State Key Laboratory of Agricultural Microbiology, Key Laboratory of Animal Embryo Engineering and Molecular Breeding of Hubei Province, Hubei Hongshan Laboratory, Frontiers Science Center for Animal Breeding and Sustainable Production, College of Animal Sciences and Technology, Huazhong Agricultural University, Wuhan, 430070, Hubei, China.
Institute of Animal Husbandry and Veterinary Sciences, Hubei Academy of Agricultural Sciences, Wuhan, 430064, China.
Arch Toxicol. 2023 Mar;97(3):805-817. doi: 10.1007/s00204-023-03445-z. Epub 2023 Jan 25.
T-2 toxin is a worldwide problem for feed and food safety, leading to livestock and human health risks. The objective of this study was to explore the mechanism of T-2 toxin-induced small intestine injury in broilers by integrating the advanced microbiomic, metabolomic and transcriptomic technologies. Four groups of 1-day-old male broilers (n = 4 cages/group, 6 birds/cage) were fed a control diet and control diet supplemented with T-2 toxin at 1.0, 3.0, and 6.0 mg/kg, respectively, for 2 weeks. Compared with the control, dietary T-2 toxin reduced feed intake, body weight gain, feed conversion ratio, and the apparent metabolic rates and induced histopathological lesions in the small intestine to varying degrees by different doses. Furthermore, the T-2 toxin decreased the activities of glutathione peroxidase, thioredoxin reductase and total antioxidant capacity but increased the concentrations of protein carbonyl and malondialdehyde in the duodenum in a dose-dependent manner. Moreover, the integrated microbiomic, metabolomic and transcriptomic analysis results revealed that the microbes, metabolites, and transcripts were primarily involved in the regulation of nucleotide and glycerophospholipid metabolism, redox homeostasis, inflammation, and apoptosis were related to the T-2 toxin-induced intestinal damage. In summary, the present study systematically elucidated the intestinal toxic mechanisms of T-2 toxin, which provides novel ideas to develop a detoxification strategy for T-2 toxin in animals.
T-2 毒素是全球范围内饲料和食品安全的问题，导致牲畜和人类健康风险。本研究的目的是通过整合先进的微生物组学、代谢组学和转录组学技术，探讨 T-2 毒素诱导肉鸡小肠损伤的机制。将 4 组 1 日龄雄性肉鸡（每组 4 个笼，每个笼 6 只）分别饲喂对照日粮和添加 T-2 毒素的对照日粮，剂量分别为 1.0、3.0 和 6.0mg/kg，连续 2 周。与对照组相比，日粮 T-2 毒素以不同剂量不同程度地降低了采食量、体重增加、饲料转化率以及表观代谢率，并诱导了小肠的组织病理学损伤。此外，T-2 毒素以剂量依赖性方式降低了十二指肠谷胱甘肽过氧化物酶、硫氧还蛋白还原酶和总抗氧化能力的活性，但增加了蛋白质羰基和丙二醛的浓度。此外，整合的微生物组学、代谢组学和转录组学分析结果表明，微生物、代谢物和转录物主要参与核苷酸和甘油磷脂代谢的调节，氧化还原稳态、炎症和细胞凋亡与 T-2 毒素诱导的肠道损伤有关。综上所述，本研究系统阐明了 T-2 毒素的肠道毒性机制，为动物体内 T-2 毒素的解毒策略提供了新的思路。
