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  • Title: Glutathione might exert an important function in caerulein-stimulated amylase release in isolated rat pancreatic acini.
    Author: Yu H, Klonowski-Stumpe H, Lüthen R.
    Journal: Pancreas; 2002 Jan; 24(1):53-62. PubMed ID: 11741183.
    Abstract:
    AIMS: The effect of different modes of thiol depletion on pancreatic exocrine secretory function and potential mechanisms of interference with the secretory process in pancreatic acinar cells were investigated. METHODOLOGY: After incubation with three thiol-modulating agents (L-buthionine sulfoximine, ethacrynic acid, and diamide) for 30 minutes, caerulein-stimulated amylase release and cholecystokinin (CCK) receptor binding characteristics were assessed in isolated rat pancreatic acini. The level of thiol groups (glutathione and protein thiols) and cytosolic-free calcium were measured in pancreatic acinar cells. RESULTS: All three thiol-modulating agents decreased caerulein (10(-10)M)-stimulated amylase release and the level of pancreatic acinar glutathione in a dose-dependent fashion without a marked increase in cell damage. Diamide also diminished the level of protein thiols. Ethacrynic acid and diamide, but not L-buthionine sulfoximine, inhibited the caerulein (10(-9)M)-induced Ca(2+) mobilization in pancreatic acinar cells. None of the three thiol-modulating agents altered the CCK receptor binding characteristics. CONCLUSION: The present findings strongly suggest an important role of glutathione in the secretory process in pancreatic acinar cells and in the secretory blockade observed in acute pancreatitis. A decrease in caerulein-induced Ca(2+) mobilization might participate in the inhibition of amylase release by some oxidative agents, but it is not the prominent cause in general.
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