BACKGROUND: Polyenylphosphatidylcholine, a mixture of polyunsaturated phospholipids, prevents the fibrosis induced by alcohol in baboons and by CCl4 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 mumol/L arachidonate supplemented with 20 mumol/L dilinoleoylphosphatidylcholine or 20 mumol/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.
BACKGROUND:Polyenylphosphatidylcholine, a mixture of polyunsaturated phospholipids, prevents the fibrosis induced by alcohol in baboons and by CCl4 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 mumol/L arachidonate supplemented with 20 mumol/L dilinoleoylphosphatidylcholine or 20 mumol/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.
Authors: A Gigliozzi; R Romeo; F Fraioli; A Cantafora; M Delle Monache; A Cardilli; A F Attili; E Scafato; L Carli; D Alvaro Journal: Dig Dis Sci Date: 1998-10 Impact factor: 3.199