Ammonia is one of the major environmental pollutants in the pig industry that seriously affects the airway health of pigs. In this study, we aimed to investigate the metabolic profiling changes of piglets’ lung tissue after the exposure of 0 ppm (CG), 20 ppm (LG) and 50 ppm (HG) ammonia for 30 days. Compared with the control group, the obvious lung lesions were observed in HG, including interstitial thickening, inflammatory cell infiltration and focal hemorrhage. The significantly increased content of malondialdehyde in HG, combined with the significantly decreased mRNA expression of antioxidase and inflammatory-regulators in exposure groups, implied that ammonia exposure induced oxidative stress and diminished the anti-inflammatory response in lung tissues. Metabolomic analyses of lung tissues revealed 15 significantly altered metabolites among the three groups including multiple amino acids, carbohydrates and lipids. The accumulation of succinic acid, linoleic acid and phosphorylethanolamine and consumption of glucose, quinolinic acid and aspartic acid in ammonia exposure groups, indicated that energy supply from glucose aerobic oxidation was suppressed and the glycolysis and lipolysis were activated in lung tissues induced by chronic ammonia exposure.

中文翻译：

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慢性氨暴露诱导仔猪肺氧化应激和糖酵解增强

氨是养猪业的主要环境污染物之一，严重影响猪的呼吸道健康。在本研究中，我们旨在研究暴露 0 ppm (CG)、20 ppm (LG) 和 50 ppm (HG) 氨 30 天后仔猪肺组织的代谢谱变化。与对照组相比，HG 可见明显的肺部病变，包括间质增厚、炎性细胞浸润和局灶性出血。HG中丙二醛含量显着增加，结合暴露组抗氧化酶和炎症调节剂的mRNA表达显着降低，表明氨暴露诱导了氧化应激并减弱了肺组织的抗炎反应。肺组织的代谢组学分析显示，三组中有 15 种代谢物发生显着改变，包括多种氨基酸、碳水化合物和脂质。氨暴露组琥珀酸、亚油酸和磷酸乙醇胺的积累以及葡萄糖、喹啉酸和天冬氨酸的消耗表明，慢性氨暴露诱导的肺组织葡萄糖有氧氧化的能量供应受到抑制，糖酵解和脂肪分解被激活.