T-2 toxin-induced intestinal damage with dysregulation of metabolism, redox homeostasis, inflammation, and apoptosis in chicks

文献类型： 外文期刊

第一作者： Liu, Meng

作者： Liu, Meng;Zhao, Ling;Wei, Jin-Tao;Huang, Yu-Xuan;Sun, Lv-Hui;Wei, Jin-Tao;Khalil, Mahmoud Mohamed;Wu, Wen-Da;Kuca, Kamil

作者机构： Huazhong Agr Univ, Coll Anim Sci & Technol, Frontiers Sci Ctr Anim Breeding & Sustainable Prod, State Key Lab Agr Microbiol, Wuhan 430070, Hubei, Peoples R China;Hubei Acad Agr Sci, Inst Anim Husb & Vet Sci, Wuhan 430064, Peoples R China;Massey Univ, Monogastr Res Ctr, Sch Agr & Environm, Palmerston North 4442, New Zealand;Nanjing Agr Univ, Coll Vet Med, MOE Joint Int Res Lab Anim Hlth & Food Safety, Nanjing, Peoples R China;Univ Hradec Kralove, Fac Sci, Dept Chem, Rokitanskeho 62, Hradec Kralove 50003, Czech Republic

关键词： T-2 toxin; Chicks; Intestine; Microbiome; Metabolome; Transcriptome

期刊名称：ARCHIVES OF TOXICOLOGY （ 2022影响因子：6.1； 五年影响因子：5.7 ）

ISSN： 0340-5761

年卷期： 2023 年

页码：

收录情况： SCI

摘要： 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.

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