Chronic exposure to pentachlorophenol alters thyroid hormones and thyroid hormone pathway mRNAs in zebrafish
- Authors
- Yu, L.Q., Zhao, G.F., Feng, M., Wen, W., Li, K., Zhang, P.W., Peng, X., Huo, W.J., and Zhou, H.D.
- ID
- ZDB-PUB-131115-7
- Date
- 2014
- Source
- Environmental toxicology and chemistry 33(1): 170-6 (Journal)
- Registered Authors
- Keywords
- Gene expression, Hypothalamic-pituitary-thyroid axis, Pentachlorophenol, Thyroid hormone, Zebrafish
- MeSH Terms
-
- Animals
- Arylsulfotransferase/genetics
- Brain/drug effects
- Brain/metabolism
- Female
- Glucuronosyltransferase/genetics
- Iodide Peroxidase/genetics
- Liver/drug effects
- Liver/metabolism
- Male
- Pentachlorophenol/toxicity*
- Prealbumin/genetics
- RNA, Messenger/metabolism
- Thyroid Hormone Receptors beta/genetics
- Thyroid Hormones/blood*
- Thyrotropin, beta Subunit/genetics
- Water Pollutants, Chemical/toxicity*
- Zebrafish/genetics
- Zebrafish/metabolism*
- Zebrafish Proteins/genetics
- PubMed
- 24123209 Full text @ Environ. Toxicol. Chem.
Pentachlorophenol (PCP) is frequently detected in the aquatic environment and has been implicated as an endocrine disruptor in fish. Here, 4-month-old zebrafish (Danio rerio) were exposed to one of four concentrations of PCP (0.1, 1, 9 and 27 μg/L) for 70 days. The effects of PCP exposure on plasma thyroid hormone levels, and the expression levels of selected genes were measured in the brain and liver. PCP exposure at 27 μg/L resulted in elevated plasma thyroxine concentrations in male and female zebrafish, and depressed 3, 5, 3'-triiodothyronine concentrations in males only. In both sexes, PCP exposure resulted in decreased mRNA expression levels of thyroid stimulating hormone β-subunit (tshβ) and thyroid hormone receptor β (trβ) in the brain, as well as increased liver levels of uridine diphosphoglucuronosyl transferase (ugt1ab) and decreased deiodinase 1 (dio1). We also identified several sex-specific effects of PCP exposure, including changes in mRNA levels for deiodinase 2 (dio2), cytosolic sulfotransferase (sult1 st5), and transthyretin (ttr) genes in the liver. Environmental PCP exposure also caused an increased malformation rate in offspring that received maternal exposure to PCP. The present study demonstrates that chronic exposure to environmental levels of PCP alters plasma thyroid hormone levels, as well as the expression of genes associated with thyroid hormone signaling and metabolism in the HPT axis and liver, resulting in abnormal zebrafish development.