摘要：SummaryLow 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 inelovl1a–/–andelovl1b–/–zebrafish with cold stress.In vitrostudies 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 byelovl1in the cold resistance of fish.Graphical abstractDisplay OmittedHighlights•elovl1, closely associated with C24:0, was activated in ZFL cells with cold stress•C20:0 and C22:0 induced Erk1/2 expression and apoptosis to impair cold tolerance•This study showed the positive role of C24:0 in the cold resistance of fishBiological sciences; Physiology; Animal physiology; Lipidomics
