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<p>T-2 toxin is a typical mycotoxin that seriously threatens human and animal health. Liver is the major target organ of T-2 toxin. To elucidate the precise hepatotoxicity mechanism and discover a natural antagonist of T-2 toxin. T-2 toxin (0, 0.5, 1, 2 mg/kg BW)-induced liver injury model, Ferrostatin-1 (1 mg/kg·BW) interference model, Parkin<sup>−/−</sup> mice model, Nrf2-activating model (tBHQ, 20 mg/kg·BW) and lycopene (5 mg/kg·BW) treatment model were constructed. Proteomics revealed that ferroptosis is a critical hepatotoxicity mechanism of T-2 toxin. Blocking ferroptosis alleviated the liver damage and mitophagy under T-2 toxin threat. However, these processes were exacerbated in Parkin<sup>−/−</sup> mice. In vivo mouse model confirmed that Nrf2 activation increased PINK-Parkin mediated mitophagy and alleviated T-2 toxin-induced ferroptosis, suggesting that Nrf2/mitophagy axis was involved in T-2 toxin-induced hepatic ferroptosis. Further analysis revealed that lycopene promoted Nrf2 nuclear translocation and PINK-Parkin mediated mitophagy to mitigate T-2 toxin-induced hepatic ferroptosis.</p>

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Lycopene mitigates T-2 toxin-induced hepatic ferroptosis by targeting the Nrf2/mitophagy axis in mice

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年2月7日

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  • Xu Yang,
  • Wenxi Song,
  • Zhi Lu,
  • Yunhe Chen,
  • Youshuang Wang,
  • Tingyu Huang,
  • Yu Liu,
  • Yiming Wang,
  • Shuai Chen,
  • Yanfei Li,
  • Xuebing Wang,
  • Cong Zhang

摘要

T-2 toxin is a typical mycotoxin that seriously threatens human and animal health. Liver is the major target organ of T-2 toxin. To elucidate the precise hepatotoxicity mechanism and discover a natural antagonist of T-2 toxin. T-2 toxin (0, 0.5, 1, 2 mg/kg BW)-induced liver injury model, Ferrostatin-1 (1 mg/kg·BW) interference model, Parkin−/− mice model, Nrf2-activating model (tBHQ, 20 mg/kg·BW) and lycopene (5 mg/kg·BW) treatment model were constructed. Proteomics revealed that ferroptosis is a critical hepatotoxicity mechanism of T-2 toxin. Blocking ferroptosis alleviated the liver damage and mitophagy under T-2 toxin threat. However, these processes were exacerbated in Parkin−/− mice. In vivo mouse model confirmed that Nrf2 activation increased PINK-Parkin mediated mitophagy and alleviated T-2 toxin-induced ferroptosis, suggesting that Nrf2/mitophagy axis was involved in T-2 toxin-induced hepatic ferroptosis. Further analysis revealed that lycopene promoted Nrf2 nuclear translocation and PINK-Parkin mediated mitophagy to mitigate T-2 toxin-induced hepatic ferroptosis.