Cm. Hart et al., OLEIC-ACID REDUCES OXIDANT STRESS IN CULTURED PULMONARY-ARTERY ENDOTHELIAL-CELLS, Experimental lung research, 23(5), 1997, pp. 405-425
Altering the fatty acid composition of cultured porcine pulmonary arte
ry endothelial cells (PAEC) modulates their susceptibility to oxidant
stress. This study demonstrates that supplementing PAEC with oleic aci
d (18:1 omega 9), but not gamma-linolenic acid (18:3 omega 6), provide
d dose-dependent protection from hydrogen peroxide (H2O2)-induced cyto
toxicity. It was hypothesized that 18:1 reduced PAEC susceptibility to
oxidant stress by altering H2O2 metabolism. To test this hypothesis,
confluent PAEC monolayers were treated with 100-200 mu M H2O2 or contr
ol conditions 24 h after supplementation with 0.1 mM 18:1, 18:3, or ve
hicle for 3 h. Intracellular [H2O2] in control cells (14.4-29.0 pM), e
stimated from the rate of aminotriazole-mediated inactivation of endog
enous catalase activity, increased following treatment with 200 mu M H
2O2 (19.0-37.3 pM). Supplementation with 18:1 attenuated increases in
intracellular [H2O2] only in oxidant-exposed cells, whereas supplement
ation with 18:3 attenuated intracellular [H2O2] only in control cells.
Supplementation with 18:1 or 18:3 tended to reduce or enhance PAEC li
pid hydroperoxide content following H2O2 exposure, respectively, but d
id not alter PAEC reduced glutathione content, the activities of gluta
thione peroxidase or catalase, or H2O2 uptake and release. Alteration
of H2O2 metabolism in cultured PAEC may contribute to the ability of f
atty acids to modulate cellular oxidant susceptibility.