PUBLICATION

Aflatoxin B1-induced early developmental hepatotoxicity in larvae zebrafish

Authors
Feng, C., Bai, H., Chang, X., Wu, Z., Dong, W., Ma, Q., Yang, J.
ID
ZDB-PUB-230828-45
Date
2023
Source
Chemosphere   340: 139940 (Journal)
Registered Authors
Dong, Wu
Keywords
Aflatoxin B1, Glutathione, Oxidative stress, Zebrafish
MeSH Terms
  • Acetylcysteine
  • Aflatoxin B1/toxicity
  • Animals
  • Chemical and Drug Induced Liver Injury*
  • Fatty Liver*
  • Larva/genetics
  • Zebrafish/genetics
PubMed
37634582 Full text @ Chemosphere
Abstract
Aflatoxin B1 (AFB1) is a ubiquitous mycotoxin that causes oxidative damage in various organs. At present, the research studies on AFB1 are primarily focused on its effects on the terrestrial environment and animals. However, its toxicity mechanism in aquatic environments and aquatic animals has not been largely explored. Thus, in this study, zebrafish was used as a model to study the toxicity mechanism of AFB1 on the liver of developing larvae. The results showed that AFB1 exposure inhibited liver development and promoted fat accumulation in the liver. Transcriptome sequencing analysis showed that AFB1 affected liver redox metabolism and oxidoreductase activity. KEGG analysis showed that AFB1 inhibited the expression of gsto1, gpx4a, mgst3a, and idh1 in the glutathione metabolizing enzyme gene pathway, resulting in hepatic oxidative stress. At the same time, AFB1 also inhibited the expression of acox1, acsl1b, pparα, fabp2, and cpt1 genes in peroxidase and PPAR metabolic pathways, inducing hepatic steatosis and lipid droplet accumulation. Antioxidant N-Acetyl-l-cysteine (NAC) preconditioning up-regulated gsto1, gpx4a and idh1 genes, and improved the AFB1-induced lipid droplet accumulation in the liver. In summary, AFB1 induced hepatic oxidative stress and steatosis, resulting in abnormal liver fat metabolism and accumulation of cellular lipid droplets. NAC could be used as a potential preventative drug to improve AFB1-induced fat accumulation.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping