PUBLICATION

Long-term exposure to triphenyl phosphate alters hormone balance and HPG, HPI, and HPT gene expression in zebrafish (Danio rerio)

Authors
Liu, X., Jung, D., Jo, A., Ji, K., Moon, H.B., Choi, K.
ID
ZDB-PUB-160213-16
Date
2016
Source
Environmental toxicology and chemistry   35(9): 2288-96 (Journal)
Registered Authors
Choi, Kyungho
Keywords
Endocrine disruptors, Flame retardants, Organophosphates, Sex hormone, Thyroid hormone
MeSH Terms
  • Animals
  • Endocrine System/drug effects*
  • Endocrine System/metabolism
  • Estradiol/blood
  • Estradiol/genetics
  • Female
  • Flame Retardants/toxicity*
  • Gene Expression/drug effects*
  • Male
  • Organophosphates/toxicity*
  • Testosterone/analogs & derivatives
  • Testosterone/blood
  • Testosterone/genetics
  • Thyroid Hormones/blood
  • Thyroid Hormones/genetics
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/blood
  • Zebrafish/metabolism*
PubMed
26865342 Full text @ Environ. Toxicol. Chem.
CTD
26865342
Abstract
With the global decline in the use of polybrominated diphenyl ethers (PBDEs), demand for alternative flame retardants, such as triphenyl phosphate (TPP), has increased substantially. TPP is now detected in various environments including aquatic ecosystems worldwide. However, studies on the toxicological consequences of chronic TPP exposure on aquatic organisms are scarce. We used the zebrafish model to investigate the effects of long-term TPP exposure on the endocrine system. For this purpose, we exposed zebrafish embryos to 5, 50 or 500 µg/L TPP for 120 d, and measured hormonal and transcriptional responses along the hypothalamus-pituitary-gonad (HPG), -interrenal (HPI), and -thyroid (HPT) axes. Exposure to TPP significantly increased plasma 17β-estradiol (E2), but decreased 11-ketotestosterone (11-KT) in both sexes. Gene expression data support these changes. In HPI axis, plasma cortisol and pomc and mr transcripts increased in females, but in males cortisol decreased while pomc increased (p < 0.05). Thyroxine (T4) and triiodothyronine (T3) increased, and trhr2 and trh expression were affected only in females (p < 0.05). In summary, long-term exposure to TPP enhanced estrogenicity in both males and females, potentially through influencing the HPG axis, but modulated the HPI, and HPT axes differently by sex, suggesting that both genomic and nongenomic responses might be involved.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping