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Histopathology, markers of liver injury, and regulatory enzymes were measured in terminal liver samples.<\/jats:p><jats:p><jats:bold>Results:\u2002<\/jats:bold> Among the ethanol group, livers showed hepatocellular necrosis together with increased levels of S\u2010adenosylhomocysteine (SAH) and reduced levels of SAM and its ratio to SAH and glutathione (GSH), together with increased malondialdehyde plus hydroxynonenol (MDA\u2003+\u2003HNE) and nitrotyrosine (NT), transcripts and protein levels of cytochrome P4502E1 (CYP2E1), activity of NADPH oxidase, and activity and protein levels of inducible nitric oxide (iNOS). These findings were attenuated partially or completely to control levels by SAM supplementation of the ethanol diet.<\/jats:p><jats:p><jats:bold>Conclusions:\u2002<\/jats:bold> The present results indicate that SAM supplementation attenuates ethanol induced liver injury through its effects on the expressions and activities of oxidative stress pathways, and are consistent with the concept that the pathogenesis of oxidative liver injury is regulated in part through altered hepatic methionine metabolism.<\/jats:p>","DOI":"10.1111\/j.1530-0277.2007.00511.x","type":"journal-article","created":{"date-parts":[[2007,9,16]],"date-time":"2007-09-16T05:39:39Z","timestamp":1189921179000},"page":"1934-1943","source":"Crossref","is-referenced-by-count":27,"title":["S\u2010Adenosylmethionine Attenuates Oxidative Liver Injury in Micropigs Fed Ethanol With a Folate\u2010Deficient Diet"],"prefix":"10.1111","volume":"31","author":[{"given":"Jesus 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