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Journal of Lipid Research, Vol. 43, 944-951, June 2002
Copyright © 2002 by Lipid Research, Inc.

In vitro mimicry of essential fatty acid deficiency in human endothelial cells by TNF impact of -3 versus -6 fatty acids

Konstantin Mayer, Reinhold Schmidt, Marion Muhly-Reinholz, Tina Bögeholz, Stephanie Gokorsch, Friedrich Grimminger and Werner Seeger¹

Medizinische Klinik II, Zentrum für Innere Medizin, Justus-Liebig-University, Klinikstr. 36, D-35392 Giessen, Germany

¹ To whom correspondence should be addressed. e-mail: werner.seeger{at}innere.med.uni-giessen.de

Severe endothelial abnormalities are a prominent feature in sepsis with cytokines such as tumor necrosis factor (TNF) being implicated in the pathogenesis. As mimic to inflammation, human umbilical vascular endothelial cells (HUVEC) were incubated with TNF for 22 h, in the absence or presence of the -6 fatty acid (FA), arachidonic acid (AA), or the alternative -3 FA eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). TNF caused marked alterations in the PUFA profile and long chain PUFA content of total phospholipids (PL) decreased. In contrast, there was a compensatory increase in mead acid [MA, 20:3(-9)], the hallmark acid of the essential fatty acid deficiency (EFAD) syndrome. Corresponding changes were noted in phosphatidylcholine, phosphatidylethanolamine, phosphatidylserine, and phosphatidylinositol, but not in the sphingomyelin fraction. Supplementation with AA, EPA, or DHA markedly increased the respective FA contents in the PL pools, suppressed the increase in MA, and resulted in a shift either toward further predominance of -6 or predominance of -3 FA.

We conclude that short-term TNF incubation of HUVEC causes an EFAD state hitherto only described for long-term malnutrition, and that endothelial cells are susceptible to differential influence by -3 versus -6 FA supplementation under these conditions.

Abbreviations: AA, 20:4-6, all-cis-5,8,11,14-eicosatetraenoic acid, arachidonic acid; CL, cardiolipin; DHA, 22:6-3, all-cis-4,7,10,13, 16,19-docosahexaenoic acid; EFAD, essential fatty acid deficiency syndrome; EPA, 20:5-3, all-cis-5,8,11,14,17-eicosapentaenoic acid; FA, fatty acids; HUVEC, human umbilical venous endothelial cells; LT, leukotriene; OA, 18:1-9, cis-9-octadecenoic acid, oleic acid; PAF, platelet-activating factor; PC, phosphatidylcholine; PE, phosphatidylethanolamine; PG, prostaglandin; PI, phosphatidylinositol; PL, phospholipid; PS, phosphatidylserine; SPH, sphingomyelin; TNF, tumor necrosis factor; 14:0, tetradecanoic acid, myristic acid; 16:0, hexadecanoic acid, palmitic acid; 16:1-7, cis-9-hexadecenoic acid, palmitoleic acid; 18:0, octadecanoic acid, stearic acid; 18:2-6, all-cis-9,12-octadecadienoic acid, linoleic acid; 20:0, eicosanoic acid, arachidic acid; 20:1-9, cis-11-eicosenoic acid; 20:2-6, all-cis-11,14-eicosadienoic acid; 20:3-9, all-cis-5,8,11-eicosatrienoic acid, mead acid; 20:3-6, all-cis-8,11,14-eicosatrienoic acid; 20:3-3, all-cis-11,14,17-eicosatrienoic acid; 22:0, docosanoic acid, behenic acid; 22:1-9, cis-13-docosenoic acid, erucic acid; 22:4-6, all-cis-7,10,13,16-docosatetraenoic acid; 22:5-3, all-cis-7,10,13,16,19-docosapentaenoic acid; 24:0, tetracosanoic acid, lignoceric acid; 24:1-9, cis-15-tetracosenoic acid, nervonic acid

Supplementary key words arachidonic acid • eicosapentaenoic acid • mead acid • phosphatidylinositol • phosphatidylcholine

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