High temperature changes the structure and function of spotted seabass (Lateolabrax maculatus) tissues and causes ER stress and mitochondrial homeostasis imbalance in liver

Global warming raises coastal water temperatures, affecting fish tissue structure, function, and survival. It is essential to understand these changes to develop effective mitigation strategies. This study investigates the changes in gill, liver, intestine, and head kidney structure and function of spotted seabass (Lateolabrax maculatus) after 56 days of cultivation at 27 degrees C (N, normal), 31 degrees C (M, moderate), and 35 degrees C (H, high). The results indicate that increased water temperature induced gill remodeling, liver vacuolization, reduced and broken intestinal villi, and increased melanin macrophages in head kidney of spotted seabass. The mRNA levels of hif alpha in gill of the H group were markedly elevated than those observed in N and M groups (P < 0.05). The mRNA levels of autophagy-related genes (beclin1, ulk1) in liver were significantly reduced in the H group in comparison to both the N and M groups (P < 0.05). The activities of trypsin (TRY), lipase (LPS), and amylase (AMS) in intestinal were lowest in H group and these levels were markedly lower than those observed in N group (P < 0.05). The mRNA levels of pro-inflammatory genes (il1 beta, il8) in intestinal were significantly elevated in H group than in N and M groups (P < 0.05). Furthermore, the activities of acid phosphatase (ACP), alkaline phosphatase (AKP), total nitric oxide synthase (T-NOS), and nitric oxide (NO) concentration in head kidney were markedly reduced in H group than N group (P < 0.05). Additionally, the mRNA levels of endoplasmic reticulum (ER) stress-related and mitochondrial homeostasis-related genes in liver indicate that high temperature induce ER stress and mitochondrial homeostasis imbalance. Conclusion: Elevated temperatures altered the morphological structure of the gill, liver, intestine, and kidney tissues in seabass, reducing oxygen absorption, self-repair, digestion, and nonspecific immune capabilities. Additionally, high temperature induced ER stress and mitochondrial homeostasis imbalance in liver, thereby inhibiting the thermal tolerance of seabass.