Apoptotic Changes, Oxidative Stress and Immunomodulatory Effects in the Liver of Japanese Seabass ( Lateolabrax japonicus ) Induced by Ammonia-Nitrogen Stress during Keep-Live Transport.

This study investigated the effects of NH-N on antioxidant responses, histoarchitecture, and immunity of Japanese seabass () during keep-live transport. The findings suggest that NH-N stress transport alters the transcription of , , , and genes, demonstrating that NH-N stress can trigger the apoptotic pathway of -- and Caspase and induce apoptosis. NH-N stress transport also evoked transcriptional upregulation of inflammatory cytokines (, , , ) and increased complement C3, C4, lysozyme (LZM) and immunoglobulin (IgM) levels, activating the innate immunological system during keep-live transport. In addition, NH-N stress transport altered changes in the levels of superoxide dismutase (SOD), catalase (CAT), glutathione-related enzymes, and heat shock proteins 70 and 90 in the liver, indicating that the antioxidant system and Hsp protected the cells from NH-N-induced oxidative stress. When excess ROS were not removed, they caused the body to respond with immunological and inflammatory responses, as well as apoptosis and tissue damage. This helps towards understanding the effect of NH-N levels on sea bass during keep-live transport.