied thyroid tissue from selenium- (SE-) and/or iodine-deficient (I-) rats before and after an acute toxic iodine overload. In I- thyroids, necrotic cells were numerous. Acute iodine administration increased this effect. Necrosis was associated with transient infiltration of inflammatory cells. In I-SE+ thyroids the tissue resumed its normal appearance. In I-SE- thyroid glands, the iodide toxicity was stronger, with greater necrosis and inflammatory reaction. The inflammation resolved but was replaced by fibrotic tissue. Fifteen days after the toxic overload, the connective tissue volume was twice the control value. Before iodide overload, the proportion of dividing cells was equal in I-SE+ and I-SE- thyroids. Three days after the iodide overload, this proportion was increased in I-SE+ thyroids but reduced in the I-SE- thyroids. Overall, the I-SE- thyroids had four times fewer dividing cells than the I-SE+ thyroids. In summary, selenium deficiency coupled to iodine deficiency increased necrosis, induced fibrosis and impeded compensatory epithelial cell proliferation. These results are compatible with histological and functional description of thyroid tissue from myxoedematous cretins.
有人提出，在黏液性水肿型克汀病的发病机制中，硒缺乏是碘缺乏的一个协同因素。提出的机制是，缺碘甲状腺中过氧化氢的生成大幅增加，且硒参与过氧化氢及其衍生自由基的控制。本研究旨在探讨与硒缺乏相关的可能受损的细胞防御机制对甲状腺坏死和组织修复的影响。为此，我们研究了急性毒性碘负荷前后缺硒（SE-）和/或缺碘（I-）大鼠的甲状腺组织。在I-甲状腺中，坏死细胞众多。急性给予碘会增强这种效应。坏死与炎症细胞的短暂浸润有关。在I-SE+甲状腺中，组织恢复正常外观。在I-SE-甲状腺中，碘化物毒性更强，坏死和炎症反应更严重。炎症消退但被纤维化组织取代。毒性负荷15天后，结缔组织体积是对照值的两倍。在碘化物负荷前，I-SE+和I-SE-甲状腺中分裂细胞的比例相等。碘化物负荷3天后，I-SE+甲状腺中该比例增加，而I-SE-甲状腺中该比例降低。总体而言，I-SE-甲状腺中的分裂细胞比I-SE+甲状腺中的少四倍。总之，硒缺乏与碘缺乏相结合会增加坏死、诱导纤维化并阻碍代偿性上皮细胞增殖。这些结果与黏液性水肿型克汀病患者甲状腺组织的组织学和功能描述相符。
