title: Polyenylphosphatidylcholine protects against alcohol but not iron-induced oxidative stress in the liver.
abstract: BACKGROUND
  We reported before that, in baboons, the alcohol-induced oxidative stress in the liver is associated with depletion of dilinoleoylphosphatidylcholine [the major component of polyenylphosphatidylcholine (PPC)] and that both can be corrected by the administration of PPC, but we did not determine whether this protection extended to iron-induced oxidative stress.
  
  
  METHODS
  To compare the effects of PPC on alcohol- and iron-induced hepatic oxidative stress, 56 Sprague Dawley male rats were pair-fed nutritionally adequate liquid diets containing ethanol (36% of energy) or isocaloric carbohydrate and PPC (3 mg/ml) or safflower oil (2.73 mg/ml), with or without 5 mg/ml carbonyl iron for 2 months. Markers of oxidative stress (4-hydroxynonenal and reduced glutathione), antioxidants (vitamin E, ubiquinol-9, and ubiquinol-10), and phosphatidylcholine (PC) species were assessed by HPLC and/or gas chromatography/mass spectrometry.
  
  
  RESULTS
  Alcohol feeding increased hepatic 4-hydroxynonenal 3-fold and decreased glutathione by 19%, ubiquinol-10 by 53%, and PC species containing arachidonate (palmitoyl- and stearoylarachidonoylphosphatidylcholines by 24% and 21%, respectively) and total phospholipids by 14%. PPC feeding prevented the rise of 4-hydroxynonenal, restored glutathione, and increased the hepatic content of dilinoleoylphosphatidylcholine and of some other PC carrying polyunsaturated fatty acids. Administration of iron alone increased hepatic iron, doubled 4-hydroxynonenal and glutathione, whereas it decreased vitamin E, ubiquinol-9, total phospholipids, and several polyunsaturated PC. Alcohol given with iron further exacerbated the hepatic oxidative stress, as documented by the increase of 4-hydroxynonenal and the decrease in glutathione and ubiquinols-10. PPC did not prevent this oxidative stress, although it increased hepatic glutathione. Hepatic dilinoleoylphosphatidylcholine content was comparable with and without dietary iron.
  
  
  CONCLUSIONS
  PPC prevents the alcohol-induced oxidative stress but only in the absence of iron overload.
authors.affiliation: Section of Liver Disease and Nutrition and Alcohol Research Center, Bronx VA Medical Center and Mount Sinai School of Medicine, New York, New York 10468, USA.
authors.forename: S I
authors.initials: SI
authors.lastname: Aleynik
authors.forename: M A
authors.initials: MA
authors.lastname: Leo
authors.forename: M K
authors.initials: MK
authors.lastname: Aleynik
authors.forename: C S
authors.initials: CS
authors.lastname: Lieber
mesh_terms: D000818:Animals; D002492:Central Nervous System Depressants / Q000494:pharmacology*; D000431:Ethanol / Q000494:pharmacology*; D005217:Fat Emulsions, Intravenous / Q000494:pharmacology*; D019266:Iron, Dietary / Q000494:pharmacology*; D015227:Lipid Peroxidation / Q000187:drug effects; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D010713:Phosphatidylcholines / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D002492:Central Nervous System Depressants; D005217:Fat Emulsions, Intravenous; D019266:Iron, Dietary; D010713:Phosphatidylcholines; C005152:lipostabil; D000431:Ethanol