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Department of Human Biology and Nutritional Sciences, University of Guelph, Guelph, Ontario, Canada N1G 2W1
1To whom correspondence should be addressed, (519) 824-4120 Ext. 3742, (519) 763-5902 Fax, kmeckling.ns@aps.uoguelph.ca
The control of proliferation and epithelial restitution are processes
that are poorly understood. The effects of (n-3), (n-6) and
trans fatty acids on proliferation of subconfluent IEC-6
cultures and restitution of wounded IEC-6 monolayers were investigated.
Incorporation of supplemented fatty acids into cellular phospholipid
was also assessed. Sulforhodamine B protein dye binding assay was
utilized to assess the proliferative effects of fatty acids on growth
of IEC-6 cultures. Incorporation of supplemental fatty acids into
cellular phospholipid was examined by thin-layer chromatography
combined with gas chromatography. The modulation of epithelial
restitution was examined by razor blade wounding confluent IEC-6
monolayers grown in media supplemented with various fatty acids.
Inhibition of eicosanoid synthesis by indomethacin during the wounding
assay was also assessed. Both (n-3) and (n-6) fatty acids significantly
inhibited growth of this intestinal epithelial cell model at
concentrations above 125 µmol/L. The trans fatty acid,
linoelaidate 18:2(n-6)trans, inhibited growth of IEC-6 cells
at concentrations above 250 µmol/L. Another trans fatty
acid, elaidate 18:1(n-9)trans, was well-tolerated at
concentrations as high as 500 µmol/L. Eicosapentanoic 20:5(n-3),
linoleic 18:2(n-6),
-linolenic 18:3(n-3),
-linolenic 18:3(n-6)
and arachidonic 20:4(n-6) acids all significantly enhanced cellular
migration in the IEC-6 model of wound healing. Eicosapentanoate,
linoleate,
-linolenate,
-linolenate and arachidonate are all
capable of improving reconstitution of epithelial integrity following
mucosal injury. Inhibition of eicosanoid synthesis reduced the
enhancement of restitution by n-6 fatty acids back to control
levels.
KEY WORDS: restitution fatty acid rats IEC-6 cells wound healing
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