Han Yujing, Li Chunqiu, Su Mingjun, Wang Zhihui, Jiang Ning, Sun Dongbo
College of Animal Science and Veterinary Medicine, Heilongjiang Bayi Agricultural University, Sartu District, Daqing 163319, P.R. China.
Oncotarget. 2017 May 16;8(20):33725-33735. doi: 10.18632/oncotarget.16736.
Lead (Pb) may damage the immune function in human and animal. Selenium (Se) has antagonistic effects on Pb. In our study, brown layer chickens were randomly allocated to control group, Se group (1 mg/kg Se), Se+Pb group (1 mg/kg Se and 350 mg/kg Pb), and Pb group (350 mg/kg Pb). The chickens were sacrificed on the 90th day; spleen tissues were subjected to observation of ultrastructure and detection of spleen-related indexes. The results revealed that in the Pb group, expression levels of the cytokines IL-1 and TNF-α significantly increased, and expression levels of IL-2 and INF-γ significantly decreased; activities of antioxidant enzyme GPX, SOD and CAT significantly decreased, and expression level of malondialdehyde (MDA) significantly increased; expression levels of mitochondrial fission-related genes (Mff and Drp1) significantly increased, and expression levels of mitochondrial fusion-related genes (Opa1, Mfn1 and Mfn2) significantly decreased; expression of autophagy-related genes (Beclin 1, Dynein, Atg 5, LC3-I and LC-II) was upregulated, while expression of mammalian target of rapamycin (mTOR) was downregulated. The results of transmission electron microscopy indicated that Pb induced mitochondrial fragmentation, and triggered autophagy in the spleen of chickens. The Se and Pb co-treatment remarkably alleviated these injuries induced by Pb in the spleen of chickens. In conclusion, Pb can induce the oxidative stress to influence the mitochondrial dynamics balance and lead to autophagy, which triggers the immune dysfunction in the spleen of chickens; the Se exhibits the antagonistic effects on lead-induced autophagy by influencing mitochondrial dynamics in the spleen of chickens.
铅（Pb）可能损害人和动物的免疫功能。硒（Se）对铅具有拮抗作用。在我们的研究中，将罗曼褐蛋鸡随机分为对照组、硒组（1毫克/千克硒）、硒+铅组（1毫克/千克硒和350毫克/千克铅）和铅组（350毫克/千克铅）。在第90天处死鸡；对脾脏组织进行超微结构观察和脾脏相关指标检测。结果显示，在铅组中，细胞因子IL-1和TNF-α的表达水平显著升高，IL-2和INF-γ的表达水平显著降低；抗氧化酶GPX、SOD和CAT的活性显著降低，丙二醛（MDA）的表达水平显著升高；线粒体裂变相关基因（Mff和Drp1）的表达水平显著升高，线粒体融合相关基因（Opa1、Mfn1和Mfn2）的表达水平显著降低；自噬相关基因（Beclin 1、动力蛋白、Atg 5、LC3-I和LC-II）的表达上调，而雷帕霉素靶蛋白（mTOR）的表达下调。透射电子显微镜结果表明，铅诱导鸡脾脏线粒体碎片化，并引发自噬。硒和铅联合处理显著减轻了铅对鸡脾脏造成的这些损伤。总之，铅可诱导氧化应激，影响线粒体动力学平衡并导致自噬，从而引发鸡脾脏免疫功能障碍；硒通过影响鸡脾脏线粒体动力学对铅诱导的自噬具有拮抗作用。
