Li Longfei, Ran Yang, Shen Xiaoyun
College of Agriculture and Biology, Liaocheng University, Liaocheng 252000, China.
College of Life Science and Agri-Forestry, Southwest University of Science and Technology, Mianyang 621010, China.
Metabolites. 2025 Aug 9;15(8):541. doi: 10.3390/metabo15080541.
: Molybdenum (Mo) is an essential trace element for animals, but too much intake can cause adverse effects. Due to the metabolic characteristics of goats and other ruminants, they are more susceptible to the cumulative effects of Mo toxicity. A high Mo intake can cause multi-organ toxicity in ruminants, but the mechanism of damage to the pancreas is still unclear. The aim of this study was to systematically analyze the key regulatory pathways of pancreatic injury induced by Mo in goats using a metabolomics approach. : Twenty male Yudong Black goats (22.34 ± 1.87 kg, six months) were randomly divided into a control group (fed a basal diet) and the Mo group (fed a basal diet supplemented with 50 mg·kg NaMoO·2HO). After 60 days of continuous feeding, their pancreatic tissues were collected and the mineral elements, antioxidant capacity, and inflammatory factors were examined. Untargeted metabolomics based on HILIC UHPLC-Q-EXACTIVE MS was used to analyze changes in metabolites. The core regulatory mechanisms were revealed by KEGG enrichment analysis. : The results demonstrated that goats in the Mo group showed obvious clinical signs, such as lethargy, loss of appetite, and unsteady gait. The pancreatic tissue of goats in the Mo group exhibited significantly elevated levels of Mo and copper, accompanied by a marked reduction in antioxidant capacity and concurrent increases in inflammatory cytokine levels. Between the Mo group and control group, 167 differentially expressed metabolites were identified. KEGG enrichment analysis showed that it disrupted multiple metabolic pathways, including glycine, serine, and threonine metabolism, cysteine and methionine metabolism, and butanoate metabolism. : This study mainly revealed, at the metabolomics level, that Mo exposure would disrupt the metabolic pathways related to antioxidant capacity in goat pancreata. It provides new insights into the molecular mechanisms of Mo-induced pancreatic injury in goats.
钼（Mo）是动物必需的微量元素，但摄入过多会产生不良影响。由于山羊和其他反刍动物的代谢特性，它们更容易受到钼中毒累积效应的影响。高钼摄入量会导致反刍动物多器官中毒，但钼对胰腺的损伤机制仍不清楚。本研究旨在采用代谢组学方法系统分析钼诱导山羊胰腺损伤的关键调控途径。
将20只雄性豫东黑山羊（22.34±1.87千克，6个月龄）随机分为对照组（饲喂基础日粮）和钼组（饲喂添加50毫克·千克钼酸钠·2H₂O的基础日粮）。连续饲喂60天后，采集它们的胰腺组织，检测其中的矿物质元素、抗氧化能力和炎症因子。采用基于亲水相互作用液相色谱-四极杆-静电场轨道阱高分辨质谱联用（HILIC UHPLC-Q-EXACTIVE MS）的非靶向代谢组学方法分析代谢物变化。通过KEGG富集分析揭示核心调控机制。
结果表明，钼组山羊出现明显的临床症状，如嗜睡、食欲不振和步态不稳。钼组山羊的胰腺组织中钼和铜的含量显著升高，同时抗氧化能力明显降低，炎症细胞因子水平升高。在钼组和对照组之间，鉴定出167种差异表达的代谢物。KEGG富集分析表明，钼干扰了多个代谢途径，包括甘氨酸、丝氨酸和苏氨酸代谢、半胱氨酸和蛋氨酸代谢以及丁酸代谢。
本研究主要在代谢组学水平上揭示了钼暴露会破坏山羊胰腺中与抗氧化能力相关的代谢途径。它为钼诱导山羊胰腺损伤的分子机制提供了新的见解。
