PUBLICATION

C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage

Authors
Sun, S., Cao, X., Gao, J.
ID
ZDB-PUB-211202-5
Date
2021
Source
iScience   24: 103409 (Journal)
Registered Authors
Keywords
Animal physiology, Biological sciences, Lipidomics, Physiology
MeSH Terms
none
PubMed
34849471 Full text @ iScience
Abstract
Low temperatures can cause severe growth inhibition and mortality in fish. Previous studies about the cold resistance of fish mainly focused on the role of unsaturated fatty acids, rather than saturated fatty acids (SFAs). In this study, the role of very-long-chain SFA synthetized by fatty acyl elongase 1 gene (elovl1) in cold resistance was explored. Both an aggravated liver oxidative stress and a mitochondrial metabolism disorder were observed in elovl1a-/- and elovl1b-/- zebrafish with cold stress. In vitro studies confirmed that high levels of C20:0 and C22:0 obviously increased the hepatocyte oxidative stress and activated the extracellular signal-regulated kinases 1/2 (Erk1/2) pathway to further induce apoptosis and inflammation. We further demonstrated that C24:0 could promote mitochondrial β-oxidation to improve the cold resistance of zebrafish. Overall, our results define a positive role of C24:0 fatty acids synthetized by elovl1 in the cold resistance of fish.
Genes / Markers
Figures
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Expression
Phenotype
No data available
Mutations / Transgenics
Allele Construct Type Affected Genomic Region
zf3816
    		Indel
    zf3817
      		Indel
      1 - 2 of 2
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      Human Disease / Model
      No data available
      Sequence Targeting Reagents
      Target Reagent Reagent Type
      elovl1aCRISPR1-elovl1aCRISPR
      elovl1bCRISPR1-elovl1bCRISPR
      1 - 2 of 2
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      Fish
      No data available
      Antibodies
      No data available
      Orthology
      No data available
      Engineered Foreign Genes
      No data available
      Mapping
      No data available
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      Citation
      Sun, S., Cao, X., Gao, J. (2021) C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage. iScience. 24:103409.