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

Aflatoxin B1-contaminated feeds and foods induce various health problems in domesticated animals humans, including tumor development hepatotoxicity. B1 also has embryotoxic effects different livestock species humans. However, it is difficult to distinguish between the indirect, maternally-mediated toxic direct embryotoxicity of aflatoxin mammals. In present study, we investigated B1-induced a zebrafish embryo model system combining toxicological, transcriptomic, immunological, biochemical approaches. Embryonic exposure induced significant changes at transcriptome level resulting elevated expression inflammatory gene network repression lipid metabolism gastrointestinal tract development-related sets. According changes, massive neutrophil granulocyte influx, nitric oxide production, yolk accumulation were observed abdominal region B1-exposed larvae. parallel, defective reduced L-arginine found our system. Our results revealed complex B1, inhibited utilization, intestinal development, inflammation.