Excess dietary iodine differentially affects thyroid gene expression in diabetes, thyroiditis‐prone versus ‐resistant BioBreeding (BB) rats

Swist, Eleonora; Chen, Qixuan; Qiao, Cunye; Caldwell, Douglas R.; Gruber, Heidi; Scoggan, Kylie A.

doi:10.1002/mnfr.201100299

Cited by 5 publications

(4 citation statements)

References 45 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Excess iodine intake affects thyroid gene expression differentially in thyroiditis-prone BioBreeding (BB) rats, compared to thyroiditis-resistant BB rats, and some of these changes occurred early enough in the disease to suggest that such alterations may play an initiating role [38]. But this can only be part of the explanation, as the incidence of insulitis is also increased by iodine, an observation which implies that iodine also has an effect on immune cells.…”

Section: Non-genetic Factorsmentioning

confidence: 95%

The Immunopathogenesis of Chronic Autoimmune Thyroiditis One Century after Hashimoto

Weetman¹

2012

Eur Thyroid J

View full text Add to dashboard Cite

Hakaru Hashimoto described 4 patients with a hitherto unknown cause for goitre, struma lymphomatosa, a century ago. He was careful to distinguish this from Riedel thyroiditis but it has become clear that fibrosis and atrophy of the thyroid are indeed components of Hashimoto thyroiditis, and in rare cases IgG4-related sclerosing disease may be an outcome. Although the cause of the lymphocytic infiltration was unknown to Hashimoto, we now know through the pioneering studies of N.R. Rose and E. Witebsky [J Immunol 1956;76:417–427] that this condition is the archetype for autoimmune destruction as a disease mechanism. In the last two decades in particular, there has been huge interest in unravelling the genetic basis for this and related autoimmune disorders. The list of polymorphisms associated with autoimmune thyroid disease grows each year, and in the case of vitiligo, which is frequently found in association with thyroid autoimmunity, we know that 27 separate susceptibility loci account for less than 20% of the heritability of this condition. Environmental and existential factors may turn out to be just as complex in number and in interactions. We can thus imagine a ‘Swiss cheese’ model for the causation of autoimmune thyroid disease, in which the effects of cumulative weaknesses line up – like the holes in slices of cheese – to allow the catastrophic event of autoimmune destruction to occur.

show abstract

Section: Non-genetic Factorsmentioning

confidence: 95%

The Immunopathogenesis of Chronic Autoimmune Thyroiditis One Century after Hashimoto

Weetman¹

2012

Eur Thyroid J

View full text Add to dashboard Cite

show abstract

“…Although there is also evidence that CIDEC-induced apoptosis is dependent on activation of caspase-8, but independent on Fas-associated protein with death domain (FADD) [47]. Nevertheless, iodine doesn't have this effect in thyroiditis-resistant BBc rats [45]. These results suggest that iodine induces apoptosis in thyroiditis-prone animals.…”

Section: Iodine Excess and Thyroid Cells Apoptosismentioning

confidence: 96%

“…CIDEC was reported to induce apoptosis via the mitochondrial pathway through the cleavage of caspases-3, -7, and -9, and release of cytochrome c from mitochondria [41]. Swist et al [45] demonstrated that high levels of iodine increased mRNA and protein levels of CIDEC in thyroiditis-prone BBdp rats. The apoptotic mechanism of Fsp27, which involves caspase-9 and mitochondrial cytochrome c, requires 174-192 amino acids of its CIDEC domain.…”

Section: Iodine Excess and Thyroid Cells Apoptosismentioning

confidence: 99%

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

Markovic¹

2017

Srp Arh Celok Lek

View full text Add to dashboard Cite

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]

show abstract

“…Some in vivo studies have been performed to investigate the cellular mechanisms and functional outcomes after EI administration. Swist et al (2011) found that a chronic high‐iodine diet increased the incidence of insulitis and thyroiditis in diabetic rats. Also, the iodine‐rich compound amiodarone has been demonstrated to be toxic towards the thyroid, lungs and liver (Xia et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

Iodine excess induces hepatic, renal and pancreatic injury in female mice as determined by attenuated total reflection Fourier‐transform infrared spectrometry

Guo

Xia

et al. 2021

J of Applied Toxicology

View full text Add to dashboard Cite

Limited knowledge of the long‐term effects of excessive iodine (EI) intake on biomolecular signatures in the liver/pancreas/kidney prompted this study. Herein, following 6 months of exposure in mice to 300, 600, 1200 or 2400 μg/L iodine, the biochemical signature of alterations to the liver/pancreas/kidney was profiled using attenuated total reflection Fourier‐transform infrared (ATR‐FTIR) spectroscopy coupled with principal component analysis‐linear discriminant analysis (PCA‐LDA). Our research showed that serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), blood urea nitrogen (BUN), serum creatinine (Scr), insulin, blood glucose levels and homeostasis model assessment for insulin resistance (HOMA‐IR) index in the 1200 and 2400 μg/L iodine‐treated groups were significantly increased compared with those in the control group. Moreover, histological analysis showed that the liver/kidney/pancreas tissues of mice exposed to EI treatment displayed substantial morphological abnormalities, such as a loss of hepatic architecture, glomerular cell vacuolation and pancreatic neutrophilic infiltration. Notably, EI treatment caused distinct biochemical signature segregation between EI‐exposed versus the control liver/pancreas/kidney. The main biochemical alterations between EI‐exposed and control groups were observed for protein phosphorylation, protein secondary structures and lipids. The ratios of amide I‐to‐amide II (1674 cm−1/1570 cm−1), α‐helix‐to‐β‐sheet (1657 cm−1/1635 cm−1), glycogen‐to‐phosphate (1030 cm−1/1086 cm−1) and the peptide aggregation (1 630 cm−1/1650 cm−1) level of EI‐treated groups significantly differed from the control group. Our study demonstrated that EI induced hepatic, renal and pancreatic injury by disturbing the structure, metabolism and function of the cell membrane. This finding provides the new method and implication for human health assessment regarding long‐term EI intake.

show abstract

Excess dietary iodine differentially affects thyroid gene expression in diabetes, thyroiditis‐prone versus ‐resistant BioBreeding (BB) rats

Abstract: Differential expression of thyroid genes in BBdp versus BBc rats caused by excess dietary iodine may be implicated in autoimmune thyroiditis and insulitis pathogenesis.

Cited by 5 publications

References 45 publications

The Immunopathogenesis of Chronic Autoimmune Thyroiditis One Century after Hashimoto

The Immunopathogenesis of Chronic Autoimmune Thyroiditis One Century after Hashimoto

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

Iodine excess induces hepatic, renal and pancreatic injury in female mice as determined by attenuated total reflection Fourier‐transform infrared spectrometry

Contact Info

Product

Resources

About