Ammonia inhalation impaired immune function and mitochondrial integrity in the broilers bursa of fabricius: Implication of oxidative stress and apoptosis
Ammonia inhalation impaired immune function and mitochondrial integrity in the broilers bursa of fabricius: Implication of oxidative stress and apoptosis
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DOI：
10.1016/j.ecoenv.2019.110078
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发表时间：
2020-03-01
影响因子：
6.8
通讯作者：
Teng, Xiaohua
中科院分区：
文献类型：
--
作者：
Shah, Syed Waqas Ali;Chen, Jianqing;Teng, Xiaohua
氨（NH3）被认为是环境污染物和对动物和人类（包括家禽）的毒性剂。以往的研究表明，NH3抑制肉鸡的免疫力。然而，氨对肉鸡法氏囊的危害作用尚不清楚。在功能上，细胞凋亡对于包括淋巴细胞群体的稳态在内的许多生理过程是非常重要的。因此，本研究旨在探讨氨对肉仔鸡BF的毒性机制。组织学观察显示BF内淋巴细胞聚集、空洞、间质细胞增多。超微结构观察显示线粒体空泡、线粒体膜变形和消失。氧化应激指标（CAT、MDA、H_2O_2、GGT、GSH-Px和GSH）表明NH_3对BF有氧化应激作用。同时，末端脱氧核苷酸转移酶介导的dUTP缺口末端标记（TUNEL）法显示凋亡细胞增加。此外，动力蛋白相关蛋白1（Drp 1）、线粒体分裂因子（Mff）、线粒体融合蛋白1和2（Mfn 1和Mfn 2）、视神经萎缩蛋白1（Opa 1）的mRNA和蛋白表达水平表明，肉鸡BF线粒体内外膜失衡，导致线粒体功能障碍。结果表明，在肉鸡BF中，凋亡相关基因Caspase-3、Caspase-9、Caspase-8、细胞色素C（Cyt-C）、p53、B细胞淋巴瘤2（Bcl-2）和Bcl-2相关X蛋白（Bax）的mRNA和蛋白表达均发生了显著变化。以上结果表明，过量NH3通过氧化应激和细胞凋亡引起BF损伤和线粒体功能障碍，并影响BF的免疫功能。这些发现为预防氨对肉仔鸡血液的毒性提供了可能的治疗靶点。
Ammonia (NH3) is considered as environmental pollutant and toxic agent for animals and humans including poultry. Previous reports demonstrated that NH3 suppressed broilers immunity. However, the harmful effects of NH3 on broilers bursa of fabricius (BF) is still unknown. Functionally, apoptosis is very important for many physiological processes including homeostasis of lymphocyte population. Therefore, the present study was aimed to investigate the underlying mechanisms of NH3 toxicity in the broilers BF. Histological observation showed lymphocyte accumulation, cavities and increased interstitial cells in BF. Ultrastructural observation indicated mitochondrial vacuoles, deformation and disappearance of mitochondrial membranes. Oxidative stress markers (CAT, MDA, H2O2, GGT, GSH-Px and GSH) showed that NH3-induced oxidative stress in BF. Meanwhile, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay revealed increased apoptotic cells. In addition, the mRNA and protein expression of dynamin-related protein 1 (Drp1), mitochondria] fission factor (Mff), mitofusin 1 and 2 (Mfn1 and Mfn2), optic atrophy 1 (Opa1) indicated imbalance between mitochondrial inner and outer membrane and results in mitochondrial dysfunction in broilers BF. The mRNA and protein expression of apoptosis-related genes including Caspase-3, Caspase-9, Caspase-8, Cytochrome-C (Cyt-C), p53, B-cell lymphoma 2 (Bcl-2) and Bcl-2 associated X protein (Bax) were significantly altered in broilers BF. Conclusively, these results displayed that excessive NH3 causes BF damage and mitochondrial dysfunction through oxidative stress and apoptosis in BF and could affect immune function of BF. These findings provide possible therapeutic targets to prevent NH3 induced toxicity in the BF of broilers.