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

Summary Low temperatures can cause severe growth inhibition and mortality in fish. Previous studies about cold resistance of fish mainly focused on the role of unsaturated fatty acids, rather than saturated fatty acids (SFA). 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 found 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 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 cold resistance of zebrafish. Overall, our results define a positive role of C24:0 fatty acids synthetized by elovl1 in cold resistance of fish.