Yin Shuang, Cui Hengmin, Peng Xi, Fang Jing, Zuo Zhicai, Deng Junliang, Wang Xun, Wu Bangyuan, Guo Hongrui
Key Laboratory of Animal Diseases and Environmental Hazards of Sichuan Province, Ya'an, Sichuan, China.
College of Veterinary Medicine, Sichuan Agricultural University, Ya'an, Sichuan, China.
Oncotarget. 2016 Jan 5;7(1):125-39. doi: 10.18632/oncotarget.6591.
This study was conducted with objective of evaluating the toxic effects of nickel chloride (NiCl2) on development of bursa of Fabricius in broilers fed on diets supplemented with 0, 300, 600 and 900 mg/kg of NiCl2 for 42 days by using the methods of experimental pathology, flow cytometry (FCM), and quantitative real-time polymerase chain reaction (qRT-PCR). The results showed that dietary NiCl2 in 300 mg/kg and over induced toxic suppression in the bursal development, which was characterized by decreasing lymphocytes histopathologically and relative weight, increasing G0/G1 phase (a prolonged nondividing state), reducing S phase (DNA replication) and proliferating index, and increasing percentages of apoptotic cells. Concurrently, the mRNA expression levels of bax, cytochrome c (cyt c), apoptotic peptidase activating factor 1 (Apaf-1), caspase-3, caspase-6, caspase-7 and caspase-9 were increased and the bcl-2 mRNA expression levels were decreased. The toxic suppression of bursal development finally impaired humoral immunity duo to the reduction of B lymphocyte population and B lymphocyte activity in the broiler chicken. This study provides new evidences for further studying the effect mechanism of Ni and Ni compoundson B-cell or bursa of Fabricius.
本研究旨在通过实验病理学、流式细胞术(FCM)和实时定量聚合酶链反应(qRT-PCR)等方法,评估氯化镍(NiCl₂)对日粮中添加0、300、600和900 mg/kg NiCl₂的肉鸡法氏囊发育的毒性作用,为期42天。结果表明,日粮中300 mg/kg及以上的NiCl₂对法氏囊发育产生毒性抑制,其特征为组织病理学上淋巴细胞减少、相对重量降低、G0/G1期增加(延长的非分裂状态)、S期(DNA复制)和增殖指数降低以及凋亡细胞百分比增加。同时,bax、细胞色素c(cyt c)、凋亡肽酶激活因子1(Apaf-1)、半胱天冬酶-3、半胱天冬酶-6、半胱天冬酶-7和半胱天冬酶-9的mRNA表达水平升高,而bcl-2 mRNA表达水平降低。法氏囊发育的毒性抑制最终损害了肉鸡的体液免疫,这是由于B淋巴细胞数量和B淋巴细胞活性降低所致。本研究为进一步研究镍及其化合物对B细胞或法氏囊的作用机制提供了新的证据。