Oxidative stress induced by portal vein embolization in fatty liver: Experimental study of a nonalcoholic steatohepatitis model.

The present study aimed to investigate whether excessive oxidative stress production or reduction of antioxidative stress potential may occur following portal vein embolization (PVE) in an experimental animal nonalcoholic steatohepatitis (NASH) model. A NASH rabbit model (n=11) was established by feeding of a fat diet for 4 weeks, and a normal diet rabbit model (n=11) was prepared as a control. The oxidative status of NASH was examined by measuring derivatives of reactive oxygen metabolites (d-ROM) for oxidative stress and biological antioxidative potential (BAP) for antioxidative potential in the NASH model and normal group. Additionally, oxidative status of PVE after 2 weeks was assessed by measuring d-ROM and BAP in the NASH and normal liver models. Oxidative status in a PVE+NASH model was also detected. In the process of NASH creation (fat diet for 4 weeks), total cholesterol was increased in the NASH group (P<0.0001). In the NASH group, PVE induced an increase in serum aspartate transaminase (P=0.0318). At 4 weeks after initiation of the fat diet, a decrease in BAP was determined as statistically significant (P<0.0001). In normal liver, d-ROM production was stimulated in the Sham group after 2 weeks (P=0.0152), but BAP was not altered (P=0.6119). In NASH liver, d-ROM production was stimulated in PVE and Sham groups (P<0.0001 and P=0.0189, respectively), but BAP did not change (P>0.05). In conclusion, decrease of antioxidant potential may promote NASH progression. Additionally, PVE appeared to cause a surge in oxidative stress in NASH liver.