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Am J Physiol Gastrointest Liver Physiol 276: G1-G6, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 1, G1-G6, January 1999

THEMES
Mechanisms of Hepatic Toxicity
V. Necrapoptosis and the mitochondrial permeability transition: shared pathways to necrosis and apoptosis*

John J. Lemasters

Department of Cell Biology & Anatomy, University of North Carolina, Chapel Hill, North Carolina 27799-7090

Opening of a high-conductance pore conducting solutes of molecular mass <1,500 Da causes onset of the mitochondrial permeability transition (MPT). Cyclosporin A blocks this pore and prevents acute necrotic cell death in several models. Confocal microscopy directly visualizes onset of the MPT during acute cytotoxicity from the movement of the green-fluorescing fluorophore, calcein, into the mitochondria from the cytosol. The MPT also plays a causative role in tumor necrosis factor-alpha -induced apoptosis in hepatocytes. Progression to apoptosis or necrosis after the MPT may depend on the presence or absence, respectively, of ATP. Often, features of both apoptotic and necrotic cell death develop after death signals and toxic stresses. The term "necrapoptosis" is introduced to emphasize the shared pathways leading to both forms of cell death.

ATP; confocal microscopy; cyclosporin A; tumor necrosis factor-alpha

* Fifth in a series of invited articles on Mechanisms of Hepatic Toxicity.




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