The effect of ammonia exposure on energy metabolism and mitochondrial dynamic proteins in chicken thymus: Through oxidative stress, apoptosis, and autophagy

Abstract

Ammonia (NH₃) gas is an atmospheric pollutant, produced from different sources. In poultry houses NH₃ is produced from the biological process of liter, manure, and protein composition. It has been well documented that NH₃ adversely effects the health of chickens. However, the underlying mechanism of NH₃ toxicity on chicken thymus is still unknown. Thymus is an important immune organ, which play a critical role in eliciting protective immune responses to ensure healing process and elimination of harmful stimuli. The results showed that NH₃ exposure reduced antioxidant activities and induced oxidative stress in thymus tissues. Histological observation showed normal morphology of chicken thymus in control group. In contrast, increased number of nuclear debris, vacuoles, and cristae break were seen in NH₃ affected chickens. Ultrastructural analysis indicated mitochondrial breakdown, disappearance, vacuoles, and chromatin condensation in NH₃ treated groups. The mRNA and protein expression of apoptosis related genes were significantly enhanced in the chicken thymus of NH₃ affected chickens compared to control group. Moreover, Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) assay results suggested that NH₃ exposure increased positive stained nuclei in the chicken thymus. Meanwhile, NH₃ exposure reduced the number of CD8⁺ T-lymphocytes, decreased the adenosine triphosphate (ATPase) activities. The mRNA and protein expression of autophagy, energy metabolism, and mitochondrial dynamics proteins were altered by NH₃ exposure. In summary, these results showed that NH₃ induced oxidative stress, apoptosis and autophagic cell death (ACD), which could be the possible causes of immune damage and structural impairment in chicken thymus.