生物学杂志

Journal of Biology ›› 2021, Vol. 38 ›› Issue (5): 23-.doi: 10.3969/j.issn. 2095-1736.2021.05.023

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Depletion of SOCS1a causes hepatic oxidative stress in zebrafish

  

  1. 1. Guangxi Key Laboratory of Beibu Gulf Marine Biodiversity Conservation, Qinzhou 535011, China;
    2. College of Light Industry and Food Engineering, Guangxi University, Nanning 530004, China;
    3. Key Laboratory of Aquatic Biodiversity and Conservation of the Chinese Academy of Sciences,
    Institute of Hydrobiology, Chinese Academy of Sciences, Wuhan 430072, China;
    4. Laboratory of Aquaculture Nutrition and Environmental Health (LANEH), School of Life Sciences,
    East China Normal University, Shanghai 200241, China
  • Online:2021-10-18 Published:2021-10-20

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Abstract: To investigate the effect of SOCS1a on liver oxidative stress in zebrafish, the liver tissues of zebrafish were analyzed by transmission electron microscopy (TEM), the activity of antioxidant enzymes and transcriptome between the SOCS1a-deficient adult zebrafish and their control siblings after feeding with high fat food and normal food for 6 weeks was assayed. Abnormal expansion, decreased ridge density of mitochondria and lipid droplet accumulation were observed in the liver of SOCS1a-deficient zebrafish. Under normal feed feeding conditions, the activities of superoxide dismutase (SOD) and glutathione reductase (GR) were lower in the liver of SOCS1a mutant compared with their control siblings by 27.813 and 3.879U/mg(prot), respectively. Under high-fat conditions, the SOD and GR activities were lower in the liver of SOCS1a mutant compared with their control siblings by 14.015 and 3.865 U/mg(prot), respectively. Transcriptome analysis showed the oxidative stress-related signaling pathway was significantly upregulated in the SOCS1a-deficient zebrafish. Overall, the SOCS1a knockout in zebrafish caused oxidative damage and oxidative stress, and the oxidative stress was more intense under the induction of high fat food.

Key words: SOCS1a knockout, zebrafish, hyperlipidemia, liver, transcriptome, oxidative stress

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