Abstract
Background
Polyenylphosphatidylcholine, a mixture of polyunsaturated phospholipids, prevents the fibrosis induced by alcohol in baboons and by CCl, in rats and opposes the associated oxidative stress.
Methods
To determine the responsible phosphatidylcholine species, a Morris hepatoma cell line (RH 7777) was incubated with 100 µmol/L arachidonate supplemented with 20 µmol/L dilinoleoylphosphatidylcholine or 20 µmol/L palmitoyllinoleoylphosphatidylcholine which comprise 42% and 24% of polyenylphosphatidylcholine, respectively or with equivalent amounts of polyenylphosphatidylcholine. Distearoylphosphatidylcholine, the saturated analog of dilinoleoylphosphatidylcholine, also was used for comparison. Two markers of lipid peroxidation (4-hydroxynonenal and F2-isoprostanes) were measured by GC/MS.
Results
Arachidonate caused 8- and 11-fold rises of cellular 4-hydroxynonenal and F2-isoprostanes, respectively; these increases were reduced more than 50% by polyenylphosphatidylcholine and dilinoleoylphosphatidylcholine. By contrast, palmitoyllinoleoylphosphatidylcholine and distearoylphosphatidylcholine had no significant effect. Lipid peroxidation was associated with a striking exacerbation of cell death, observed microscopically, and documented by a 2.5-fold decrease in cellular DNA and a 2- to 3-fold increase in lactic dehydrogenase leakage. Dilinoleoylphosphatidylcholine and polyenylphosphatidylcholine decreased the release of lactic dehydrogenase (47% and 67%, respectively); whereas, palmitoyllinoleoylphosphatidylcholine had no effect.
Conclusions
An in vitro system of oxidative stress revealed that polyenylphosphatidylcholine is a potent antioxidant and that dilinoleoylphosphatidylcholine is mainly responsible for this protective effect; whereas, its saturated counterpart distearoylphosphatidylcholine is inactive.
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