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The purpose of this study was to observe the histopathological lesions and oxidative damage induced by dietary nickel chloride (NiCl 2 ) in the thymus.A total of 280 one-day-old avian broilers were divided into four groups and fed on a corn-soybean basal diet as the control diet or the same basal diet supplemented with 300, 600, and 900 mg/kg of NiCl 2 for 42 days.In the NiCl 2 -treated groups, the broiler weight and thymic relative weight were significantly (P < 0.05 or P < 0.01) decreased.Histopathologically, thymic corpuscles were increased and enlarged; the reticular cells were degenerate and necrotic, and lymphocytes were slightly decreased and loosely arranged in the medulla of thymus in the 600 mg/kg and 900 mg/kg groups.The activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px), and the ability to inhibit hydroxy radical and glutathione (GSH) content were significantly (P < 0.05 or P < 0.01) lower in the NiCl2-treated groups than those in the control group, while MDA content was higher.The abovementioned results demonstrated that dietary NiCl 2 in excess of 300 mg/kg could reduce the broiler weight and thymic relative weight, and cause histopathological lesions and oxidative damage in the thymus, which finally impaired the thymic function.
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Tang et al. (2014) studied this question.
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