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

SIMPLE SUMMARY: Excreta produced by fish during preservation transport can increase ammonia-nitrogen (NH(3)-N) levels in transport water and reduce survival rates. However, studies on the effects of NH(3)-N stress on Japanese seabass during transport are limited. The objective of this study was to investigate the effects of NH(3)-N stress on tissue damage, oxidative stress, apoptosis and immunity in Japanese seabass during transport, and to determine tolerance and response to NH(3)-N toxicity. The results of this study provide insight into the impact of environmental factors on Japanese seabass during maintenance of live transport, which can be considered during transport in terms of improving the quality of transport water, among other things, to develop optimal procedures for live fish transport and improve survival rates during transport. ABSTRACT: This study investigated the effects of NH(3)-N on antioxidant responses, histoarchitecture, and immunity of Japanese seabass (Lateolabrax japonicus) during keep-live transport. The findings suggest that NH(3)-N stress transport alters the transcription of P53, Caspase 9, Bcl2, Caspase 3 and Bax genes, demonstrating that NH(3)-N stress can trigger the apoptotic pathway of P53-Bax-Bcl2 and Caspase and induce apoptosis. NH(3)-N stress transport also evoked transcriptional upregulation of inflammatory cytokines (tumor necrosis factor α (TNF-α), Toll-like receptor 3 (TLR-3), nuclear factor kappa β (NF-κB), interleukin 6 (IL-6) and interleukin 1β (IL-1β)) and increased complement C3, C4, lysozyme (LZM) and immunoglobulin (IgM) levels, activating the innate immunological system during keep-live transport. In addition, NH(3)-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(3)-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(3)-N levels on sea bass during keep-live transport.