PUBLICATION

Gonadal impairment and parental transfer of tris (2-butoxyethyl) phosphate in zebrafish after long-term exposure to environmentally relevant concentrations

Authors
Huang, Y., Liu, J., Yu, L., Liu, C., Wang, J.
ID
ZDB-PUB-181130-25
Date
2018
Source
Chemosphere   218: 449-457 (Journal)
Registered Authors
Yu, Liqun
Keywords
Gonadal impairment, Parental transfer, Tris (2-butoxyethyl) phosphate, Zebrafish
MeSH Terms
  • Animals
  • Endocrine Disruptors/toxicity
  • Female
  • Gene Expression/drug effects
  • Gonads/drug effects*
  • Larva/drug effects
  • Male
  • Maternal Exposure/adverse effects
  • Organophosphates/metabolism
  • Organophosphates/toxicity*
  • Paternal Exposure/adverse effects
  • Reproduction/drug effects
  • Sex Factors
  • Water Pollutants, Chemical/toxicity*
  • Zebrafish/growth & development*
  • Zebrafish/metabolism
PubMed
30497028 Full text @ Chemosphere
Abstract
Tris (2-butoxyethyl) phosphate (TBOEP) is a ubiquitous environmental contaminant due to its overuse. TBOEP has been found to cause reproductive toxicity and endocrine disruption during acute toxic experiment. In this study, we examined the effects of TBOEP on growth in initial generation (F0) zebrafish and transgenerational effects on growth of first generation (F1) larvae after parental long-term exposure (120 d) to environmentally relevant concentrations (0, 0.1, 1, 10 and 100 μg/L). Exposure to TBOEP resulted in significantly less growth as measured by body length, body weight and gonadosomatic index (GSI) in F0 females but not F0 males. Furthermore, the bioaccumulation of TBOEP in gonad, the alteration of the gene transcriptions in the hypothalamic-pituitary-gonadal (HPG) axis, and the delay in gonadal development in both female and male zebrafish were demonstrated. In addition, the residues of TBOEP were detected in F1 larvae after parental exposure, resulting in lower survival and shorter body length, as well as faster heart rate. And no significant changes in gene expressions along the growth hormone/insulin-like growth factor (GH/IGF) axis and the hypothalamic-pituitary-thyroid (HPT) axis were found in F1 larvae. In conclusion, these results indicated that long-term parental exposure to environmentally relevant concentrations of TBOEP could inhibit the development of progeny by parental gonadal impairment and by TBOEP transfer to offspring, instead of gene transcription in GH/IGF and HPT axes.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping