Deoxynivalenol toxicity along the gut–liver–brain axis in animal models: Mechanisms of action and strategies for mitigation

Abstract

Deoxynivalenol (DON), a trichothecene mycotoxin commonly found in cereals and animal feed, exerts systemic toxicity affecting intestinal, hepatic, and neural function. This review critically examines DON-induced damage along the gut–liver–brain axis in animal models, highlighting shared molecular mechanisms including oxidative stress, inflammatory signaling, and impaired antioxidant responses. DON disrupts intestinal barrier integrity, alters microbiota composition, promotes hepatic inflammation and apoptosis, and can impair neurochemical balance via direct and gut-mediated pathways. We also summarize the prevalence of DON contamination globally, with detection rates exceeding 60 % in some regions. In response to these risks, various mitigation strategies have been explored. This review evaluates the efficacy and safety of bioactive compounds such as vitamins, plant polyphenols, probiotics, and yeast derivatives, as well as synthetic agents, in reducing DON toxicity. Mechanisms of action include antioxidant defense, mycotoxin binding, and modulation of host immunity. Despite progress, knowledge gaps remain in long-term exposure effects, combinatory mycotoxin toxicity, and feed additive standardization. Integrative and translational approaches are needed to ensure effective DON risk management in food-producing systems.