PUBLICATION

Chronic dietary exposure of zebrafish to PAH mixtures results in carcinogenic but not genotoxic effects

Authors
Larcher, T., Perrichon, P., Vignet, C., Ledevin, M., Le Menach, K., Lyphout, L., Landi, L., Clerandeau, C., Lebihanic, F., Ménard, D., Burgeot, T., Budzinski, H., Akcha, F., Cachot, J., Cousin, X.
ID
ZDB-PUB-140513-68
Date
2014
Source
Environmental science and pollution research international   21(24): 13833-49 (Journal)
Registered Authors
Cousin, Xavier
Keywords
none
MeSH Terms
  • Animal Feed/analysis
  • Animals
  • Carcinogens/analysis
  • Carcinogens/toxicity*
  • DNA Damage/drug effects
  • Petroleum/analysis
  • Petroleum/toxicity
  • Polycyclic Aromatic Hydrocarbons/analysis
  • Polycyclic Aromatic Hydrocarbons/toxicity*
  • Zebrafish/genetics
  • Zebrafish/growth & development*
PubMed
24777325 Full text @ Environ. Sci. Pollut. Res. Int.
Abstract
Polycyclic aromatic hydrocarbons (PAHs) are ubiquitous contaminants that can be present at high levels as mixtures in polluted aquatic environments. Many PAHs are potent mutagens and several are well-known carcinogens. Despite numerous studies on individual compounds, little is known about the toxicity of PAHs mixtures that are encountered in environmental situations. In the present work, zebrafish were continuously fed from 5 days post-fertilisation to 14 months post-fertilisation (mpf) with a diet spiked with fractions of either pyrolytic (PY), petrogenic light oil (LO), or petrogenic heavy oil (HO) origin at three concentrations. A decrease in survival was identified after 3 mpf in fish fed with the highest concentration of HO or LO, but not for PY. All PAH fractions caused preneoplastic and neoplastic disorders in long-term-exposed animals. Target tissues were almost exclusively of epithelial origin, with the bile duct epithelium being the most susceptible to chronic exposure to all PAH fractions, and with germ cells being the second most responsive cells. Significantly higher incidences of neoplasms were observed with increasing PAH concentration and exposure duration. The most severe carcinogenic effects were induced by dietary exposure to HO compared to exposure to LO or PY (45, 30 and 7 %, respectively, after 9 to 10 months of exposure to an intermediate concentration of PAHs). In contrast, earliest carcinogenic effects were detected as soon as 3 mpf after exposure to LO, including the lowest concentration, or to PY. PAH bioactivation and genotoxicity in blood was assessed by ethoxyresorufin-O-deethylase activity quantification and comet and micronuclei assays, respectively, but none of these were positive. Chronic dietary exposure of zebrafish to PAH mixtures results in carcinogenotoxic events that impair survival and physiology of exposed fish.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping