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 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...

Descripción completa

Guardado en:

Detalles Bibliográficos
Autores principales:	Shouxiang Sun, Xiaojuan Cao, Jian Gao
Formato:	article
Lenguaje:	EN
Publicado:	Elsevier 2021
Materias:	Biological sciences Physiology Animal physiology Lipidomics Science Q
Acceso en línea:	https://doaj.org/article/f299753919c14609a250255871d05243
Etiquetas:	Agregar Etiqueta Sin Etiquetas, Sea el primero en etiquetar este registro!

id	oai:doaj.org-article:f299753919c14609a250255871d05243
record_format	dspace
spelling	oai:doaj.org-article:f299753919c14609a250255871d052432021-11-20T05:11:21ZC24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage2589-004210.1016/j.isci.2021.103409https://doaj.org/article/f299753919c14609a250255871d052432021-12-01T00:00:00Zhttp://www.sciencedirect.com/science/article/pii/S2589004221013808https://doaj.org/toc/2589-0042Summary: 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.Shouxiang SunXiaojuan CaoJian GaoElsevierarticleBiological sciencesPhysiologyAnimal physiologyLipidomicsScienceQENiScience, Vol 24, Iss 12, Pp 103409- (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	Biological sciences Physiology Animal physiology Lipidomics Science Q
spellingShingle	Biological sciences Physiology Animal physiology Lipidomics Science Q Shouxiang Sun Xiaojuan Cao Jian Gao C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage
description	Summary: 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.
format	article
author	Shouxiang Sun Xiaojuan Cao Jian Gao
author_facet	Shouxiang Sun Xiaojuan Cao Jian Gao
author_sort	Shouxiang Sun
title	C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage
title_short	C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage
title_full	C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage
title_fullStr	C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage
title_full_unstemmed	C24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage
title_sort	c24:0 avoids cold exposure-induced oxidative stress and fatty acid β-oxidation damage
publisher	Elsevier
publishDate	2021
url	https://doaj.org/article/f299753919c14609a250255871d05243
work_keys_str_mv	AT shouxiangsun c240avoidscoldexposureinducedoxidativestressandfattyacidboxidationdamage AT xiaojuancao c240avoidscoldexposureinducedoxidativestressandfattyacidboxidationdamage AT jiangao c240avoidscoldexposureinducedoxidativestressandfattyacidboxidationdamage
_version_	1718419575864819712

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

Ejemplares similares