UPR-mediated apoptosis induced by ammonia nitrogen stress is contributed to gills damage in Litopenaeus vannamei

Ammonia nitrogen concentration is a critical factor affecting shrimp health in aquaculture, with the gills being the main target organ of ammonia nitrogen toxicity. This study investigated the role of unfolded protein response (UPR)-mediated apoptosis in ammonia-induced gill damage in L. vannamei . The experiment found that ammonia nitrogen stress significantly triggered apoptosis and tissue damage in gill tissue cells, and increased the cumulative mortality rate of L. vannamei ( p < 0.05), while activated the IRE1-XBP1, ATF6 and PERK-eIF2α pathways, thus indicating UPR activation. Further in-depth research found that under ammonia nitrogen stress, the activation of the UPR significantly upregulated the expression levels of apoptosis-related genes and enhanced the activity of Caspase 3 in the gills of shrimp ( p < 0.05), increased the number of apoptotic cells and aggravated tissue damage. In contrast, inhibition of different branches of the UPR exerted distinct effects. Notably, inhibiting the PERK-eIF2α pathway alleviated ammonia nitrogen-induced apoptosis and tissue damage, thereby increasing the survival rate of shrimp. In conclusion, ammonia nitrogen stress induced apoptosis and tissue damage in the gill cells of L. vannamei by activating the UPR, leading to increased mortality, among which the PERK-eIF2α pathway played a key pro-apoptotic role in this process. • Ammonia nitrogen stress induces UPR and triggers apoptosis in L. vannamei . • Persistent UPR exacerbates tissue damage and apoptosis under ammonia nitrogen stress. • The key pathway that mediates apoptosis under UPR is the PERK-eIF2α pathway.