Ann Emerg Med 2001 Sep;38(3):346-7
Children's Hospital, Boston MA.
[Medline record in process]
PMID: 11524662, UI: 21415373
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J Hepatol 2001 Mar;34(3):386-94
Department of Biomedical Sciences, University of Sassari, Italy.
BACKGROUND: 5'-Methylthioadenosine (MTA), a product of S-adenosylmethionine (SAM) catabolism, could undergo oxidation by mono-oxygenases and auto-oxidation. MTA and SAM effects on oxidative liver injury were evaluated in CCl4-treated rats. METHODS: Male Wistar rats were killed 1-48 h after poisoning with a single intraperitoneal CCl4 dose (0.15 ml/100 g) or with the same dose twice a week for 14 weeks. Daily doses of MTA or SAM (384 micromol/kg), started 1 week before acute CCl4 administration or with chronic treatment, were continued up to the time of sacrifice. RESULTS: Acute and chronic CCl4 intoxication decreased MTA and, to a lesser extent, SAM and reduced glutathione (GSH) liver levels. MTA administration increased liver MTA without affecting SAM and GSH. SAM treatment caused complete/partial recovery of these compounds. MTA and, to a lesser extent, SAM prevented an increase in liver phospholipid hydroperoxides in acutely and chronically intoxicated rats and in prolyl hydroxylase activity and trichrome-positive areas in chronically treated rats. MTA prevented upregulation of Tgf-beta1, Collagen-alpha1 (I) and Tgf-alpha genes in liver of chronically intoxicated rats, and TGF-beta1-induced transdifferentiation to myofibroblasts and growth stimulation by platelet-derived growth factor-b of stellate cells in vitro. CONCLUSIONS: MTA and SAM protect against oxidative liver injury through partially different mechanisms.
PMID: 11322199, UI: 21219541
JAMA 2001 Aug 8;286(6):664-5
PMID: 11508310, UI: 21390250
Med J Aust 2001 Jun 18;174(12):665-6; discussion 666-7
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PMID: 11480696, UI: 21373009
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