We see an awful lot of people "advised" (by anyone they talk to and most especially anyone who speaks beyond their understanding) to take iodine simply because the word "thyroid" has been mentioned in relation to their disorder. Doesn't seem to matter whether they have hyperthyroidism, hypothyroidism, cancer, whether it is primary, secondary or tertiary, autoimmune or diet-related. The universal assumption is that because the thyroid absorbs iodine, people should take more iodine.
There are bound to be circumstances in which some extra iodine might be helpful. But this paper suggests a potentially important reason for high iodine treatment to be avoided in autoimmune thyroiditis.
Of course, this is in mice, they don't have classic Hashimoto's, etc.
I certainly hope that follow-up research clarifies further. For now, this probably should be in the "hmm, that could be interesting" pile.
Cell Immunol. 2019 Jul 2:103948. doi: 10.1016/j.cellimm.2019.103948. [Epub ahead of print]
High iodine induces DNA damage in autoimmune thyroiditis partially by inhibiting the DNA repair protein MTH1.
Li F1, Wu Y2, Chen L2, Hu L2, Zhu F2, He Q2.
Author information
1 Thyroid Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China. Electronic address: cd20070410@zju.edu.cn.
2 Thyroid Disease Diagnosis and Treatment Center, The First Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou 310003, China.
Abstract
This study aims to investigate the level of DNA damage in high iodine (HI)-induced autoimmune thyroiditis (AIT), and to explore the role of DNA repair protein MutT homolog-1 (MTH1) in this process. The levels of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-8 were measured using qRT-PCR and ELISA. The apoptosis was evaluated using TUNEL staining. The pathological changes of thyroid tissues were evaluated using hematoxylin and eosin (HE) staining. The DNA damage was assessed by determining the expression of 8-hydroxy-2'deoxyguanosine (8-OHdG; an indicator of oxidative DNA damage) and performing the Comet assay. Our results showed that both the HI-treated NOD.H-2h4 mice (experimental AIT mice) and the HI-treated mouse thyroid follicular epithelial cells showed enhanced inflammation, apoptosis, and DNA damage level, accompanied by decreased MTH1 expression. Importantly, overexpression of MTH1 effectively abrogated the HI-induced enhancement of inflammation, apoptosis, and DNA damage in mouse thyroid follicular epithelial cells. In conclusion, HI treatment induces DNA damage in AIT, at least in part, by inhibiting the DNA repair protein MTH1.
Copyright © 2019 Elsevier Inc. All rights reserved.
KEYWORDS:
Apoptosis; DNA damage; Inflammation; Iodine; MTH1
PMID: 31311621
DOI: 10.1016/j.cellimm.2019.103948