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
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.
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
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping