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<p>Deoxynivalenol (DON) is a prevalent foodborne mycotoxin severely compromising livestock and poultry health and food safety. This study evaluated gallic acid (GA) —a top-performing candidate among screened polyphenols—in counteracting DON toxicity. In chicken embryo fibroblasts, 0.5 μM DON reduced viability to ~55% and induced oxidative stress, while co-treatment with 160 μM GA restored viability to ~79%. In chicks, DON caused hepatic injury and intestinal villus shortening, effects that GA effectively mitigated. Transcriptomic and biochemical assays revealed that DON triggers ferroptosis by disrupting iron homeostasis and lipid peroxidation elevation, whereas GA activated the Nrf2 pathway and upregulated key cytoprotective genes (<i>GPX4</i>, <i>FTH1</i>, <i>SLC7A11</i>, <i>HO-1</i>) to inhibit ferroptosis. These results demonstrate that GA antagonizes DON toxicity primarily through Nrf2-mediated ferroptosis suppression. In summary, this investigation provided not only a mechanistic basis for GA’s standalone application but also a rationale for targeted combinatorial therapy from multi-mechanistic perspectives to alleviate DON-induced damage and safeguard animal health and food safety.</p><p></p>

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Gallic acid antagonizes deoxynivalenol toxicity by inhibiting DON-induced ferroptosis

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年3月5日

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  • Haorong Wang,
  • Jiacui Xu,
  • Jinghan Feng,
  • Yifan Zhang,
  • Zixian Zhao,
  • Yan Lv,
  • Chuanqi Wang,
  • Jing Zhang,
  • Yongxing Ai

摘要

Deoxynivalenol (DON) is a prevalent foodborne mycotoxin severely compromising livestock and poultry health and food safety. This study evaluated gallic acid (GA) —a top-performing candidate among screened polyphenols—in counteracting DON toxicity. In chicken embryo fibroblasts, 0.5 μM DON reduced viability to ~55% and induced oxidative stress, while co-treatment with 160 μM GA restored viability to ~79%. In chicks, DON caused hepatic injury and intestinal villus shortening, effects that GA effectively mitigated. Transcriptomic and biochemical assays revealed that DON triggers ferroptosis by disrupting iron homeostasis and lipid peroxidation elevation, whereas GA activated the Nrf2 pathway and upregulated key cytoprotective genes (GPX4, FTH1, SLC7A11, HO-1) to inhibit ferroptosis. These results demonstrate that GA antagonizes DON toxicity primarily through Nrf2-mediated ferroptosis suppression. In summary, this investigation provided not only a mechanistic basis for GA’s standalone application but also a rationale for targeted combinatorial therapy from multi-mechanistic perspectives to alleviate DON-induced damage and safeguard animal health and food safety.