Biochemical changes in transplanted rat liver stored in University of Wisconsin and Euro-Collins solutions.
BACKGROUND: Liver ischemia/reperfusion injury is a severe problem in transplantation, and preservation solutions could be critical for liver viability. The aim of our study was to evaluate the cytosolic and mitochondrial glutathione levels, the glyoxalase II activity, and the mitochondrial hydroperoxide contents of livers stored in different preservation solutions for 7 or 24 h and after transplantation. MATERIALS AND METHODS: Orthotopic liver transplantation was performed without reconstruction of the hepatic artery. The livers were stored at 4 degrees C for 7 or 24 h in University of Wisconsin or Euro-Collins solutions. Portions of livers before and after transplantation were homogenized and mitochondria isolated. RESULTS: Cytosolic glutathione levels were decreased in all stored livers and after transplantation. In livers stored with University of Wisconsin solution, mitochondrial glutathione was unchanged during cold storage and no significant decrease has been found after reperfusion, whereas in livers stored in Euro-Collins solution, mitochondrial glutathione was decreased and a further significant decrease was found 30 min after reperfusion. Mitochondrial hydroperoxides were higher in livers stored in Euro-Collins solution than in University of Wisconsin solution after 30 min of reperfusion. Mitochondrial glyoxalase II did not show any change by reperfusion. CONCLUSION: We have demonstrated that rat liver stored in Euro-Collins solution suffered a severe depletion of mitochondrial GSH and a concomitant increase of hydroperoxides. The data obtained suggested that the livers stored with University of Wisconsin solution were probably less prone to ischemia/reperfusion injury after liver transplantation.[1]References
- Biochemical changes in transplanted rat liver stored in University of Wisconsin and Euro-Collins solutions. Jassem, W., Battino, M., Cinti, C., Norton, S.J., Saba, V., Principato, G. J. Surg. Res. (2000) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg