Ischemia-reperfusion (I/Rp) injury to the liver occurs after liver transplantation, shock or in surgical procedures in which
vascular supply to the liver is temporarily abrogated. The extent of I/Rp-mediated injury is dependent on several factors
including duration of ischemia, and in liver transplantation the injury depends also on the temperature of the liver and the
type of preservation solution used (1
). A variety of proteases has been found to be important in mediating I/Rp injury in several organs. Cytoplasmic calcium concentrations
rise dramatically during both ischemia and reperfusion, mainly due to release from intracellular organelles (2
–7
). Increased cytoplasmic calcium concentrations activate several calcium-dependent systems including calpain-like proteases
(8
–11
). Calpain-like proteolytic activity has recently been found to be involved in the pathogenesis of the ischemic brain (12
), heart (13
), kidney (14
), and liver (15
). Other factors may also contribute to increased calpain-like activities such as increased synthesis of calpains, inhibition
by calpastatin, or increased phospholipase activity (16
).