Atmospheric ammonia causes histopathological lesions, cell cycle blockage, and apoptosis of spleen in chickens

Abstract

This experiment was conducted to investigate the effect of atmospheric ammonia (NH3) on histological changes, cell cycle distribution, and apoptosis of the spleen in chickens. Two hundred forty chickens were randomly allocated to the control group (without NH3 challenge) and NH3 group (70 ± 5 ppm NH3). The experiment lasted for 8 days. The results showed that NH3 exposure caused decreased relative weight ( P < 0.05), dysplasia of white pulps, obvious ultrastructural lesions, upregulation of G0G1 phase cells, excessive apoptosis, and oxidative stress ( P < 0.05) in the spleen. The mechanisms of cell cycle blockage were closely related to the upregulation of the P53 and P21 genes ( P < 0.05), the downregulation of the cyclin D1 and CDK6 genes ( P < 0.05), and the decrease of proliferating cell nuclear antigen (PCNA) protein ( P < 0.05). The activated apoptosis resulted from the increased gene and protein expression of Bax and caspase-3 ( P < 0.05), and the decreased gene and protein expression of Bcl-2 ( P < 0.05). The results suggested that 70 ± 5 ppm NH3 caused the spleen dysplasia, which was closely related to the cell cycle arrest and mitochondrial apoptotic pathway activation.