College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
College of Wildlife and Protected Area, Northeast Forestry University, Harbin 150040, Heilongjiang, PR China.
Pestic Biochem Physiol. 2024 Feb;199:105761. doi: 10.1016/j.pestbp.2023.105761. Epub 2023 Dec 30.
Excessive acetochlor residues present ecological and food safety challenges. Here, broiler chicks were exposed to varied acetochlor doses to first assess its effects on the gut. Subsequent dietary supplementation with omega-3 was used to assess its anti-contamination effects. Pathologically, acetochlor induced notable ileal lesions including inflammation, barrier disruption, tight junction loss, and cellular anomalies. Mechanistically, acetochlor stimulated the TNFα/TNFR1 and TLR4/NF-κB/NLRP3 pathways, promoting RIPK1/RIPK3 complex formation, MLKL phosphorylation, NLRP3 inflammasome activation, Caspase-1 activation, and GSDMD shearing with inflammatory factor release. These mechanisms elucidate ileal cell death patterns essential for understanding chicken enteritis. Omega-3 supplementation showed promise in mitigating inflammation, though its precise counteractive role remains unclear. Our findings suggest early omega-3 intervention offered protective benefits against acetochlor's adverse intestinal effects, emphasizing its potential poultry health management role. Harnessing dietary interventions' therapeutic potential will be pivotal in ensuring sustainable poultry production and food safety despite persistent environmental contaminants.
过量的乙草胺残留对生态和食品安全构成挑战。本研究通过暴露于不同剂量的乙草胺来评估其对肉鸡肠道的影响,并通过后续的膳食补充ω-3 来评估其抗污染效果。组织病理学观察发现,乙草胺诱导了显著的回肠损伤,包括炎症、屏障破坏、紧密连接丢失和细胞异常。在机制上,乙草胺激活了 TNFα/TNFR1 和 TLR4/NF-κB/NLRP3 途径,促进 RIPK1/RIPK3 复合物形成、MLKL 磷酸化、NLRP3 炎性体激活、Caspase-1 激活和 GSDMD 剪切,导致炎症因子释放。这些机制阐明了理解鸡肠炎所必需的回肠细胞死亡模式。ω-3 补充显示出减轻炎症的潜力,但确切的拮抗作用尚不清楚。我们的研究结果表明,早期补充 ω-3 提供了对乙草胺肠道不良影响的保护作用,强调了其在禽类健康管理中的潜在作用。尽管环境污染物持续存在,利用膳食干预的治疗潜力对于确保可持续的家禽生产和食品安全将至关重要。