title: Glutathione decreased parenteral nutrition-induced hepatocyte injury in infant rabbits.
abstract: BACKGROUND
  This study was designed to explore the mechanisms in parenteral nutrition (PN)-associated hepatic dysfunction, and the possible effectiveness of glutathione (GSH) to alleviate this injury.
  
  
  METHODS
  Thirty 1-week-old New Zealand rabbits were divided into 3 groups: 10 in the control group (maternal fed); 10 in the PN group (PN for 10 days); and 10 in the GSH + PN group (PN plus glutathione for 10 days). At the end of the study, blood biochemistry analysis and liver histologic examination were performed by light and electronic microscope; malondialdehyde (MDA) content of liver tissues and apoptotic hepatocytes were also measured.
  
  
  RESULTS
  Direct bilirubin and bile acid in the PN group were significantly higher than that in the control group and in the GSH + PN group (p < .05, for both). In the PN group, there were some cholestatic or steatotic changes. In the GSH + PN group, histologic changes were reduced compared with the PN group. The electron microscopy appearances were in agreement with the histologic findings. MDA value was higher in the PN group than in the control group and in the GSH + PN group (p < .05, respectively). Terminal deoxynucleotidyl transferase mediated nick end labeling (TUNEL) assays showed that the rate of apoptotic hepatocytes in the PN group was the highest and the control group was the lowest among 3 groups (comparison between groups, p < .01, individually.)
  
  
  CONCLUSIONS
  The study showed that PN can induce hepatic dysfunction in infant rabbits. GSH can effectively reduce this injury. The study implies that oxidative stress and apoptosis contribute to PN-associated hepatic dysfunction.
authors.affiliation: Department of Pediatric Surgery, Xinhua Hospital and Shanghai Children's Medical Center, School of Medicine, Shanghai Jiaotong University, Shanghai, China.
authors.forename: Li
authors.initials: L
authors.lastname: Hong
authors.forename: Jiang
authors.initials: J
authors.lastname: Wu
authors.forename: Wei
authors.initials: W
authors.lastname: Cai
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D017209:Apoptosis; D001663:Bilirubin / Q000097:blood; D001774:Blood Chemical Analysis; D056486:Chemical and Drug Induced Liver Injury; D005978:Glutathione / Q000627:therapeutic use*; D022781:Hepatocytes / Q000187:drug effects / Q000378:metabolism; D020287:In Situ Nick-End Labeling; D008099:Liver / Q000378:metabolism* / Q000473:pathology / Q000648:ultrastructure; D008107:Liver Diseases / Q000378:metabolism / Q000473:pathology; D008315:Malondialdehyde / Q000032:analysis; D008854:Microscopy, Electron; D018384:Oxidative Stress; D010288:Parenteral Nutrition / Q000009:adverse effects*; D011817:Rabbits; D011897:Random Allocation; D013047:Specific Pathogen-Free Organisms
chemical_list: D008315:Malondialdehyde; D005978:Glutathione; D001663:Bilirubin