Abstract：
Ammonia has been reported to have a variety of toxicity to aquatic animals, farm animals and humans. However, its potential toxicity on the intestines remains unknown. L-selenomethionine is one of the important organic selenium sources. However, the mitigating effect of L-selenomethionine on ammonia exposure toxicity is still lacking. Therefore, in this study, the mechanism of toxic action of ammonia on intestinal tract and the detoxification effect of L-selenomethionine were examined. We evaluated the intestinal toxicity of ammonia and the alleviating effect of L-selenomethionine in an in vivo model, and then verified it in vitro model by a variety of cutting-edge experimental techniques. Our results showed that ammonia exposure causes oxidative stress, necroptosis, Th1/Th2 imbalance and inflammation in the intestinal tissue and the intestinal cells, and L-selenomethionine had a significant mitigation effect on the changes of these indexes induced by ammonia. In conclusion, ammonia exposure caused oxidative stress and Th1/Th2 imbalance in the porcine small intestine and IPEC-J2 cells, and that excessive ROS accumulation-mediated necroptosis targeted inflammatory responses, resulting in the destruction of tight connections of intestinal cells, thereby causing intestinal barrier dysfunction. L-selenomethionine could effectively reduce the intestinal injury caused by ammonia exposure and antagonize the toxic effect of ammonia.
摘要：
据报道，氨对水生动物具有多种毒性，农场动物和人类。然而,它对肠道的潜在毒性仍然未知。L-硒代蛋氨酸是重要的有机硒源之一。然而,L-硒代蛋氨酸对氨暴露毒性的缓解作用尚缺乏。因此,在这项研究中，研究了氨对肠道的毒性作用机理和L-硒代蛋氨酸的解毒作用。我们在体内模型中评估了氨的肠道毒性和L-硒代蛋氨酸的缓解作用，然后通过多种尖端实验技术对其体外模型进行验证。我们的结果表明，氨暴露会导致氧化应激，坏死,Th1/Th2失衡和炎症在肠组织和肠细胞，和L-硒代蛋氨酸对氨引起的这些指标的变化有明显的缓解作用。总之,氨暴露引起猪小肠和IPEC-J2细胞的氧化应激和Th1/Th2失衡，过量的ROS积累介导的坏死靶向炎症反应，导致肠道细胞紧密连接的破坏，从而引起肠屏障功能障碍。L-硒代蛋氨酸能有效减轻氨暴露对肠道的损伤,拮抗氨的毒性作用。
