title: Dilinoleoylphosphatidylcholine is the active antioxidant of polyenylphosphatidylcholine.
abstract: 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.affiliation: Section of Liver Disease & Nutrition and Alcohol Research Center, Bronx VA Medical Center, New York, NY, USA.
authors.forename: S I
authors.initials: SI
authors.lastname: Aleynik
authors.forename: M A
authors.initials: MA
authors.lastname: Leo
authors.forename: U
authors.initials: U
authors.lastname: Takeshige
authors.forename: M K
authors.initials: MK
authors.lastname: Aleynik
authors.forename: C S
authors.initials: CS
authors.lastname: Lieber
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D016718:Arachidonic Acid / Q000633:toxicity; D006528:Carcinoma, Hepatocellular / Q000139:chemically induced / Q000473:pathology; D016923:Cell Death / Q000187:drug effects / Q000235:genetics; D002470:Cell Survival / Q000187:drug effects / Q000235:genetics; D004273:DNA, Neoplasm / Q000187:drug effects; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation / Q000187:drug effects; D008114:Liver Neoplasms, Experimental / Q000139:chemically induced / Q000473:pathology; D018384:Oxidative Stress; D010713:Phosphatidylcholines / Q000494:pharmacology*; D051381:Rats; D014407:Tumor Cells, Cultured
chemical_list: D000975:Antioxidants; D004273:DNA, Neoplasm; D010713:Phosphatidylcholines; C005152:lipostabil; D016718:Arachidonic Acid; C002448:1,2-linoleoylphosphatidylcholine; D007770:L-Lactate Dehydrogenase