C24:0 Avoids Cold Exposure-Induced Oxidative Stress and Impaired Fatty Acid β -Oxidation

As we know, 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 through fatty acid elongase 1 gene (elovl1) in cold resistance was explored. The aggravated liver oxidative stress and the disorder of mitochondrial metabolism were found in elovl1a-/- and elovl1b-/- zebrafish with cold stress. In vitro experiments confirmed that high levels of C20:0 and C22:0 significantly increased the hepatocytes oxidative stress and activated mitogen-activated protein kinase (Mapk) pathway to further induce apoptosis and inflammation. We further demonstrated that C24:0 promoted mitochondrial β-oxidation through ceramide synthetase to produce Cer24:0 to improve cold resistance. Overall, our results define a positive role of C24:0 fatty acids synthetized by through elovl1 in cold resistance of fish.