title: Oxidative stress, hepatocellular integrity, and hepatic function after initial reperfusion in human hepatic transplantation.
abstract: BACKGROUND
  The mechanisms underlying liver graft dysfunction are not completely defined, although much of the injury derives from oxidative stress in organ reperfusion. The antioxidant glutathione in its reduced form (GSH) is an important agent to detoxify oxygen species after reperfusion. However, this effect might be limited by low concentrations at the end of cold storage. The objective of this study was to evaluate GSH and glutathione oxidized (GSSG) hepatic levels pre- and postreperfusion and correlate with hepatocellular injury and liver function in the 5 subsequent days after transplantation.
  
  
  METHODS
  Liver biopsies were taken immediately before implant and 2 hours after venous reperfusion in 34 grafts, determining GSH, GSSG levels, and GSSG/GSH ratio. Aminotransferases (ALT, AST) and PT were measured for 5 days.
  
  
  RESULTS
  There was a strong decrease in GSH concentration (P <.0001), increase of GSSG levels (P <.01), and increase of the GSSG/GSH ratio (P <.0001). No correlations were found between GSH, GSSG, or GSH/GSSH levels and AST, ALT, and PT.
  
  
  CONCLUSIONS
  Glutathione levels showed significant changes after 2 hours of reperfusion, due to intense oxidative stress. Therapies to replenish GSH should be considered as a protective measure to avoid liver graft dysfunction after transplantation.
authors.affiliation: Liver Transplantation Group, Irmandade Santa Casa de Misericórdia de Porto Alegre, Brazil. tomgrez@terra.com.br
authors.forename: T J M
authors.initials: TJ
authors.lastname: Grezzana
authors.forename: C O
authors.initials: CO
authors.lastname: Corso
authors.forename: M L
authors.initials: ML
authors.lastname: Zanotelli
authors.forename: C A
authors.initials: CA
authors.lastname: Marroni
authors.forename: A B M
authors.initials: AB
authors.lastname: Brandão
authors.forename: E
authors.initials: E
authors.lastname: Schlindwein
authors.forename: I
authors.initials: I
authors.lastname: Leipnitz
authors.forename: M H M
authors.initials: MH
authors.lastname: Meine
authors.forename: A
authors.initials: A
authors.lastname: Fleck
authors.forename: A
authors.initials: A
authors.lastname: Cassal
authors.forename: L
authors.initials: L
authors.lastname: Hope
authors.forename: R
authors.initials: R
authors.lastname: Hoppen
authors.forename: G
authors.initials: G
authors.lastname: Kiss
authors.forename: A L M
authors.initials: AL
authors.lastname: Gleisner
authors.forename: T
authors.initials: T
authors.lastname: Cerski
authors.forename: A
authors.initials: A
authors.lastname: Bellò-Klein
authors.forename: V
authors.initials: V
authors.lastname: Severo
authors.forename: C
authors.initials: C
authors.lastname: Innocenti
authors.forename: G P C
authors.initials: GP
authors.lastname: Cantisani
mesh_terms: D000241:Adenosine; D000328:Adult; D000493:Allopurinol; D002423:Cause of Death; D005260:Female; D005978:Glutathione / Q000378:metabolism; D019803:Glutathione Disulfide / Q000378:metabolism; D022781:Hepatocytes / Q000166:cytology*; D006801:Humans; D007328:Insulin; D008099:Liver; D008111:Liver Function Tests; D016031:Liver Transplantation / Q000401:mortality / Q000502:physiology*; D008297:Male; D009926:Organ Preservation / Q000379:methods; D019188:Organ Preservation Solutions; D018384:Oxidative Stress / Q000502:physiology*; D011887:Raffinose; D015427:Reperfusion Injury; D012189:Retrospective Studies
chemical_list: D007328:Insulin; D019188:Organ Preservation Solutions; C055206:University of Wisconsin-lactobionate solution; D000493:Allopurinol; D005978:Glutathione; D000241:Adenosine; D011887:Raffinose; D019803:Glutathione Disulfide