Uptake and metabolic conversion of saturated and unsaturated fatty acids in Hep2 human larynx tumor cells

Research on fatty acid metabolism in cultured human larynx tumor cells Hep2 was carried out. The cells were incubated with either a saturated (palmitic) or a polyunsaturated (linoleic, α -linolenic and eicosatrienoic (n-6)) radioactive fatty acid (0.66 μ M, 24 h). The best incorporation capacity was...

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Published inProstaglandins, leukotrienes and essential fatty acids Vol. 65; no. 5-6; pp. 295 - 300
Main Authors Albino, L., Polo, M.P., de Bravo, M.G., de Alaniz, M.J.T.
Format Journal Article
LanguageEnglish
Published Kidlington Elsevier Ltd 01.11.2001
Elsevier
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Summary:Research on fatty acid metabolism in cultured human larynx tumor cells Hep2 was carried out. The cells were incubated with either a saturated (palmitic) or a polyunsaturated (linoleic, α -linolenic and eicosatrienoic (n-6)) radioactive fatty acid (0.66 μ M, 24 h). The best incorporation capacity was observed in the linoleic acid followed by α -linolenic, palmitic and eicosatrienoic acids. All fatty acids tested were anabolized to higher derivatives within their own family. Palmitic acid was primarily monodesaturated rather than elongated, proving to have a very active Δ 9 desaturase activity. With respect to polyunsaturated acid metabolism, the conversion of α -linolenic acid to higher homologs, although better than linoleic acid, occurred far less efficiently than that observed in other non-highly undifferentiated human tumor cells. This impairment in higher polyunsaturated fatty acid biosynthesis, reflected in the low levels of arachidonic acid in the fatty acid composition, would not reside in the Δ 5 desaturation step since Hep2 cells can readily convert eicosatrienoic acid into arachidonic acid. Considering the potential regulatory role of specific polyunsaturated fatty acids in the cell proliferative control, the knowledge of the metabolism of fatty acids in this human tumor cell would be important for designing future experiments in order to clarify the mechanism involved in balance, proliferation and cell death.
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ISSN:0952-3278
1532-2823
DOI:10.1054/plef.2001.0328