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氯化镍(NiCl2)通过氧化损伤诱导肉鸡法氏囊的组织病理学病变。

Nickel Chloride (NiCl2) Induces Histopathological Lesions via Oxidative Damage in the Broiler's Bursa of Fabricius.

作者信息

Yin Shuang, Guo Hongrui, Cui Hengmin, Peng Xi, Fang Jing, Zuo Zhicai, Deng Junliang, Wang Xun, Tang Kun, Li Jian

机构信息

Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Ya'an, China.

College of Veterinary Medicine, Sichuan Agricultural University, Ya'an, 625014, China.

出版信息

Biol Trace Elem Res. 2016 May;171(1):214-23. doi: 10.1007/s12011-015-0528-8. Epub 2015 Oct 6.

DOI:10.1007/s12011-015-0528-8
PMID:26440478
Abstract

The purpose of this study was to investigate the histopathological lesions, oxidative damage, changes of immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) contents in the bursa of Fabricius and serum immunoglobulins (IgG, IgM, IgA) induced by dietary nickel chloride (NiCl2). Two hundred and eighty-one-day-old broilers were randomly divided into four groups and fed on a control diet and three experimental diets supplemented with 300, 600, and 900 mg/kg of NiCl2 for 42 days. Lesions were observed in the NiCl2-treated groups. Histopathologically, lymphocytes were decreased in lymphoid follicles with thinner cortices and wider medullae. Concurrently, the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxyl radical and glutathione (GSH) contents were significantly (p < 0.05 or p < 0.01) decreased, while malondialdehyde (MDA) contents were increased in the NiCl2-treated groups. The serum IgG, IgM, and bursa IgG and IgM contents were significantly (p < 0.05 or p < 0.01) lower in the NiCl2-treated groups than those in the control group. The above-mentioned results show that dietary NiCl2 in excess of 300 mg/kg can cause histopathological lesions via oxidative damage, which finally impairs the function of the bursa of Fabricius and reduces IgG and IgM contents of the serum and the bursa of Fabricius. The study is aimed to provide helpful materials for studies on Ni- or Ni compounds-induced B cell toxicity in both human and other animals in the future.

摘要

本研究旨在探讨日粮中氯化镍(NiCl₂)诱导的法氏囊组织病理学损伤、氧化损伤、免疫球蛋白G(IgG)、免疫球蛋白M(IgM)和免疫球蛋白A(IgA)含量变化以及血清免疫球蛋白(IgG、IgM、IgA)情况。将281日龄的肉鸡随机分为四组,分别饲喂基础日粮和添加300、600和900 mg/kg NiCl₂的三种试验日粮,持续42天。在NiCl₂处理组中观察到了病变。组织病理学检查显示,淋巴滤泡中的淋巴细胞减少,皮质变薄,髓质增宽。同时,超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GSH-Px)的活性以及抑制羟自由基的能力和谷胱甘肽(GSH)含量在NiCl₂处理组中显著(p < 0.05或p < 0.01)降低,而丙二醛(MDA)含量增加。NiCl₂处理组的血清IgG、IgM以及法氏囊IgG和IgM含量显著(p < 0.05或p < 0.01)低于对照组。上述结果表明,日粮中NiCl₂超过300 mg/kg可通过氧化损伤引起组织病理学病变,最终损害法氏囊功能,降低血清和法氏囊中IgG和IgM的含量。该研究旨在为未来关于镍或镍化合物对人和其他动物B细胞毒性的研究提供有用资料。

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