Recent advances in the mechanism of deoxynivalenol-induced hepatotoxicity and protective strategies.

Deoxynivalenol (DON) is a type B trichothecene mycotoxin produced by fusarium species, which widely contaminates grains and feed, posing a serious threat to human and animal health, with the liver as one of its key target organs. This review summarises in vivo and in vitro studies indicating that DON induces liver injury through multiple synergistic mechanisms, among which ferroptosis has attracted increasing attention; other core mechanisms include ribosomal stress response triggered by ribosomal function inhibition, reactive oxygen species (ROS) burst and lipid peroxidation (LPO), inflammatory cascades, and various forms of programmed cell death. In terms of protective mechanisms, the innovative potential of diverse protective strategies is highlighted: natural compounds exert significant hepatoprotective effects by activating the nuclear factor erythroid 2-related factor 2 (Nrf2) antioxidant pathway, inhibiting nuclear factor-kappa B kinase subunit beta (NF-κB) inflammatory signalling, and interfering with ferroptosis, while probiotic microorganisms, nanomaterials, epigenetic modulators, and physicochemical methods also show considerable detoxification capacity. Despite significant progress, future research should focus on the cumulative effects of long-term low-dose exposure and the combined toxicity of multiple mycotoxins, with emphasis on species specificity and dose dependency. Centering on the "GPX4-ferroptosis" axis, this review integrates research data to establish a comprehensive evidence chain, elucidate the "target-mechanism-consequence" logic of DON-induced hepatotoxicity, and provide a crucial theoretical basis for understanding its mechanisms and developing effective prevention and control strategies.