Premium
Quantitative fatty acid analyses in cultured porcine pulmonary artery endothelial cells: The combined effects of fatty acid supplementation and oxidant exposure
Author(s) -
Hart C. Michael,
Tolson J. Keith,
Block Edward R.
Publication year - 1992
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041530111
Subject(s) - fatty acid , chemistry , phospholipid , hydrogen peroxide , biochemistry , membrane
Supplemental fatty acids can modify the oxidant susceptibility of pulmonary artery endothelial cells (PAEC) in monolayer culture. In addition, in vivo dietary modifications have altered tissue and animal susceptibility to a variety of forms of oxidant stress. These modifications of oxidant injury have been attributed to changes in the numbers of fatty acid double bonds in cell lipids. We tested this hypothesis by incubating porcine PAEC in culture medium supplemented with either 0.1 mM oieic acid (18: 1ω9) or with an equivalent volume of ethanol vehicle alone (ETOH‐0.1%) for 3 h. After supplementation, PAEC were exposed to either oxidant stress, 100 μM hydrogen peroxide (H 2 O 2 ) in Hanks' balanced salt solution (HBSS), or to control condition, HBSS alone, for 30 min. Supplemented PAEC were exposed to HBSS or H 2 O 2 either immediately or 24, 48, or 72 h after supplementation. Supplementation with 18:1 protected PAEC from H 2 O 2 ‐induced injury at all time points. The fatty acid composition of PAEC phospholipid (PL), triglyceride (TG), and free fatty acid (FFA) subclasses was determined using thin layer and gas chromatography. The PL fraction contained the majority of PAEC fatty acids, and H 2 O 2 reduced the polyunsaturates in this fraction regardless of supplementation. Supplementation with 18:1 increased the 18:1 content of PAEC PL, TG, and FFA at all time points, modified other fatty acids to a lesser extent, but failed to alter the overall number of fatty acid double bonds at all time points. These results indicate that modification of double bond number does not fully explain the mechanisms by which changes in lipid composition can modulate oxidant injury. © 1992 Wiley‐Liss, Inc © 1992 Wiley‐Liss, Inc.