4.7 Article

Toxic responses of liver in Lateolabrax maculatus during hypoxia and re-oxygenation

期刊

AQUATIC TOXICOLOGY
卷 236, 期 -, 页码 -

出版社

ELSEVIER
DOI: 10.1016/j.aquatox.2021.105841

关键词

Lateolabrax maculatus; Hypoxia; Re-oxygenation; Liver function; Apoptosis

资金

  1. Central Publicinterest Scientific Institution Basal Research Fund, CAFS [2020TD21, 2019ZD0501]
  2. National Natural Science Foundation of China [31802281]
  3. Natural Science Foundation of Guangdong Province, China [2018A030313137]
  4. Guangzhou Municipal Science and Technology Project [201906010028]
  5. Special Scientific Research Funds for Central Nonprofit Institutes, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences [2021SD11]

向作者/读者索取更多资源

Estuarine environments experience fluctuating oxygen levels, which negatively impact the liver function of hypoxia-sensitive spotted sea bass. Hypoxia leads to increased transaminase activity and decreased protein levels, while re-oxygenation partially restores protein synthesis but exacerbates apoptosis and purine metabolism dysregulation. These findings highlight the severe impact of hypoxia on hepatocyte function in spotted sea bass.
Estuarine environmental have been reported to undergo significant fluctuations in oxygen concentrations with hypoxic conditions and subsequent re-oxygenation events being of significant concern for resident fish populations. In this study we assessed the toxicological effects of hypoxia and re-oxygenation on the liver of hypoxiasensitive spotted sea bass (Lateolabrax maculatus) that were exposed to hypoxia (1.17 mg/L dissolved oxygen) for 12 h and then re-oxygenated for 12 h. The activities of glutamic-pyruvic transaminase and glutamic-oxalacetic transaminase in serum significantly increased under hypoxia (p < 0.05) and continued to increase during reoxygenation (p < 0.05), indicating that normal liver function might be disrupted by hypoxia and might become worse during re-oxygenation for 12h. Total protein, albumin, and globulin levels in serum decreased under hypoxia but began to return to normal during re-oxygenation, showing that protein synthesis in the liver decreased during hypoxia but could be restored by re-oxygenation. We also used RNA-Seq technology to identify changes in gene expression in the liver during hypoxia and re-oxygenation. Transcriptome sequencing revealed that the hypoxia-inducible factor (HIF-1) signaling pathway, apoptosis, and purine metabolism transcripts were significantly enriched under hypoxia and re-oxygenation conditions. A total of 15 and 16 apoptosis-related genes were induced by hypoxia and re-oxygenation stress, respectively. The apoptosis index increased from the normal to the hypoxic condition and was highest under re-oxygenation. Additionally, 19 and 29 genes, that are involved in purine metabolism in the liver of L. maculatus during hypoxia and re-oxygenation, respectively, were dysregulated. Unexpectedly, the serum uric acid level significantly increased during hypoxia and significantly decreased under re-oxygenation, indicating the presence of purine metabolic disorder in the liver of L. maculatus. These results illustrate that hypoxia poses a pronounced threat to hepatocyte function in L. maculatus and that liver damage is difficult to reverse with 12 h of re-oxygenation, and it may actually become worse when reoxygenation is established.

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