['Since the late stages of alcoholic liver injury are associated with decreased activity of methionine adenosyltransferase (MAT), we wondered whether this already occurs at the early stages and what is the mechanism involved.', 'Sprague-Dawley rats (n = 32) were pair-fed ethanol (36% of energy) or isocaloric carbohydrates (control) in Lieber-DeCarli liquid diets, with or without polyenylphosphatidylcholine (PPC).', 'After 2 months, there was a striking depletion of S-adenosylmethionine (measured by high-performance liquid chromatography) from 68.2 +/- 5.1 to 36.2 +/- 3.4 nmol/g, associated with a reduction in hepatic reduced glutathione (GSH) from 4.95 +/- 0.20 to 4.09 +/- 0.08 micro mol/g, and an increase from 0.24 +/- 0.02 to 0.47 +/- 0.07 nmol/g of 4-hydroxynonenal (4-HNE), a reliable marker of lipid peroxidation. Hepatic S-adenosylmethionine (SAMe) correlated positively with GSH (r = 0.5916) and negatively with 4-HNE (r = -0.6375). Feeding PPC corrected all values and MAT activity did not differ significantly between groups.'] Does polyenylphosphatidylcholine correct the alcohol-induced hepatic oxidative stress by restoring s-adenosylmethionine?