Ammonia-induced testicular tissue damage: Apoptosis and autophagy pathways mediated by regulating Cyt C/Bcl-2 and p62/LC3B pathways

Abstract

Ammonia gas (NH₃) is a major hazard in animal husbandry that negatively affects animal growth and reproductive activities. Although the adverse effects of ammonia on livestock health and performance have been studied, its specific effects on the male reproductive system and its underlying biological mechanisms remain unclear. The aim of this study was to investigate the effects of ammonia exposure on male reproduction and its potential mechanisms of action. Immunohistochemistry revealed a significant increase in IL-10 expression in mouse testicular tissues under ammonia-induced stress. Ammonia exposure significantly decreased anti-apoptotic factor Bcl-2 and anti-autophagy factor p62 expression, coupled with increased expression of pro-apoptotic factors, including p53, Caspase-8, Bax, and Apaf, as well as the pro-autophagy factors Beclin1, ATG5, LC3B, the ratio of Bax/Bcl-2 and the ratio of P53/Bcl-2. The fluorescence intensity of the Cyt C apoptotic gene and pro-autophagy factor LC3B in immune tissues was significantly higher than that in the normal control group. In summary, ammonia exposure significantly affects the reproductive ability of male mice by inducing inflammation, apoptosis, and autophagic damage in the testes. Our findings provide insights into ammonia-induced reproductive disorders, which will contribute to the management and control of ammonia in animal husbandry, thereby reducing the negative effects of ammonia on the reproductive health of livestock and poultry and improving the quality and yield of livestock products.