Dietary Vanadium Induces Lymphocyte Apoptosis in the Bursa of Fabricius of Broilers
2012
Cui, Wei | Cui, Hengmin | Peng, Xi | Fang, Jing | Zuo, Zhicai | Liu, Xiaodong | Wu, Bangyuan
The purpose of this 42-day study was to investigate the apoptosis in the bursa of Fabricius induced by different levels of dietary vanadium. A total of 420 1-day-old avian broilers were divided into 6 groups in which there were 7 replicates in each group and 10 broilers in each replicate and fed on a corn–soybean basal diet as control diet (vanadium 0.073 mg/kg) or the same diet amended to contain 5, 15, 30, 45, and 60 mg/kg vanadium supplied as ammonium metavanadate (NH4VO3). Ultrastructurally, mitochondrial injury and increased numbers of apoptotic cells with condensed nuclei were observed in the 30, 45, and 60 mg/kg groups. As measured by flow cytometry, the percentages of apoptotic lymphocytes were significantly increased in the 15-, 30-, 45-, and 60-mg/kg groups when compared with those of control group. Meanwhile, the terminal deoxynucleotidyl transferase 2′-deoxyuridine 5′-triphosphate nick end-labeling assay showed that there were increased numbers of apoptotic cells in the 30-, 45-, and 60-mg/kg groups. Immunohistochemical tests showed increased numbers of positive cells under Bax and caspase-3 protein detection and decreased Bcl-2 protein in the 15-, 30-, 45-, and 60-mg/kg groups. The vanadium content of the bursa was found to be significantly increased in the 30-, 45-, and 60-mg/kg groups. These results suggested that dietary vanadium in excess of 15 mg/kg could cause lymphocyte apoptosis in the bursa of Fabricius and impact humoral immunity in broilers. Lymphocyte apoptosis in the bursa induced by high levels of dietary vanadium is associated with mitochondrial injury and changes in levels of apoptogenic proteins, such as Bcl-2, Bax, and caspase-3.
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