As the number of reported deoxynivalenol (DON) contamination incidents increased steadily over the past decades, there has been a widespread interest in understanding the cellular mechanisms of the toxicological effects of DON using in vitro systems and omics technologies. The present investigation was conducted to understand the metabolomic changes in human hepatocellular carcinoma cells (HepG2) exposed to 10 μM DON for short term (4 h) and long term (12 h) periods, using a non-targeted metabolomics approach. Our results revealed a remarkable metabolic shift from short term to long term exposure to DON in HepG2 cells. Our metabolomics data also confirmed the role of DON induced oxidative stress in DON toxicity. Coupled with pattern recognition and pathway analysis, effects of DON on redox homeostasis, energy balance, lipid metabolism, and potential toxicological mechanisms were discussed, which would facilitate further studies on the risk assessment of the dietary mycotoxin DON.

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