From the hypothesis that in TNF-alpha -resistant cells the activity of mito
chondrial phospholipase A2 could be reversed by a lysophospholipid acyltran
sferase, we report that the mitochondrial reacylation of phosphatidylcholin
e as phosphatidylethanolamine was considerably higher in C6 (TNF-alpha -res
istant) than in WEHI-164 (TNF-alpha -sensitive) cells. TNF-alpha did not mo
dify the phospholipids' reacylation in C6, while in WEHI-164 it was increas
ed several-fold. These results suggest that TNF-alpha is not sufficient to
restore the barrier permeability in sensitive cells, but may be enough to e
xplain the absence of permeability change in resistant cells, AcylCoA ester
s, depending on whether the acyl group is unsaturated or saturated (palmiti
c acid), could control membrane permeability either by participating in the
reacylation of phospholipids or keeping the pore in a closed state. The an
alysis of the endogenous acvlCoA ester pools of both cell lines show that t
he amount of palmitoylCoA is higher in resistant than sensitive cell lines.
TNF-alpha treatment does not change these results. (C) 2001 Academic Press
.