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The purpose of this study was to observe the histopathological lesions and oxidative damage induced by dietary nickel chloride (NiCl2) 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 NiCl2 for 42 days. In the NiCl2-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 above-mentioned results demonstrated that dietary NiCl2 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.

Effects of Nickel Chloride on Histopathological Lesions and Oxidative Damage in the Thymus