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Biochem Biophys Res Commun. 2007 Jun 29;358(2):500-5. Epub 2007 May 2.

Necrosis and apoptosis: sequence of liver damage following reperfusion after 60 min ischemia in rats.

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College of Pharmacy, Sungkyunkwan University, 300 Cheoncheon-Dong, Jangan-Gu, Suwon-Si, Gyeonggi-Do, Republic of Korea.


This study evaluated the time-dependent modes of cell death that occur during the course of reperfusion after 60 min ischemia. The serum ALT level increased immediately after reperfusion, peaked at 6 h and then declined gradually thereafter. This was supported by the H&E staining of the liver tissues taken at 2 h reperfusion, which revealed massive peri-portal necrosis. The succinate driven mitochondrial-swelling rate, release of cytochrome c into the cytoplasm, increase in caspase-3 activity and TUNEL stained tissue were measured to determine the changes in the biochemical markers of apoptosis. The biochemical markers of apoptosis increased by 2 h of reperfusion, peaked at 6 h and remained elevated throughout the 24 h reperfusion period. Cyclosporin A, an inhibitor of the mitochondrial permeability transition (MPT), inhibited MPT opening, the release of cytochrome c and caspase-3 activation. This indicates that necrotic death occurs particularly in the peri-portal region in the initial period of reperfusion, and delayed apoptotic death occurs primarily in the peri-central region in the liver tissues undergoing I/R.

[Indexed for MEDLINE]

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