The chloride channel blocker anthracene 9-carboxylate inhibits fatty acid incorporation into phospholipid in cultured human airway epithelial cells.
This study investigated whether making epithelial cell membranes impermeable to Cl- movement affects incorporation of fatty acids into membrane constituents. Epithelial cells were isolated from human nasal polyps, cultured for 5-7 days, and used to test the effect of anthracene 9-carboxylate (9-AC), known to inhibit Cl- conductance across the epithelial membrane, on the incorporation and desaturation of [1-14C]linoleic acid (C18:2,n-6) in experiments of up to 4 h duration. 9-AC (5 mM) reduced C18:2,n-6 incorporation into phospholipid by 60-70%, and increased incorporation of C18:2,n-6 into triacylglycerol by 50-100%. The decrease in C18:2,n-6 incorporation into phospholipid was rapid and dependent on the concentration of 9-AC. Substitution of extracellular Cl- with gluconate significantly decreased C18:2,n-6 incorporation into phospholipid, suggesting that the effect of 9-AC may occur by inhibiting Cl- conductance. Lipid analysis of cells exposed to 50 microM-C18:2 revealed that, as a consequence of the effect of 9-AC, the level of C18:2,n-6 in cell membrane phospholipid was significantly lowered. The relative rate of C18:2,n-6 desaturation was not apparently changed by 9-AC. These data suggest that Cl- conductance may play a role in fatty acid incorporation into epithelial cell membrane phospholipids.[1]References
- The chloride channel blocker anthracene 9-carboxylate inhibits fatty acid incorporation into phospholipid in cultured human airway epithelial cells. Kang, J.X., Man, S.F., Brown, N.E., Labrecque, P.A., Clandinin, M.T. Biochem. J. (1992) [Pubmed]
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