PUBLICATION

Embryonic exposure to low concentrations of aflatoxin B1 triggers global transcriptomic changes, defective yolk lipid mobilization, abnormal gastrointestinal tract development and inflammation in zebrafish

Authors
Ivanovics, B., Gazsi, G., Reining, M., Berta, I., Poliska, S., Toth, M., Domokos, A., Nagy, B., Staszny, A., Cserhati, M., Csosz, E., Bacsi, A., Csenki-Bakos, Z., Acs, A., Urbanyi, B., Czimmerer, Z.
ID
ZDB-PUB-210411-12
Date
2021
Source
Journal of hazardous materials   416: 125788 (Journal)
Registered Authors
Urbanyi, Bela
Keywords
Aflatoxin B1, Embryonic toxicity, Gastrointestinal tract development, Inflammation, L-arginine, Yolk lipid mobilization, Zebrafish
MeSH Terms
  • Aflatoxin B1*/toxicity
  • Animals
  • Gastrointestinal Tract
  • Humans
  • Inflammation/chemically induced
  • Inflammation/genetics
  • Lipid Mobilization
  • Transcriptome
  • Zebrafish*/genetics
PubMed
33838512 Full text @ J. Hazard. Mater.
Abstract
Aflatoxin B1-contaminated feeds and foods induce various health problems in domesticated animals and humans, including tumor development and hepatotoxicity. Aflatoxin B1 also has embryotoxic effects in different livestock species and humans. However, it is difficult to distinguish between the indirect, maternally-mediated toxic effects and the direct embryotoxicity of aflatoxin B1 in mammals. In the present study, we investigated the aflatoxin B1-induced direct embryotoxic effects in a zebrafish embryo model system combining toxicological, transcriptomic, immunological, and biochemical approaches. Embryonic exposure to aflatoxin B1 induced significant changes at the transcriptome level resulting in elevated expression of inflammatory gene network and repression of lipid metabolism and gastrointestinal tract development-related gene sets. According to the gene expression changes, massive neutrophil granulocyte influx, elevated nitric oxide production, and yolk lipid accumulation were observed in the abdominal region of aflatoxin B1-exposed larvae. In parallel, aflatoxin B1-induced defective gastrointestinal tract development and reduced L-arginine level were found in our model system. Our results revealed the complex direct embryotoxic effects of aflatoxin B1, including inhibited lipid utilization, defective intestinal development, and inflammation.
Genes / Markers
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Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping