Changes of thyroid hormone levels and related gene expression in zebrafish on early life stage exposure to triadimefon
- Authors
- Liu, S., Chang, J., Zhao, Y., and Zhu, G.
- ID
- ZDB-PUB-111027-25
- Date
- 2011
- Source
- Environmental Toxicology and Pharmacology 32(3): 472-477 (Journal)
- Registered Authors
- Keywords
- triadmifeon, hypothalamic-pituitary-thyroid axis, gene expression, thyroid hormone, zebrafish
- MeSH Terms
-
- Animals
- Embryo, Nonmammalian
- Endocrine Disruptors/toxicity
- Female
- Gene Expression Regulation, Developmental/drug effects*
- Hypothalamus/drug effects
- Iodide Peroxidase/genetics
- Male
- Pituitary Gland/drug effects
- Thyroid Gland/drug effects
- Thyroid Hormone Receptors alpha/genetics
- Thyroid Hormone Receptors beta/genetics
- Thyroid Hormones/metabolism*
- Thyrotropin, beta Subunit/genetics
- Triazoles/toxicity*
- Triiodothyronine/metabolism
- Water Pollutants, Chemical/adverse effects
- Zebrafish/embryology
- Zebrafish/genetics*
- Zebrafish Proteins/genetics
- PubMed
- 22004968 Full text @ Environ. Toxicol. Pharmacol.
- CTD
- 22004968
In this study, zebrafish was exposed to triadimefon. Thyroid hormones levels and the expression of related genes in the hypothalamic–pituitary–thyroid (HPT) axis, including thyroid-stimulating hormone (TSH-beta), deiodinases (dio1 and dio2) and the thyroid hormone receptor (thraa and thrb) were evaluated. After triadimefon exposure, increased T4 can be explained by increased thyroid-stimulating hormone (TSH-beta). The conversion of T4 to T3 (deiodinase type I-dio1) was decreased, which reduced the T3 level. Thyroid hormone receptor beta (thrb) mRNA levels were significantly down-regulated, possibly as a response to the decreased T3 levels. The overall results indicated that triadimefon exposure could alter gene expression in the HPT axis and that mechanisms of disruption of thyroid status by triadimefon could occur at several steps in the synthesis, regulation, and action of thyroid hormones.