title: Augmentation of mitochondrial reduced glutathione by S-adenosyl-L-methionine administration in ischemia-reperfusion injury of the rat steatotic liver induced by choline-methionine-deficient diet.
abstract: We examined whether warm ischemia-reperfusion (I/R) damage of the rat steatotic liver can be reduced by administration of S-adenosyl-L-methionine (SAMe). We examined the effect of SAMe on the mitochondrial reduced-glutathione (GSH) pool. Sixty minutes of partial left lobar vascular clamping followed by 2 h of reperfusion were employed for a model of hepatic warm ischemia. Either 5% dextrose or SAMe was injected intraperitoneally 2 h before I/R in steatotic rats (S-D5% or S-SAMe group). Serum liver enzyme concentrations 2 h after reperfusion were significantly lower in the S-SAMe group than in the S-D5% group. The cytosolic and mitochondrial GSH concentrations after I/R were significantly higher in the S-SAMe group than in the S-D5% group (p < 0.05). The cytosolic and mitochondrial oxidized-glutathione/GSH ratios after I/R were significantly greater in the S-D5% group than in the S-SAMe group (p < 0.01). The adenosine triphosphate concentration was higher in the S-SAMe group than in the S-D5% group (p = 0.0515). These results show that hepatocellular and mitochondrial oxidative stress after I/R in the steatotic liver can be reduced by administration of SAMe. The results also show that mitochondrial function and hepatocellular integrity can be restored by administration of SAMe in steatotic rats.
authors.affiliation: Department of Surgery, Showa University Fujigaoka Hospital, Yokohama, Japan.
authors.forename: Y
authors.initials: Y
authors.lastname: Kaneshiro
authors.forename: H
authors.initials: H
authors.lastname: Nakano
authors.forename: K
authors.initials: K
authors.lastname: Kumada
authors.forename: K
authors.initials: K
authors.lastname: Boudjema
authors.forename: N
authors.initials: N
authors.lastname: Kitamura
authors.forename: H
authors.initials: H
authors.lastname: Shimura
authors.forename: A
authors.initials: A
authors.lastname: Barama
authors.forename: G
authors.initials: G
authors.lastname: Kigawa
authors.forename: M
authors.initials: M
authors.lastname: Tatsuno
authors.forename: Y
authors.initials: Y
authors.lastname: Fujiwara
authors.forename: Y
authors.initials: Y
authors.lastname: Baek
authors.forename: J
authors.initials: J
authors.lastname: Sasaki
authors.forename: H
authors.initials: H
authors.lastname: Nagasaki
authors.forename: M
authors.initials: M
authors.lastname: Yamaguchi
mesh_terms: D000818:Animals; D002796:Choline Deficiency / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism*; D019803:Glutathione Disulfide / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D008099:Liver / Q000098:blood supply*; D008297:Male; D008715:Methionine / Q000172:deficiency*; D008930:Mitochondria, Liver / Q000378:metabolism*; D010084:Oxidation-Reduction; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000378:metabolism*; D012436:S-Adenosylmethionine / Q000494:pharmacology*
chemical_list: D012436:S-Adenosylmethionine; D008715:Methionine; D005978:Glutathione; D019803:Glutathione Disulfide