Abstract
Abstract In liver transplantation primary graft nonfunction (PGN) occurs in 10–15% of all cases. The cause of PGN is likely associated with free radical and lipid peroxidation at reperfusion, however, the mechanism of PGN is still unknown. We investigated in rats the electron leakage of mitochondria, i.e., free radical generation, and lipid peroxidation of mitochondria after cold ischemia to clarify the mechanism of PGN. After cold ischemia, generation of free radical was recognized, but decreased in proportion to cold ischemic time. The chemiluminescence value increased slightly after 8 h of cold ischemia, however, thereafter gradually decreased. Mitochondrial ATP synthesis also decreased in proportion to cold ischemic time. From these results we concluded that free radical generation occurs while the mitochondria maintain energy synthesis and the generation of free radical decreases with cold preservation. Although mitochondria with cold ischemia suffer lipid peroxidation with ease, leaked electrons from the mitochondria are not a main cause of the lipid peroxidation of mitochondria at reperfusion.
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