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

Area of Science:

• Environmental Toxicology
• Nutritional Science
• Gastroenterology

Background:

• Selenium (Se) is crucial for intestinal redox balance; deficiency impairs antioxidant capacity.
• Trimethyltin chloride (TMT) is an environmental pollutant inducing oxidative stress (OS).
• The combined effects of Se deficiency and TMT on ileal injury mechanisms are not fully understood.

Purpose of the Study:

• To elucidate the mechanism of ileal inflammatory injury from combined Se deficiency and TMT exposure in chickens.
• To investigate the roles of oxidative stress, endoplasmic reticulum stress (ERS), and pyroptosis in this injury.
• To identify potential nutritional interventions for environmental enterotoxicity.

Main Methods:

• In vivo chicken models and in vitro experiments were utilized.
• Assessed ileal antioxidant systems, reactive oxygen species (ROS) accumulation, and intestinal barrier function.
• Investigated the PERK/CHOP endoplasmic reticulum stress (ERS) pathway and pyroptosis markers.
• Employed pharmacological inhibitors (NAC for ROS, MCC950 for pyroptosis).

Main Results:

• Se deficiency or TMT alone disrupted antioxidant systems, increased ROS, activated PERK/CHOP ERS, promoted pyroptosis, and damaged the intestinal barrier.
• Combined exposure synergistically exacerbated these ileal lesions.
• NAC treatment suppressed ROS/ERS/pyroptosis; MCC950 mitigated inflammatory responses.

Conclusions:

• TMT exacerbates Se deficiency-induced ileitis in chickens via a ROS/ERS-mediated pyroptosis axis.
• This study clarifies the interaction between environmental pollutants and trace elements in intestinal injury.
• Findings suggest potential nutritional targets for mitigating environmental enterotoxicity.