An integrated transcriptomic and metabolomic analysis reveals hepatic physiological responses of Perca fluviatilis to heat stress.

Abstract

Heat stress negatively affects the growth and health of fish. In this study, Eurasian perch (Perca fluviatilis) were exposed to control (18°C, CK) and heat stress (25°C, HS) conditions. Using liver transcriptomics and metabolomics in conjunction with physiological and biochemical indicators, we investigated the mechanisms underlying their thermal response. The results revealed that heat stress in P. fluviatilis led to liver cell damage, characterized by vacuolar degeneration and inflammatory cell infiltration. Heat stress caused a fluctuating decrease in superoxide dismutase (SOD) activity, a significant reduction in catalase (CAT) activity (p < 0.05) and a transient increase in glutathione peroxidase (GSH-Px) activity at 24 h, followed by a sustained decrease. Malondialdehyde (MDA) content significantly increased in the later stages. Adenosine triphosphatase (ATPase) activity exhibited phase-specific oscillations, and adenosine triphosphate (ATP) content decreased overall, while lactate dehydrogenase (LDH) activity displayed complex time-dependent variations. In total, 536 significantly differentially expressed genes and 262 differentially abundant metabolites were identified through combined transcriptomic and metabolomic analyses. Integrated multi-omics analysis revealed that key pathways involved in the heat stress response include alanine, aspartate and glutamate metabolism; purine metabolism; mitophagy; autophagy and apoptosis; cyclic guanosine monophosphate-protein kinase G (cGMP-PKG) signalling; oestrogen signalling; and lipid metabolism-associated pathways. These findings indicate that acute heat stress induces hepatic oxidative damage, energy-metabolism disturbance and multiomics alterations in P. fluviatilis. This study provides a basis for understanding the hepatic responses of temperate freshwater fish to elevated temperatures.