Dissolved oxygen (DO) affects aquatic animals at a fundamental level so that the differences in its metabolic strategies under prolonged hypoxic conditions need an urgent exploration. In this experiment, largemouth bass (Micropterus salmoides) were chronically exposed (6 weeks) to severe hypoxia (S-HYP, DO: 2.0 ± 0.4 mg/L) and mild hypoxia (M-HYP, DO: 5.1 ± 0.4 mg/L). Compared to the control group (CON, DO:8.4 ± 0.4 mg/L), 1196 and 232 differentially expressed genes (DEGs) were obtained in S-HYP and M-HPY groups via transcriptome analysis, respectively. In S-HYP, lipolysis was promoted while anabolism was blocked. Meanwhile, significantly less fat droplet area was observed in the liver histology of S-HYP. Additionally, the cell cycle also responded to hypoxia, being blocked in the G1 phase with the suspension of DNA replication process. In M-HYP, the processing of protein in the endoplasmic reticulum and the synthesis of various aminoacyl t-RNA were inhibited, and a novel balance of the urea cycle might be established in the biosynthesis of arginine. The key DEGs involved in the above metabolic pathways, such as atgl, cpt1, arg1, etc., were validated by Q-PCR yielding results consistent with transcriptome data. This study indicates that the largemouth bass is prone to increase the proportion of lipid as an energy supply to adapt to the reprogramming of energy metabolism, while reducing the rate of cell proliferation to adapt to chronic severe hypoxia. This is also an undescribed observation in fish liver metabolism that largemouth bass may transform the synthesis and processing strategies of protein when exposed to chronic mild hypoxia.
Keywords: Cell cycle; Chronic hypoxia; Lipid metabolism; Micropterus salmoides; Mild hypoxia; Protein processing.
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