Abstract

Global warming is threatening the survival and growth of cold-water fish, and the methods to improve the high-temperature adaptability of cold-water fish need to be explored urgently. This study aims to explore the mechanism of improving high temperature tolerance of rainbow trout by temperature acclimation (TA). Rainbow trout were acclimated by two modes at 22 °C, including fluctuating TA (FA) and constant TA (CA), and thereafter subjected to heat stress (HS) at 25 °C. Results showed that TA markedly increased the critical temperature maximum (CTmax) of rainbow trout. Secondly, the levels of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in serum and malondialdehyde (MDA) in liver of CA + HS group significantly decreased compared to those in HS group without TA, indicating the reduction of liver injury by CA. Moreover, HS significantly induced ROS production and reduced mitochondrial membrane potential (MMP) in rainbow trout liver, but TA reduced the levels of ROS and increased the MMP in liver of rainbow trout after HS, indicating the reduced oxidative stress and mitochondrial damage. Furthermore, TA up-regulated the expression of genes related to mitochondrial autophagy, fusion, fission and biogenesis, as well as the expression of marker proteins of autophagy (LC3II) and mitophagy (Parkin) in the liver, so as to maintain mitochondrial homeostasis. Moreover, TA also inhibited the occurrence of apoptosis (decrease in bax/bcl-2), which may be owing to the reduced ROS and mitochondrial damage by TA. Interestingly, CA significantly up-regulated the genes expression of methyltransferase in the liver, which may inhibit the genes or transcription factors related to oxidative stress and apoptosis by DNA methylation. In conclusion, TA increased the upper limit of heat tolerance of rainbow trout by improving mitochondrial quality and inhibiting apoptosis in liver. This study will provide an effective solution to the risk of high temperature in cold-water fish culture.

Full Text
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