Grass carp (Ctenopharyngodon idella) resist heat stress by maintaining mitochondrial quality and enhancing energy production.

This study aims to explore the resistance mechanism of grass carp (Ctenopharyngodon idella) to heat stress (HS). Grass carp were cultured at 28°C, and then exposed to 30°C, 32°C or 34°C with a heating rate of 1°C/d, respectively. The results show that serum aspartate aminotransferase (AST), alanine aminotransferase (ALT) levels and liver malondialdehyde (MDA) content significantly increased after HS. In contrast, liver total antioxidant capacity (T-AOC) was significantly reduced after HS. Additionally, serum triglyceride (TG) and free fatty acid (FFA) levels increased after HS. Notably, the hepatic adenosine triphosphate (ATP) content of grass carp exposed to 30°C and 32°C was significantly higher than that of those exposed to 28°C. However, the liver ATP content of grass carp exposed to 34°C was significantly reduced compared to other groups. Further, the liver mitochondrial DNA copies significantly increased after HS. The expression of mitochondrial biogenesis genes (pgc-1α, nrf1/2, tfam) and mitophagy genes (beclin1, atg5, atg7, pink1, parkin) was upregulated in grass carp after HS. However, the expression of mitochondrial fission gene (drp1) was significantly upregulated in grass carp exposed to 34°C compared to other groups, whereas no corresponding change was observed in the expression of mitochondrial fusion gene (mfn1/2) in grass carp exposed to 34°C. In conclusion, when grass carp were exposed to 30°C or 32°C, mitochondrial homoeostasis can be maintained via regulating mitochondrial quality, providing enough energy for grass carp to resist HS. However, when grass carp was exposed to 34°C, mitochondrial homoeostasis was impaired, leading to inadequate energy for grass carp to resist HS.