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High Concentrations of Atmospheric Ammonia Induce Alterations in the Hepatic Proteome of Broilers (<i>Gallus gallus</i>): An iTRAQ-Based Quantitative Proteomic Analysis

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NIAID Data Ecosystem2026-03-08 收录
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With the development of the poultry industry, ammonia, as a main contaminant in the air, is causing increasing problems with broiler health. To date, most studies of ammonia toxicity have focused on the nervous system and the gastrointestinal tract in mammals. However, few detailed studies have been conducted on the hepatic response to ammonia toxicity in poultry. The molecular mechanisms that underlie these effects remain unclear. In the present study, our group applied isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomic analysis to investigate changes in the protein profile change in hepatic tissue of broilers exposed to high concentrations of atmospheric ammonia, with the goal of characterizing the molecular mechanisms of chronic liver injury from exposure to high ambient levels of ammonia. Overall, 30 differentially expressed proteins that are involved in nutrient metabolism (energy, lipid, and amino acid), immune response, transcriptional and translational regulation, stress response, and detoxification were identified. In particular, two of these proteins, beta-1 galactosidase (GLB1) and a kinase (PRKA) anchor protein 8-like (AKAP8 L), were previously suggested to be potential biomarkers of chronic liver injury. In addition to the changes in the protein profile, serum parameters and histochemical analyses of hepatic tissue also showed extensive hepatic damage in ammonia-exposed broilers. Altogether, these findings suggest that longtime exposure to high concentrations of atmospheric ammonia can trigger chronic hepatic injury in broilers via different mechanisms, providing new information that can be used for intervention using nutritional strategies in the future.

随着家禽养殖业的发展,氨气作为空气中的主要污染物,对肉鸡健康造成的危害日益凸显。迄今为止,有关氨气毒性的研究大多聚焦于哺乳动物的神经系统与胃肠道,但针对家禽氨气毒性的肝脏应答机制的详细研究仍较为匮乏,其背后的分子调控机制尚未明确。本研究中,我们团队采用基于同位素相对与绝对定量标记(isobaric tags for relative and absolute quantitation, iTRAQ)的定量蛋白质组学分析方法,探究高浓度大气氨气暴露后肉鸡肝脏组织的蛋白质组表达谱变化,旨在阐明长期暴露于高浓度环境氨气所引发的慢性肝损伤的分子机制。本研究共鉴定出30个差异表达蛋白,这些蛋白涉及营养代谢(能量、脂质与氨基酸代谢)、免疫应答、转录与翻译调控、应激反应及解毒作用等多个生物学过程。其中,β-1半乳糖苷酶(beta-1 galactosidase,GLB1)与蛋白激酶(PRKA)锚定蛋白8样(AKAP8L)这两种蛋白,此前已被报道可作为慢性肝损伤的潜在生物标志物。除蛋白质组表达谱的变化外,血清生化指标检测与肝脏组织化学分析结果也显示,氨气暴露组肉鸡存在广泛的肝脏损伤。综上,本研究结果表明,长期暴露于高浓度大气氨气可通过多种分子机制诱发肉鸡慢性肝损伤,为未来采用营养策略进行干预提供了新的理论依据。

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2015-04-22
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