Islet damage attributed to impaired exocrine cells during pancreas preservation and isolation procedure remains
elusive, although released exocrine enzymes could directly damage islets. The aim of this study is to investigate the
cellular mechanisms associated with exocrine cells and their possible impact on the islet cell survival and function after
isolation. Mouse pancreata were stored in cold University of Wisconsin preservation solution for 0, 24 and 48 h and
incubated with or without collagenase at 37°C for 15 min. During preservation, the percentage of exocrine cells with
necrosis, which means impaired cellular membrane that allows intracellular enzymes to be released, remains low (<10%)
regardless of preservation time; whereas the percentage of exocrine cells with apoptosis, which means impaired nucleus
and possible intact cellular membrane, increases over time of preservation. After collagenase-free incubation, however,
the percentage of exocrine cells with necrosis became higher in longer preservation time, and more than 60% of the
necrotic exocrine cells contained apoptosis as well. Islet cells located in pancreata with intact structure are almost kept
away either from necrotic or apoptotic changes even after 48 h preservation followed by collagenase-free incubation.
However, when islets are isolated after collagenase-containing incubation, the percentage of islet cells with necrosis
increases over time of preservation up to approximately 40%. This study suggests that exocrine cells with necrosis could
cause damage of isolated islets when the pancreas is dissociated and that the necrosis in exocrine cells might be induced
mainly as the conversion from apoptosis that has already existed during preservation.