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

We examined whether warm ischemia-reperfusion (I/R) damage of the rat steatotic liver can be reduced by administration of S-adenosyl-L-methi onine (SAMe). We examined the effect of SAMe on the mitochondrial redu ced-glutathione (GSH) pool. Sixty minutes of partial left lobar vascul ar clamping followed by 2 h of reperfusion were employed for a model o f hepatic warm ischemia. Either 5% dextrose or SAMe was injected intra peritoneally 2 h before I/R in steatotic rats (S-D5% or S-SAMe group). Serum liver enzyme concentrations 2 h after reperfusion were signific antly lower in the S-SAMe group than in the S-D5% group. The cytosolic and mitochondrial GSH concentrations after I/R were significantly hig her in the S-SAMe group than in the S-D5% group (p < 0.05). The cytoso lic and mitochondrial oxidized-glutathione/GSH ratios after I/R were s ignificantly greater in the S-D5% group than in the S-SAMe group (p < 0.01). The adenosine triphosphate concentration was higher in the S-SA Me group than in the S-D5% group (p = 0.0515). These results show that hepatocellular and mitochondrial oxidative stress after I/R in the st eatotic liver can be reduced by administration of SAMe. The results al so show that mitochondrial function and hepatocellular integrity can b e restored by administration of SAMe in steatotic rats.