The pancreas is vulnerable to
ethanol toxicity, but the pathogenesis of
alcoholic pancreatitis is not fully defined. The intracellular oxidative balance and the characteristics of the secretion of isolated rat pancreatic acinar cells stimulated with the
cholecystokinin analogue
cerulein were assayed after acute oral
ethanol (4 g/kg) load. Pancreatic acinar cells from
ethanol-treated rats showed a significant (p < 0.02) lower content of total
glutathione and
protein sulfhydryls, and higher levels of
oxidized glutathione (p < 0.03),
malondialdehyde, and
protein carbonyls (p < 0.05).
Ethanol-intoxicated acinar cells showed a lower baseline
amylase output compared to controls, with the difference being significantly exacerbated by
cerulein stimulation. After
cerulein, the release of
protein carbonyls by
ethanol-treated cells was significantly increased, whereas that of
protein sulfhydryls was significantly decreased. In conclusion,
ethanol oxidatively damages pancreatic acinar cells;
cerulein stimulation is followed by a lower output of
amylase and by a higher release of oxidized
proteins by pancreatic acinar cells from
ethanol-treated rats. These findings may account for the decreased exocrine function, intraductular plug formation, and
protein precipitation in
alcoholic pancreatitis.