RESUMEN
Oxygen is a critical factor for most organisms and this is especially true for aquatic animals. Unfortunately, high-density aquaculture farming practices and environmental degradation will inevitably lead to hypoxic stress in fishes such as largemouth bass (Micropterus salmoides). Thus, characterizing the physiological responses during acute hypoxia exposure is extremely important for understanding the adaptation mechanisms of largemouth bass to hypoxia. The present study aimed to investigate mitochondrial function and Ca2+ exchange in largemouth bass under hypoxic conditions. Largemouth bass were subjected to hypoxia (1.2 ± 0.2 mg/L) for 24 h Liver mitochondria and endoplasmic reticulum (ER) parameters were analyzed. We used Liquid chromatography-mass spectrometry (LC-MS) to further elucidate the pattern of energy metabolism. Changes of Ca2+ concentrations were observed in primary hepatocytes of largemouth bass under hypoxic conditions. Our results indicate that the morphology and function of the mitochondria and ER were altered under hypoxia. First, the occurrence of autophagy was accompanied by reactive oxygen species (ROS) generation and electron transport chain (ETC) activity modulation under hypoxia. Second, hypoxia enhanced mitochondrial fusion and fission, mitochondrial biosynthesis, and ER quality control in the early stages of hypoxic stress (before 8 h). Third, hypoxia modulated tricarboxylic acid (TCA) cycle flux and caused the accumulation of TCA intermediate metabolites (citric acid and oxoglutaric acid). Additionally, Ca2+ efflux in the ER was observed., and the genes for Ca2+ transporters presented high expression levels in cellular and mitochondrial membranes. Collectively, the above physiological responses of the mitochondria and ER contributed to maintaining energy production to withstand the hypoxic stress in largemouth bass. These results provide novel insights into the physiological and metabolic changes in largemouth bass under hypoxic conditions.
