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Acta Physiologica 2012; Volume 206, Supplement 693
Joint FEPS and Spanish Physiological Society Scientific Congress 2012
9/8/2012-9/11/2012
Santiago de Compostela, Spain
MODIFICATION OF MEMBRANE FATTY ACID COMPOSITION AFFECTS CELL DEATH AND ANTIOXIDANT DEFENCES IN CERULEIN-STIMULATED AR42J CELLS.
Abstract number: P128
Lopez-Millan1 MB, Santana1 C, Martinez-Burgos1 MA, Martinez de Victoria1 E, Manas1 M, Yago1 MD
1Department of Physiology, Institute of Nutrition and Food Technology
Objectives:
Fatty acids are important regulators of cell function, both in normal and pathological conditions. We sought to determine whether previous modification of membrane fatty acid profile influences cell death and antioxidant defences in pancreatic AR42J cells challenged with cerulein as a noxious stimulus.
Materials:
AR42J cells were cultured for 72 h in medium enriched with 18:1n-9 (50 μM) or n-3 PUFA (15 mM 20:5n-3 + 10 mM 22:6n-3). Cells cultured in standard medium were used as control1. Gas-liquid chromatography was used to confirm the incorporation of fatty acids into cell membranes. Next, cells were treated for 24h with vehicle or with cerulein at 10-8 M or 10-7 M. Cell death was assessed by flow-cytometry (Immunostep kit). Reduced glutathione (GSH) content was measured in cell lysates (Cayman kit). Means were compared using Student's t-test or one-way ANOVA plus DMS post-hoc test where appropriate; values were considered to be significantly different when P < 0.05.
Results:
Membranes of AR42J cells were enriched with the specific fatty acids provided in the culture medium. Cell death pattern resulting from cerulein stimulation was influenced by membrane fatty acid composition. Cerulein treatment decreased markedly GSH content in cells from the Control group, but a large increase was found in those cells cultivated with 18:1n-9 (oleic acid).
Conclusions:
Cell damage in cerulein-treated pancreatic AR42J cells is modulated by previous modification of membrane fatty acid profile, which may be of pathophysiological relevance.
To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 693 :P128