GRADUAL WARMING STRESS ON GILL TISSUE DAMAGE AND PHYSIOLOGICAL HOMEOSTASIS IN LARGE YELLOW CROAKER (LARIMICHTHYS CROCEA)

This study aimed to determine the temperature threshold for gill tissue damage and the physiological response mechanisms in large yellow croaker (Larimichthys crocea) under gradual warming, using 10-month-old fish exposed to a temperature increase from 26 °C to 33 °C at 1 °C/24 h, with simultaneous monitoring of dissolved oxygen (DO) and analysis of gill pathology, oxidative stress, oxygen transport, and energy metabolism. The results showed that at 28-29℃, mild gill damage such as epithelial hyperplasia and gill filament congestion occurred; at 30℃ and above, irreversible damage including lamellar fusion, epithelial vacuolization, and cell shedding appeared. The activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), and total antioxidant capacity (T-AOC) first increased and then decreased, while malondialdehyde (MDA) content continued to rise. The expression levels of heat shock protein genes hsp70 and hsp90 were significantly positively correlated with increasing water temperature. The expression of oxygen transport-related genes HIF-1α and Hbae4 first increased and then decreased, peaking at 30℃ and 31℃, respectively, and reaching the lowest levels at 33℃. The expression of idh3g decreased significantly at 28℃ and then recovered, while ATP content showed no significant change throughout the process. This study indicates that gradual warming and the accompanying decline in dissolved oxygen synergistically induce structural damage, oxidative stress imbalance, and energy metabolism disorders in the gill tissue of L. crocea, with 29—30℃ being the key temperature node for the transition from adaptive regulation to severe structural damage. This study preliminarily reveals the physiological response mechanisms of L. crocea gill tissue to high-temperature stress, providing a theoretical basis for water temperature regulation in healthy aquaculture.