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氨气暴露导致猪溶质载体家族基因网络的破坏。

Ammonia exposure causes the disruption of the solute carrier family gene network in pigs.

机构信息

College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, People's Republic of China.

College of Animal Science and Technology, Northeast Agricultural University, Harbin 150030, People's Republic of China.

出版信息

Ecotoxicol Environ Saf. 2021 Mar 1;210:111870. doi: 10.1016/j.ecoenv.2020.111870. Epub 2021 Jan 10.

Abstract

Ammonia is the main harmful gas in livestock houses. However, the toxic mechanism of ammonia is still unclear. Therefore, we examined the effects of ammonia exposure on different tissues of fattening pigs by histological analysis and transcriptome techniques in this study. The results showed that there were varying degrees of pathological changes in liver, kidney, hypothalamus, jejunum, lungs, spleen, heart and trachea of fattening pigs under ammonia exposure. Notably, the extent of damage in liver, kidney, jejunum, lungs, hypothalamus and trachea was more severe than that in heart and spleen. Transcriptome results showed that ammonia exposure caused changes in 349, 335, 340, 229, 120, 578, 407 and 115 differentially expressed genes in liver, kidney, spleen, lung, trachea, hypothalamus, jejunum and heart, respectively. Interestingly, the changes in solute vector (SLC) family genes were found in all 8 tissues, and the verified gene results (SLC11A1, SLC17A7, SLC17A6, SLC6A4, SLC22A7, SLC25A3, SLC28A3, SLC7A2, SLC6A6, SLC38A5, SLC22A12, SLC34A1, SLC26A1, SLC26A6, SLC27A5, SLC22A8 and SLC44A4) were consistent with qRT-PCR results. In conclusion, ammonia exposure can cause pathological changes in many tissues and organs of fattening pigs and changes in the SCL family gene network. Importantly, the SCL family is involved in the toxic mechanism of ammonia. Our findings will provide a new insight for better assessing the mechanism of ammonia toxicity.

摘要

氨是畜舍中主要的有害气体。然而,氨的毒性机制尚不清楚。因此,本研究通过组织学分析和转录组技术研究了氨暴露对育肥猪不同组织的影响。结果表明,氨暴露下育肥猪的肝脏、肾脏、下丘脑、空肠、肺、脾脏、心脏和气管均有不同程度的病理变化。值得注意的是,肝脏、肾脏、空肠、肺、下丘脑和气管的损伤程度比心脏和脾脏严重。转录组结果表明,氨暴露导致肝脏、肾脏、脾脏、肺、气管、下丘脑、空肠和心脏分别有 349、335、340、229、120、578、407 和 115 个差异表达基因发生变化。有趣的是,在所有 8 种组织中均发现溶质载体(SLC)家族基因发生变化,且验证基因结果(SLC11A1、SLC17A7、SLC17A6、SLC6A4、SLC22A7、SLC25A3、SLC28A3、SLC7A2、SLC6A6、SLC38A5、SLC22A12、SLC34A1、SLC26A1、SLC26A6、SLC27A5、SLC22A8 和 SLC44A4)与 qRT-PCR 结果一致。综上所述,氨暴露可引起育肥猪许多组织和器官的病理变化,并导致 SLC 家族基因网络的变化。重要的是,SLC 家族参与了氨的毒性机制。我们的研究结果为更好地评估氨毒性机制提供了新的见解。

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