PUBLICATION

Proteomic analysis of male zebrafish livers chronically exposed to perfluorononanoic acid

Authors
Zhang, W., Liu, Y., Zhang, H., and Dai, J.
ID
ZDB-PUB-110512-16
Date
2012
Source
Environment International   42: 20-30 (Journal)
Registered Authors
Zhang, Wei
Keywords
perfluorononanoic acid, proteomics, 2-D DIGE, hepatotoxicity, PPAR, male zebrafish
MeSH Terms
  • Animals
  • Fatty Acids/metabolism
  • Fluorocarbons/toxicity*
  • Gene Expression
  • Liver/metabolism*
  • Liver/pathology
  • Male
  • Peroxisome Proliferator-Activated Receptors/genetics
  • Peroxisome Proliferator-Activated Receptors/metabolism
  • Proteome/metabolism
  • Proteomics/methods
  • RNA, Messenger/metabolism
  • Signal Transduction
  • Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
  • Surface-Active Agents/toxicity*
  • Tandem Mass Spectrometry
  • Two-Dimensional Difference Gel Electrophoresis
  • Water Pollutants, Chemical/toxicity
  • Zebrafish/metabolism*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism*
PubMed
21481936 Full text @ Environ. Int.
Abstract
Perfluorononanoic acid (PFNA), a synthetic perfluorinated carboxylic acid and fluorosurfactant, is a known environmental contaminant found in people and wildlife. To understand the hepatotoxicity mechanism of PFNA, male zebrafish (n=200) were exposed to differing concentrations of PFNA (0, 0.1, 0.5, and 1.0mg/L) for 180days. A two-dimensional difference gel electrophoresis (2-D DIGE) approach coupled with MALDI-TOF-MS/MS analysis was employed to detect and identify the differential expressed proteins. A total of 57 proteins were successfully identified and categorized into functional classes that included metabolism (amino acid metabolism, TCA cycle and pyruvate metabolism, gluconeogenesis and glycolysis, protein metabolism and modification, and nucleotides metabolism), structure and motility, stress and defense, signal transduction, and cell communication. Our proteomic analyses added new perspective to PFNA hepatotoxicity in zebrafish. Results regarding mRNA levels demonstrated that the involvement of peroxisome proliferator-activated receptors (PPARs) could not sufficiently explain the hepatotoxicity mechanism of PFAAs in zebrafish. The extensive protein variations indicated that multiple cellular pathways were involved in and suggested that multiple protein molecules should be simultaneously targeted as an effective strategy to counter PFNA toxicity. Other potential modes should be further investigated.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping