Abstract
BackgroundAmmonia (NH3) is a well-known environmental pollution gas, threatening human health. NH3 is also the most harmful gas to poultry for many years. Some studies have found NH3 can damage eyes, respiratory system, and digestive system. However, molecular mechanism of NH3 toxicity on chicken livers remains unclear. MethodsIn this study, we selected chicken liver as research object and successfully duplicated NH3 poisoning model of chickens. The ultrastructure of chicken livers was observed. The activities of ATPases (Na+K+-ATPase, Mg++-ATPase, Ca++-ATPase, and Ca++Mg++-ATPase) and the expression of energy metabolism-related genes (HK1, HK2, PK, PFK, PDHX, CS, LDHA, LDHB, AMPK, SDHA, SDHB, and avUCP) and autophagy-related genes (PI3K, LC3I, LC3II, Beclin1, SQSTM1, mTOR, ULK1, ATG5, ATG12, and ATG13) were measured to explore the effect of NH3 on energy metabolism and autophagy in chicken livers.ResultsOur results showed that excess NH3 caused liver tissue damage. Meanwhile, ATPases activities were inhibited during NH3 treatment. Moreover, we found that NH3 exposure altered the expression of energy metabolism-related and autophagy-related genes. NH3-induced compensatory increase of AMPK activated autophagy process through inhibiting mTOR and promoting ULK1. In addition. there was dose-dependent and time-dependent effects on all detected indexes in NH3-caused chicken liver damage. ConclusionExcess NH3 induced energy metabolism disorder and autophagy via AMPK/mTOR/ULK1 pathway in chicken livers.