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Organic iodine inhibits deoxyribonucleic acid synthesis and growth in FRTL-5 thyroid cells
G P Becks1, M C Eggo, G N Burrow
1Banting and Best Department of Medical Research, University of Toronto, Ontario, Canada.
Abstract:
FRTL-5 thyroid epithelial cells in culture were used to study the possible inhibitory effects of iodine on thyroid growth. NaI exerted a dose-dependent, thyroid epithelial cell-specific inhibitory effect on [methyl-3H]thymidine incorporation into DNA, reduced the DNA content in the cell layer, and limited the increase in cell number mediated by TSH. The inhibitory effects of sodium iodide applied to growth stimulated by TSH-, cAMP-, and non-cAMP-dependent mechanisms and were prevented by 1-methylimidazole-2-thiol (methimazole) and 2-ethylthioisonicotinamide (ethionamide). The latter findings indicate that the inhibitory effects of NaI are mediated by some iodine-containing organic compound. The inhibitory effects of organic iodine on growth subsided 24-48 h after removal of excess NaI from the culture medium. In contrast, NaI had no effect on normal rat kidney fibroblast or thyroid fibroblast [methyl-3H]thymidine incorporation stimulated by epidermal growth factor or serum. These data demonstrate a specific inhibitory effect of organic iodine on thyroid epithelial cell growth.
Insights
Excess iodine specifically inhibits thyroid epithelial cell growth by affecting DNA synthesis and cell proliferation. These effects are mediated by organic iodine compounds and are reversible upon removal of excess sodium iodide.
Area of Science:
- Endocrinology
- Cell Biology
- Molecular Biology
Background:
- Thyroid growth is regulated by various factors, including thyroid-stimulating hormone (TSH).
- The role of iodine concentration in modulating thyroid cell proliferation requires further elucidation.
- Understanding cellular mechanisms of growth inhibition is crucial for managing thyroid disorders.
Purpose of the Study:
- To investigate the inhibitory effects of iodine on thyroid epithelial cell growth in vitro.
- To determine if these effects are specific to thyroid cells and mediated by organic iodine compounds.
- To explore the reversibility of iodine-induced growth inhibition.
Main Methods:
- Utilized FRTL-5 rat thyroid epithelial cells in cell culture.
- Assessed DNA synthesis via [methyl-3H]thymidine incorporation.
- Measured DNA content and cell number.
- Investigated effects of sodium iodide (NaI) on TSH-, cAMP-, and non-cAMP-dependent growth.
- Tested the role of methimazole and ethionamide in preventing NaI effects.
- Evaluated NaI effects on non-thyroid cells (rat kidney fibroblasts, thyroid fibroblasts).
Main Results:
- Sodium iodide (NaI) demonstrated a dose-dependent, thyroid epithelial cell-specific inhibition of DNA synthesis.
- NaI reduced cellular DNA content and limited TSH-stimulated cell proliferation.
- Inhibitory effects were observed across TSH-, cAMP-, and non-cAMP-dependent growth pathways.
- Inhibition was prevented by methimazole and ethionamide, suggesting mediation by organic iodine compounds.
- Effects subsided 24-48 hours after NaI removal, indicating reversibility.
- NaI had no significant effect on the growth of rat kidney or thyroid fibroblasts.
Conclusions:
- Organic iodine exerts a specific inhibitory effect on thyroid epithelial cell growth.
- The mechanism involves interference with DNA synthesis and cell proliferation pathways.
- These findings highlight a potential mechanism for iodine's influence on thyroid homeostasis.