Multi-Omics Analysis of Hepatopancreatic Responses to Ammonia Nitrogen Stress in Diploid Pacific Oysters (Magallana gigas)
TL;DR
It is shown that diploid Pacific oysters initiate early protective responses to maintain normal cellular function, but these responses may become insufficient under prolonged ammonia nitrogen stress, improving understanding of the physiological and molecular mechanisms underlying ammonia toxicity in Pacific oysters.
Abstract
Simple Summary Ammonia nitrogen accumulation in aquaculture systems can adversely affect the health and survival of cultured shellfish. To investigate the time-dependent response of diploid Pacific oysters to ammonia nitrogen stress, hepatopancreatic samples were collected before exposure (0 h) and after 6 and 48 h of exposure to 10 mg/L ammonia nitrogen. Hepatopancreatic tissue damage became progressively more severe with exposure duration. Antioxidant defenses were rapidly activated at 6 h, whereas prolonged exposure resulted in decreased activities of some antioxidant enzymes despite continued tissue injury. Integrated analyses of gene expression and metabolic profiles indicated coordinated changes in membrane transport, intracellular degradation and recycling, antioxidant defense, and nucleotide, amino acid, and lipid metabolism. These results indicate that diploid Pacific oysters initiate early protective responses to maintain normal cellular function, but these responses may become insufficient under prolonged ammonia nitrogen stress. The findings improve our understanding of the physiological and molecular mechanisms underlying ammonia toxicity in Pacific oysters and may contribute to improved water-quality management and health maintenance in oyster aquaculture.