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<p>Selenium (Se) is a vital micronutrient in maintaining intestinal redox homeostasis, and its deficiency weakens antioxidant capacity and aggravates inflammatory injury. Trimethyltin chloride (TMT), a widespread environmental pollutant with strong bioaccumulation, triggers oxidative stress (OS) at low levels, and its toxicity may be more severe in Se-deficient areas. However, the mechanism of ileal inflammatory injury caused by Se deficiency combined with TMT exposure remains unclear.</p><p>Using in vivo chicken models and in vitro experiments, we demonstrated that Se deficiency or TMT alone disrupted ileal antioxidant systems, increased ROS accumulation, activated the PERK/CHOP endoplasmic reticulum stress (ERS) pathway, promoted pyroptosis, and damaged intestinal barrier function, while combined exposure synergistically worsened these lesions. Pharmacological inhibition revealed that the ROS scavenger NAC suppressed PERK/CHOP signaling and reduced ERS and pyroptosis, and the pyroptosis inhibitor MCC950 mitigated inflammatory responses.</p><p>Overall, TMT aggravates Se deficiency-induced ileitis in chickens through the ROS/ERS-mediated pyroptosis axis. This study clarifies the interaction between environmental pollutants and trace elements, offering potential nutritional intervention targets for environmental enterotoxicity.</p>

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TMT Exacerbates Selenium-Deficient Enteritis in Gallus by Mediating Pyroptosis Through ROS/ERS

  • 期刊论文

  • 发表日期：

    2026年7月23日

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  • Shize Wang,
  • Yutian Lei,
  • Yuting Dong,
  • Kang Yang,
  • Tong Xu,
  • Hongjin Lin

摘要

Selenium (Se) is a vital micronutrient in maintaining intestinal redox homeostasis, and its deficiency weakens antioxidant capacity and aggravates inflammatory injury. Trimethyltin chloride (TMT), a widespread environmental pollutant with strong bioaccumulation, triggers oxidative stress (OS) at low levels, and its toxicity may be more severe in Se-deficient areas. However, the mechanism of ileal inflammatory injury caused by Se deficiency combined with TMT exposure remains unclear.

Using in vivo chicken models and in vitro experiments, we demonstrated that Se deficiency or TMT alone disrupted ileal antioxidant systems, increased ROS accumulation, activated the PERK/CHOP endoplasmic reticulum stress (ERS) pathway, promoted pyroptosis, and damaged intestinal barrier function, while combined exposure synergistically worsened these lesions. Pharmacological inhibition revealed that the ROS scavenger NAC suppressed PERK/CHOP signaling and reduced ERS and pyroptosis, and the pyroptosis inhibitor MCC950 mitigated inflammatory responses.

Overall, TMT aggravates Se deficiency-induced ileitis in chickens through the ROS/ERS-mediated pyroptosis axis. This study clarifies the interaction between environmental pollutants and trace elements, offering potential nutritional intervention targets for environmental enterotoxicity.