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

Shouxiang Sun; Xiaojuan Cao; Jian Gao

doi:10.1016/j.isci.2021.103409

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

iScience. 2021 Nov 9;24(12):103409. doi: 10.1016/j.isci.2021.103409. eCollection 2021 Dec 17.

Authors

Shouxiang Sun¹, Xiaojuan Cao^{1

2}, Jian Gao^{1

2}

Affiliations

¹ College of Fisheries, Key Lab of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, No.1 Shizishan Stress, Hongshan District, Wuhan 430070, Hubei Province, China.
² College of Fisheries, Engineering Research Center of Green Development for Conventional Aquatic Biological Industry in the Yangtze River Economic Belt, Ministry of Education/Hubei Provincial Engineering Laboratory for Pond Aquaculture, Huazhong Agricultural University, Wuhan 430070, China.

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.

Keywords: Animal physiology; Biological sciences; Lipidomics; Physiology.