Role of Ferroptosis in the Redox Biology of Mycotoxins

Ferroptosis, an iron‐dependent regulated cell death process driven by lipid peroxidation, has emerged as a pivotal mechanism in mycotoxin‐induced redox pathology. This review synthesizes the molecular interplay between fungal secondary metabolites (e.g., aflatoxin B1, deoxynivalenol) and ferroptotic pathways, revealing how mycotoxins subvert cellular iron homeostasis through transferrin receptor 1 (TfR1) upregulation and ferritinophagy‐mediated iron release, while concurrently inactivating glutathione peroxidase 4 (GPX4) and depleting reduced glutathione. Through integrative analysis of tissue‐specific toxicity profiles (hepatic > renal > intestinal), we propose a “two‐hit” model wherein mycotoxin bioactivation synergizes with organ‐specific ferroptosis vulnerability to drive pathological outcomes. Conversely, dietary interventions utilizing selenium‐enriched compounds and polyphenolic antioxidants demonstrate dual protective mechanisms: chelating redox‐active iron pools while preserving GPX4 activity and membrane phospholipid integrity. In addition, we evaluated the therapeutic strategies of intervening ferroptosis from food components to alleviate mycotoxin‐induced pathology, providing a translational framework for innovation in livestock health and food safety.