Reversibility of Proliferative Thyroid Lesions Induced by Iodine Deficiency in a Laboratory Zebrafish Colony
- Murray, K.N., Wolf, J.C., Spagnoli, S.T., Lains, D., Budrow, N., Kent, M.L.
- Zebrafish 15(6): 558-565 (Journal)
- Registered Authors
- Kent, Michael, Lains, David, Murray, Katy, Wolf, Jeffrey C.
- hyperplasia, iodine, neoplasia, thyroid, zebrafish
- MeSH Terms
- Adenoma/prevention & control
- Hyperplasia/prevention & control
- Iodine/administration & dosage*
- Thyroid Gland/drug effects
- Thyroid Gland/pathology
- Thyroid Neoplasms/prevention & control
- Thyroid Neoplasms/veterinary*
- 30136899 Full text @ Zebrafish
Murray, K.N., Wolf, J.C., Spagnoli, S.T., Lains, D., Budrow, N., Kent, M.L. (2018) Reversibility of Proliferative Thyroid Lesions Induced by Iodine Deficiency in a Laboratory Zebrafish Colony. Zebrafish. 15(6):558-565.
A laboratory zebrafish colony developed red masses, predominantly under the jaw, in a significant portion of the population. The masses were diagnosed histopathologically as thyroid follicular hyperplasia, adenoma, or carcinoma in accordance with published morphologic criteria. After switching to a higher iodine brand of salt used to maintain a low level of salinity within the water system and a small diet change, the thyroid lesions regressed dramatically. Within 5 months the masses were no longer grossly visible. At the population level, external evaluations and histopathological assessments of whole-body sections document a regression in the prevalence of thyroid neoplasia and hyperplasia to normal thyroid conformation by 11 months after salt change. These findings suggest that a wide range of proliferative thyroid lesions, including neoplasms, in zebrafish may be hormone-dependent, even following lesion development. In addition, these results suggest that zebrafish have an adaptive ability to absorb iodine from water and food, which should be considered in discussions to standardize diets and when describing environmental parameters in publications.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes