Effects of acute high-temperature stress on respiratory metabolism, tissue structure, and glycolipid metabolism in subadult Procambarus clarkii

Abstract

Procambarus clarkii, widely farmed in rice-crayfish systems, is vulnerable to high-temperature stress during summer. This study aimed to investigate its physiological and metabolic responses to acute heat stress. Subadult crayfish (13.72 ± 1.91 g) were exposed to 33 °C for 96 h (21 °C as control), and samples of gill, hepatopancreas, and muscle tissues were collected at 6, 12, 24, 48, and 96 h. Histological changes were observed using paraffin sectioning, while metabolic enzyme activities, substrate levels, and lipid metabolism-related gene expression were analyzed. The 96-h upper incipient lethal temperature (UILT₅₀) was determined to be 34.5 °C. Elevated temperatures significantly increased oxygen consumption, ammonia excretion, and overall metabolic rate, although the oxygen-to-nitrogen ratio remained stable. After 96 h of heat exposure, gill tissues showed reduced hemocytes, distorted filaments, and epithelial damage. In the hepatopancreas, B cell numbers increased and lipid droplets in R cells decreased. Energy metabolism shifted over time: during early stress (0-48 h), glucose was the primary energy source, with glycolysis as the main pathway; during later stress (48-96 h), lipid catabolism became dominant. Adipose triglyceride lipase (ATGL), rather than hormone-sensitive lipase (HSL), played a key role in lipid mobilization. These findings suggest that acute heat stress disrupts respiratory metabolism, damages key tissues, and drives a shift in energy strategy from carbohydrates to lipids in P. clarkii.