Pathological Effects Of Nickel Chloride On Bursa Of Fabricius In Broiler Chickens

Objective of this study was to observe nickel chloride (NiC12)-caused pathological injury in the growth of bursa of Fabricius of broiler chickens. Two hundred and eighty avian broilers were randomly divided into four groups and fed on diets supplemented with 0,300, 600 and 900 mg/kg of NiC12 for 42 days. At 14,28 and 42 days during the experiment, bursae were collected and pathological injuriy parameters were detected by using methods of experimental pathology, flow cytometry (FCM), quantitative real-time polymerase chain reaction (qRT-PCR), and ELISA. In comparison with the control group, results obtained in this study were as follows:1. Volume and weight of bursa of Fabricius were reduced in the NiCl2-treated groups. Histopathologically, lymphocytes were decreased in lymphoid follicles with thinner cortices and wider medullae.2. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) contents were significantly decreased (P<0.05 or P<0.01), and malondialdehyde (MDA) contents was increased (P<0.05 or P<0.01) in NiCl2-treated groups. Also, mRNA expression levels of CuZn-SOD, Mn-SOD, CAT, GSH-Px were significantly decreased (P<0.05 or P<0.01).3. Percentages of G0/G1 phase were increased (P<0.05 or P<0.01) and the percentages of S phase and proliferating index were reduced (P＜0.05 or P<0.01) in high NiCl2 groups.4. Percentages of apoptotic cells were increased (P<0.05 or P＜0.01). Also, mRNA expression levels of Bax, Cyt C, Apaf-1, Caspase-3, Caspase-6, Caspase-7 and Caspase-9 were increased (P＜0.05 or P＜0.01) and Bcl-2 mRNA expression levels were decreased (P＜0.05 or P＜0.01) in three NiCl2-treated groups.5. IgG and IgM contents in the bursa and serum were significantly decreased (P< 0.05 or P<0.01) in NiC12-treated groups.In conclusion, dietary NiC12 in 300 mg/kg and over causes bursal immunotoxicity in the broiler chicken, which reduces the bursal immune function. Development inhibition, arrested cell cycle, apoptosis and oxidative damage in the bursa are pathological basis and molecular basis of the NiCl2-induced bursal immune dysfunction. Reduction of T lymphocytes and immunoglobulin contents is direct reason of the NiCl2-induced bursal immune dysfunction.