Longlong Song, Ming Liu, Quancheng Li, Qingli Gong, Yan Liu
Global warming presents a substantial threat to aquatic ectotherms, including the economically significant Atlantic salmon (Salmo salar). Although warm acclimation can increase heat tolerance, little is known about the dynamic processes and cellular responses associated with the acquisition and loss of this increased tolerance. This study investigated changes in critical thermal maximum (CTmax), liver structure, hepatic antioxidant activity, and heat shock protein (HSP) expression in Atlantic salmon during prolonged warm acclimation followed by cold acclimation back to baseline temperature. CTmax increased by approximately 1.7 °C during warm acclimation, with no further significant increase observed after 7 days of warming. During subsequent cold acclimation, the acquired CTmax declined slowly, remaining elevated for over 20 days. Long-term warm acclimation induced liver damage, with partial recovery observed during the one-month cold acclimation period. Molecularly, hepatic antioxidant responses were transiently activated during warm acclimation and increased again at later stages of subsequent cold acclimation, with GSH remaining elevated throughout both phases. For heat shock responses, hsp70 and hsp90 expressions increased during warm acclimation and returned to baseline during early cold acclimation, whereas HSP70 and HSP90 protein levels remained elevated. Furthermore, the expression patterns of the paralogous genes serpinh1b-1 and serpinh1b-2 differed, likely indicating functional divergence. This study provides a comprehensive temporal profile of thermal acclimation dynamics in Atlantic salmon, highlighting the asymmetric rates of thermal tolerance acquisition and loss, as well as the regulation of molecular defense mechanisms. These findings provide new temporal insight into thermal plasticity and associated cellular defense responses in the context of climate-related warming.