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Arsenic (III) or/and copper (II) exposure induce immunotoxicity through trigger oxidative stress, inflammation and immune imbalance in the bursa of chicken.
Ecotoxicology and Environmental Safety ( IF 6.2 ) Pub Date : 2019-12-30 , DOI: 10.1016/j.ecoenv.2019.110127
Juanjuan Liu 1 , Yu Wang 1 , Hongjing Zhao 1 , Mengyao Mu 1 , Menghao Guo 1 , Xiaopan Nie 1 , Ying Sun 1 , Mingwei Xing 1
Affiliation  

The environmental hazards of arsenic (As) and copper (Cu) contamination have swept through quite a few districts worldwide. Whereas, molecular mechanisms involved in As- and Cu-induced immunotoxicity in Gallus gallus bursa of Fabricius (BF) are complex and elusive. Male Hy-line chickens were exposed to arsenic trioxide (As2O3; 30 mg/kg) and copper sulfate (CuSO4; 300 mg/kg) alone or in combination, respectively, to examine the potential ecotoxicity of them. The ions homeostasis and BF index of chicken had distinct changes after As or/and Cu exposure. Moreover, As or/and Cu treatment significantly increased the MDA content and NOS activity, and simultaneously resulted in reductions in CAT and AHR activities. Subsequently, it was further exhibited up-regulations of nuclear factor-κB (NF-κB), inflammatory mediators and pro-inflammation cytokines accompanied by depletion of anti-inflammatory cytokines and severe pathological conditions. Moreover, decreased ratio of IFN-γ/IL-4 and increased level of IL-17 illustrated an imbalance of the immune response. Meanwhile, incremental mRNA transcription and protein levels of heat shock proteins (HSPs) alleviated toxicity caused by As or/and Cu. Importantly, exposure to both contaminants significantly soared the BF injury in comparison with exposure to As or Cu alone. All these results illustrated that exposure to As2O3 or/and CuSO4 elicited BF tissue damage and ions changes, and its severity was associated with prolonged persistence of oxidative damage, accompanied by a dysregulated immune response which played a vital role in inflammatory injury. Additionally, combined management of As2O3 and CuSO4 could exacerbate BF injury.

中文翻译:

砷(III)或/和铜(II)的暴露通过触发鸡的法氏囊中的氧化应激,炎症和免疫失衡而诱导免疫毒性。

砷(As)和铜(Cu)污染对环境的危害已席卷全球许多地区。然而,As和Cu诱导的法氏囊鸡(BF)鸡胚囊免疫毒性的分子机制是复杂且难以捉摸的。将雄性Hy-line鸡单独或组合暴露于三氧化二砷(As2O3; 30 mg / kg)和硫酸铜(CuSO4; 300 mg / kg),以检查它们的潜在生态毒性。暴露于砷或铜后,鸡的离子稳态和BF指数发生明显变化。此外,砷或铜的处理显着增加了MDA含量和NOS活性,同时导致CAT和AHR活性降低。随后,它进一步表现出核因子-κB(NF-κB)的上调,炎性介质和促炎细胞因子,并伴有消炎细胞因子耗竭和严重的病理状况。此外,IFN-γ/ IL-4的比率降低和IL-17的水平升高说明了免疫反应的失衡。同时,热休克蛋白(HSP)的mRNA转录水平和蛋白水平的增加减轻了As或/和Cu引起的毒性。重要的是,与仅暴露于砷或铜相比,暴露于两种污染物会大大增加BF伤害。所有这些结果说明,暴露于As2O3或/和CuSO4会引起BF组织损伤和离子变化,其严重程度与氧化损伤的持续存在有关,并伴有免疫反应失调,这在炎症性损伤中起着至关重要的作用。此外,
更新日期:2019-12-30
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