Thyroid endocrine system disruption by pentachlorophenol: An in vitro and in vivo assay
- Authors
- Guo, Y., and Zhou, B.
- ID
- ZDB-PUB-130905-28
- Date
- 2013
- Source
- Aquatic toxicology (Amsterdam, Netherlands) 142-143C: 138-145 (Journal)
- Registered Authors
- Guo, YongYong, Zhou, BingSheng
- Keywords
- pentachlorophenol, T-Screen assay, zebrafish larvae, thyroid endocrine disruption, hypothalamic-pituitary-thyroid (HPT) axis
- MeSH Terms
-
- Animals
- Cell Line
- Cell Survival/drug effects
- Embryo, Nonmammalian
- Endocrine Disruptors/toxicity
- Endocrine System/drug effects*
- Gene Expression Regulation/drug effects
- Larva/chemistry
- Larva/drug effects
- Pentachlorophenol/toxicity*
- Rats
- Thyroid Gland/drug effects*
- Water Pollutants, Chemical/toxicity*
- Zebrafish/embryology
- Zebrafish/physiology*
- PubMed
- 24001430 Full text @ Aquat. Toxicol.
- CTD
- 24001430
The present study aimed to evaluate the disruption caused to the thyroid endocrine system by pentachlorophenol (PCP) using in vitro and in vivo assays. In the in vitro assay, rat pituitary GH3 cells were exposed to 0, 0.1, 0.3, and 1.0 µM PCP. PCP exposure significantly downregulated basal and triiodothyronine (T3)-induced Dio 1 transcription, indicating the antagonistic activity of PCP in vitro. In the in vivo assay, zebrafish embryos were exposed to 0, 1, 3, and 10 µg/L of PCP until 14 days post-fertilization. PCP exposure resulted in decreased thyroxine (T4) levels, but elevated contents of whole-body T3. PCP exposure significantly upregulated the mRNA expression of genes along hypothalamic–pituitary–thyroid (HPT) axis, including those encoding thyroid-stimulating hormone, sodium/iodide symporter, thyroglobulin, Dio 1 and Dio 2, alpha and beta thyroid hormone receptor, and uridinediphosphate-glucuronosyl-transferase. PCP exposure did not influence the transcription of the transthyretin (TTR) gene. The results indicate that PCP potentially disrupts the thyroid endocrine system both in vitro and in vivo.