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Deregulation of iron homeostasis and cold‐preservation injury to rat liver stored in University of Wisconsin solution
Author(s) -
Wyllie Samuel,
Seu Philip,
Gao Feng Q.,
Goss John A.
Publication year - 2003
Publication title -
liver transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.814
H-Index - 150
eISSN - 1527-6473
pISSN - 1527-6465
DOI - 10.1053/jlts.2003.50065
Subject(s) - viaspan , homeostasis , ferritin , cold storage , liver injury , medicine , liver transplantation , heme , metabolism , heme oxygenase , reactive oxygen species , endocrinology , biochemistry , transplantation , chemistry , biology , enzyme , horticulture
Very little is known about iron metabolism and the mediators of iron metabolism in liver subjected to cold storage before transplantation. Therefore, in this study, we investigated the effect of cold storage on iron homeostasis in the rat liver. When livers were stored at 4°C in University of Wisconsin solution for up to 6 and 24 hours, significant increases occurred in the labile iron pool, ferritin protein, and heme oxygenase activity. Significant decreases in heme content and iron regulatory protein 1 and 2 binding activities occurred by 24 hours. Liver injury indicated by significant increases in University of Wisconsin solution transaminase activity and liver lipid hydroperoxide levels occurred by 6 and 24 hours. Taken together, these results suggest that during pretransplantation cold storage of the liver, an aberrant iron homeostasis develops that contributes to preservation injury, and predisposes the liver to reperfusion injury by iron‐dependent reactive oxygen species/Fenton reaction.