Paper Information

Title: 

MISSING LINK BETWEEN EXCESS IODINE AND AUTOIMMUNE THYROID DISEASES

Type: POSTER
Author(s): MOSHTAGHI KASHANIAN GH.R.*,MIRSHEKARI T.,SOUKHTANLOU M.,HASANIFARD L.,DABIRI SH.,SHAPIRO D.
 
 *PHYSIOLOGY RESEARCH CENTER AND DEPARTMENT OF BIOCHEMISTRY, MEDICAL SCHOOL, KERMAN UNIVERSITY OF MEDICAL SCIENCES, KERMAN, IRAN
 
Name of Seminar: IRANIAN CONGRESS OF PHYSIOLOGY AND PHARMACOLOGY
Type of Seminar:  CONGRESS
Sponsor:  PHYSIOLOGY AND PHARMACOLOGY SOCIETY, MASHHAD UNIVERSITY OF MEDICAL SCIENCE
Date:  2009Volume 19
 
 
Abstract: 

The mechanisms by which excess iodine is associated with thyroid autoimmunities are still unknown, though several hypotheses have been put forward. To determine possible mechanisms, a series of in vivo, ex vivo and in vitro experiments were carried out. While consumption of excess iodine for 45 day by rats did not noticeably change circulating levels of total and free T4 or T3, it caused pathological changes of thyroid gland that were similar to alterations usually observed in human autoimmune thyroid diseases. Additionally, in vitro experiments showed that albumin has a binding affinity for iodine at 37oC with an instantaneous saturable mechanism. The results of cell culture experiments also showed a significant (p<0.001) decrease in Km of iodine uptake and increase (p<0.001) in the amount of iodine uptake of FRTL-5 cells, when albumin was used as a carrier system for the iodine. Finally, addition of radioactive iodine to the sera of healthy human showed 10.42±2.76% of total I125 attached to different proteins, while consumption of I131 by patients with thyroid autoimmunities showed 18.88±9.19% binding to proteins with different pattern from the one detected for healthy subjects. In conclusion, the present results may be the first report showing carrier systems for iodine (pre-albumin, albumin, globulin, and lipoproteins), and that iodination of these proteins increases uptake of iodine by thyrocytes. In addition, increased iodination of these proteins or changes in their concentration may activate circulating immune cells to attack thyroid gland as the largest iodine pool, thereby initiating autoimmune thyroid diseases.

 
Keyword(s): EXCESS IODINE, AUTOIMMUNE THYROID DISEASES, FRTL-5 CELL LINE, IODINE UPTAKE, IODINE CARRIER PROTEIN
 
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