tribromo-2-fluoro-ethane

• 分子结构分类: 有机化合物 - 有机卤素化合物 - 有机氟化物
• 英文名称: tribromo-2-fluoro-ethane
• 英文别名: Tribrom-2-fluor-aethan；HBFC-131B3b；1,1,1-tribromo-2-fluoroethane
• 化学式: C₂H₂Br₃F
• 分子量: 284.748
• InChiKey: OXNGNBHGFPJLTC-UHFFFAOYSA-N

计算性质

• 辛醇/水分配系数(LogP)：
  2.9
• 重原子数：
  6
• 可旋转键数：
  0
• 环数：
  0.0
• sp3杂化的碳原子比例：
  1.0
• 拓扑面积：
  0
• 氢给体数：
  0
• 氢受体数：
  1

反应信息

• 作为产物：
  描述：

  1,1,2,2-四溴乙烷 在 mercury(II) fluoride 作用下， 生成 tribromo-2-fluoro-ethane
  参考文献：
  名称：

  Iodine Excess and Hyperthyroidism

  摘要：

  150 mug iodine are daily required for thyroid hormone synthesis. The thyroid gland has intrinsic mechanisms that maintain normal thyroid function even in the presence of iodine excess. Large quantities of iodide are present in drugs, antiseptics, contrast media and food preservatives. Iodine induced hyperthyroidism is frequently observed in patients affected by euthyroid iodine deficient goiter when suddenly exposed to excess iodine. Possibly the presence of autonomous thyroid function permits the synthesis and release of excess quantities of thyroid hormones. The presence of thyroid autoimmunity in patients residing in iodine-insufficient areas who develop iodine-induced hyperthyroidism has not been unanimously observed. In iodine-sufficient areas, iodine-induced hyperthyroidism has been reported in euthyroid patients with previous thyroid diseases. Euthyroid patients previously treated with antithyroid drugs for Graves' disease are prone to develop iodine-induced hyperthyroidism. As well, excess iodine in hyperthyroid Graves' disease patients may reduce the effectiveness of the antithyroid drugs. Occasionally iodine-induced hyperthyroidism has been observed in euthyroid patients with a previous episode of post-partum thyroiditis, amiodarone destructive or type II thyrotoxicosis and recombinant interferon-cu induced destructive thyrotoxicosis. Amiodarone administration may induce thyrotoxicosis. Two mechanisms are responsible for this condition. One is related to excess iodine released from the drug, approximately 9 mg of iodine following a daily dose of 300 mg amiodarone. This condition is an iodine-induced thyrotoxicosis or type I amiodarone-induced thyrotoxicosis. The other mechanism is due to the amiodarone molecule that induces a destruction of the thyroid follicles with a release of preformed hormones. This condition is called amiodarone-induced destructive thyrotoxicosis or type II thyrotoxicosis. Patients developing type I thyrotoxicosis in general have preexisting nodular goiter whereas those developing type II thyrotoxicosis have a normal thyroid gland. The latter group of patients, after recovering from the destructive process, may develop permanent hypothyroidism as the consequence of fibrosis of the gland.

  DOI：

  10.1089/105072501300176453

文献信息

• Henne, Journal of the American Chemical Society, 1938, vol. 60, p. 1570
  作者：Henne

  DOI：——

  日期：——
• Swarts, Bulletin de la Societe Chimique de France, 1919, vol. <4>25, p. 168
  作者：Swarts

  DOI：——

  日期：——
• Sterols. XXIX. Urane Derivatives
  作者：Russell E. Marker、Oliver Kamm、Thomas S. Oakwood、Eugene L. Wittle、Elmer J. Lawson

  DOI：10.1021/ja01272a022

  日期：1938.5
• Henne; Renoll, Journal of the American Chemical Society, 1936, vol. 58, p. 888
  作者：Henne、Renoll

  DOI：——

  日期：——
• Swarts, vol. <3>33, p. 441
  作者：Swarts

  DOI：——

  日期：——