Broilers in four groups were fed a basal diet supplemented with 60 mg/kg zinc oxide (60-ZnO; control), or 20, 60, or 100 mg/kg ZnO nanoparticles (20-, 60-, and 100-nano-ZnO, respectively). Compared with the controls, after 14 days, birds in the 20- and 60-nano-ZnO groups had significantly greater weight gains and better feed conversion ratios. However, the body weight of birds in the 100-nano-ZnO group was dramatically reduced after 28 days. Relative to the control group, the total antioxidant capability (T-AOC) in serum and liver tissue was significantly higher in the 20-nano-ZnO group at all time points and also significantly higher in the 60- and 100-nano-ZnO groups in serum on days 28 and 35 and in liver tissues on days 21 and 28. Compared with the controls, the activity of copper-zinc superoxide dismutase (Cu-Zn-SOD) was significantly greater in the 60- and 100-nano-ZnO groups in serum on days 28 and 35 and in liver tissues after 21 days. Catalase activity in serum samples was significantly higher in the 20- and 60-nano-ZnO groups relative to the control and 100-nano-ZnO birds, but catalase activity in liver tissue was not affected by different nano-ZnO levels. Malondialdehyde content in serum and liver tissues was significantly reduced in the 20-, 60-, and 100-nano-ZnO groups compared with that in the control group at all time points except day 42. Taken together, our data indicate that appropriate concentration of dietary ZnO nanoparticles improves growth performance and antioxidative capabilities in broilers, and 20 mg/kg nano-ZnO is the optimal concentration.

The experiment was conducted to investigate the effect of atmospheric ammonia (NH3) on histological changes, cell cycle distribution, and apoptosis of spleen in chickens. 240 chickens were randomly allocated to control group (without NH3 challenge) and NH3 group (70±5 ppm NH3). The experiment lasted for eight days. The results showed that NH3 exposure caused the decreased relative weight (P<0.05), dysplasia of lymphatic follicle, up-regulation of G0G1 phase cells, excessive apoptosis, and increase of reactive oxygen spcecies (ROS) activated cells (P<0.05) in the spleen. The mechanisms of cell cycle blockage were closely related to the upregulation of p53, p21 gene (P<0.05), the downregulation of cyclinD1, cdk6 gene (P<0.05), and the decrease of Proliferating Cell Nuclear Antigen (PCNA) protein (P<0.05). The activated apoptosis could resulted from the increased gene and protein expressions of bax and caspase-3 (P<0.05), and the decreased gene and protein expressions of bcl-2 (P<0.05). The results suggested that 70±5 ppm NH3 caused the spleen dysplasia, which were closely related to the cell cycle arrest and mitochondria apoptotic pathway activation.