...
  • 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Srpski Arhiv za Celokupno Lekarstvo >Role of iodine in pathogenesis of thyroid disease - is induction of apoptosis consequence of iodine cytotoxicity?
【24h】

Role of iodine in pathogenesis of thyroid disease - is induction of apoptosis consequence of iodine cytotoxicity?

机译：碘在甲状腺疾病发病机理中的作用-诱导凋亡是碘细胞毒性的结果吗？

获取原文
   

获取外文期刊封面封底 >>

       
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Iodine is one of the best-characterized environmental factors associated with autoimmune thyroid disease (ATD). Epidemiological studies have shown that ATD incidence has increased following the introduction of salt iodination in the 1920s; in addition, ATD patients can improve upon iodine restriction. In animal models such as BioBreeding/Worcester and Buffalo rats, obese chicken strain, and non-obese diabetic H-2h4 mice, excess iodine is associated with autoimmunity. Analyses of Hashimoto thyroiditis (HT) have shown enlarged number of apoptotic follicular cells, and the destruction is an effect of death receptormediated apoptosis. Excess of iodine induces rapid apoptosis of goitrogen Wistar pretreated rats, possibly connected with inhibition of polyamine synthesis, inhibitors of DNA fragmentation. Percentage of apoptotic cells was statistically higher in patients with HT than in those with euthyroid goiter, with significant increase of caspase 32. Genes for Bcl-2 and Bax proteins are under the transcriptional control of p53. In TAD-2 cell cultures, apoptosis is p53-independed, suggesting that DNA damage is not primarily evoked by potassium iodide (KI). High concentrations of NaI increase the proportion of apoptotic cells in FTRL5 thyroid cell line. Iodide cytotoxicity is inhibited by a TPO inhibitor and is relieved with an anti-oxidant agent. Chronic iodine excess induces apoptosis and necrosis of thyroid follicular and endothelial cells, leading to thyroglobulin accumulation in connective tissue. Iodide excess requires peroxidase enzymatic activity to induce apoptosis. Ionic iodide is not directly toxic, whereas its molecular form I2 mediates the apoptotic effect of KI. [Project of the Serbian Ministry of Education, Science and Technological Development, Grant no. OI-175059]
机译：碘是与自身免疫性甲状腺疾病（ATD）相关的最典型的环境因素之一。流行病学研究表明，在1920年代引入盐碘化之后，ATD的发病率增加了。此外，ATD患者可以通过限制碘来改善。在诸如BioBreeding / Worcester和Buffalo大鼠，肥胖鸡毒株和非肥胖糖尿病H-2h4小鼠的动物模型中，过量的碘与自身免疫有关。桥本甲状腺炎（HT）的分析显示凋亡的卵泡细胞数量增加，破坏是死亡受体介导的细胞凋亡的作用。过量的碘会诱导Wistar预处理大鼠的Goitrogen Wistar快速凋亡，可能与多胺合成的抑制，DNA片段的抑制剂有关。 HT患者的凋亡细胞百分比在统计学上高于正常甲状腺肿的患者，其中caspase 32显着增加。Bcl-2和Bax蛋白的基因处于p53的转录控制之下。在TAD-2细胞培养物中，凋亡不受p53的影响，这表明DNA损伤主要不是由碘化钾（KI）引起的。高浓度的NaI可增加FTRL5甲状腺细胞系中凋亡细胞的比例。碘化物的细胞毒性被TPO抑制剂抑制，并被抗氧化剂缓解。长期过量的碘会诱导甲状腺滤泡和内皮细胞凋亡和坏死，从而导致甲状腺球蛋白在结缔组织中蓄积。碘化物过量需要过氧化物酶的酶促活性才能诱导细胞凋亡。离子碘化物没有直接毒性，而其分子形式I2则介导KI的凋亡作用。 [塞尔维亚教育，科学和技术发展部的项目，赠款OI-175059]

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号