PUBLICATION

Effects of exposure to microcystin-LR at environmentally relevant concentrations on the metabolism of thyroid hormones in adult zebrafish (Danio rerio)

Authors
Liu, Z., Li, D., Hu, Q., Tang, R., Li, L.
ID
ZDB-PUB-161110-9
Date
2016
Source
Toxicon : official journal of the International Society on Toxinology   124: 15-25 (Journal)
Registered Authors
Li, Li
Keywords
Histology, Iodothyronine deiodinases, Microcystin-LR, Thyroid hormones, Zebrafish
MeSH Terms
  • Animals
  • Female
  • Homeostasis
  • Iodide Peroxidase/metabolism
  • Male
  • Microcystins/toxicity*
  • Thyroid Gland/drug effects
  • Thyroid Gland/metabolism
  • Thyroid Gland/pathology
  • Thyroid Hormones/metabolism*
  • Transcription, Genetic
  • Zebrafish
PubMed
27826021 Full text @ Toxicon.
Abstract
Microcystin-LR (MC-LR) has the potential to disturb thyroid hormone homeostasis. However, the effects of MC-LR at environmentally relevant concentrations on the thyroid system in adult fish are still unclear. In this study, adult zebrafish were exposed to 0, 1, 5, and 25 μg/L MC-LR for 7, 14, 21, and 28 days. Whole-body thyroid hormones (THs) levels and thyroid follicle histology were used to assess thyroid function. The transcription of corticotropin-releasing hormone (crh), thyroid-stimulating hormone (tsh), transthyretin (ttr), thyroid hormone receptors (trs) genes, and the activities of iodothyronine deiodinases (IDs) were investigated to study the process of TH metabolism disruption. No differences in the histopathology of thyroid follicles and unchanged T4 levels were observed in adult zebrafish. A significant decline in T3 levels associated with a decrease in ID2 activity in male zebrafish was observed at 21 days exposure. Moreover, the mRNA expression of tsh, ttr and trs appeared to be a dynamic process as expression first decreased and then increased with continued exposure. These results indicated that exposure to MC-LR did not inhibit the production of TH. The decrease in ID2 activity may be an important factor in the decline of T3 levels. Furthermore, it seems that the fish triggered a compensatory mechanism to maintain TH homeostasis in respond to environmental concentrations of MC-LR which induced TH disruption.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping