PUBLICATION

Disruption of endocrine function in H295R cell in vitro and in zebrafish in vivo by naphthenic acids

Authors
Wang, J., Cao, X., Sun, J., Huang, Y., Tang, X.
ID
ZDB-PUB-150616-7
Date
2015
Source
Journal of hazardous materials   299: 1-9 (Journal)
Registered Authors
Keywords
Estrogen receptor, Naphthenic acids, Steroidogenesis, VTG
MeSH Terms
  • Animals
  • Carboxylic Acids/toxicity*
  • Cell Line, Tumor
  • Endocrine Disruptors/toxicity*
  • Estrogens/metabolism
  • Female
  • Gene Expression Profiling
  • Humans
  • In Vitro Techniques
  • Male
  • Progesterone/metabolism
  • Zebrafish
PubMed
26073515 Full text @ J. Hazard. Mater.
Abstract
Oil sands process-affected water (OSPW) have been reported to exhibit endocrine disrupting effects on aquatic organisms. Although the responsible compounds are unknown, naphthenic acids (NAs) have been considered to be implicated. The current study was designed to investigate the endocrine disruption of OSPW extracted NAs (OS-NAs) and commercial NAs (C-NAs) using a combination of in vitro and in vivo assays. The effects of OS-NAs and C-NAs on steroidogenesis were assessed both at hormone levels and expression levels of hormone-related genes in the H295R cells. The transcriptions of biomarker genes involved in endocrine systems in zebrafish larvae were investigated to detect the effects of OS-NAs and C-NAs on endocrine function in vivo. Exposure to OS-NAs and C-NAs significantly increased production of 17β-estradiol (E2) and progesterone (P4), and decreased production of testosterone (T). Both OS-NAs and C-NAs significantly induced the expression of several genes involved in steroidogenesis. The abundances of transcripts of biomarker gene CYP19b, ERα, and VTG were significantly up-regulated in zebrafish larvae exposed to OS-NAs and C-NAs, which indicated that NAs had negative effects on estrogen-responsive gene transcription in vivo. These results indicated that NAs should be partly responsible for the endocrine disrupting effects of OSPW.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping