Deoxynivalenol: Emerging Toxic Mechanisms and Control Strategies, Current and Future Perspectives

Deoxynivalenol (DON) is the most frequently present mycotoxin contaminant in food and feed, causing a variety of toxic effects in humans and animals. Currently, a series of mechanisms involved in DON toxicity have been identified. In addition to the activation of oxidative stress and the MAPK signaling pathway, DON can activate hypoxia-inducible factor-1 alpha, which further regulates reactive oxygen species production and cancer cell apoptosis. Noncoding RNA and signaling pathways including Wnt/beta-catenin, FOXO, and TLR4/NF-kappa B also participate in DON toxicity. The intestinal microbiota and the brain-gut axis play a crucial role in DON-induced growth inhibition. In view of the synergistic toxic effect of DON and other mycotoxins, strategies to detect DON and control it biologically and the development of enzymes for the biodegradation of various mycotoxins and their introduction in the market are the current and future research hotspots.

Automated summary

Deoxynivalenol (DON) is a common mycotoxin contaminant in food and feed, posing toxic effects on humans and animals. Various mechanisms, such as oxidative stress, MAPK signaling pathway, hypoxia-inducible factor-1 alpha, noncoding RNA, and signaling pathways including Wnt/beta-catenin, FOXO, and TLR4/NF-kappa B, contribute to DON toxicity. The intestinal microbiota and brain-gut axis also play a crucial role in DON-induced growth inhibition. Detection, biological control, and enzyme degradation of mycotoxins are the current and future research priorities.