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KMID : 0848120060310040127
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International Journal of Oral Biology
2006 Volume.31 No. 4 p.127 ~ p.133
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Dual Effect of H2O2 on the Regulation of Cholecystokinin-induced Amylase Release in Rat Pancreatic Acinar Cells
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An Jeong-Mi
Rhie Jin-Hak
Seo Jeong-Taeg
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Abstract
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[H2O2], a member of reactive oxygen species (ROS), is known to be involved in the mediation of physiological functions in a variety of cell types. However, little has been known about the physiological role of in exocrine cells. Therefore, in the present study, the effect of on cholecystokinin (CCK)-evoked mobilization and amylase release was investigated in rat pancreatic acinar cells. Stimulation of the acinar cells with sulfated octapeptide form of CCK (CCK-8S) induced biphasic increase in amylase release. Addition of enhanced amylase release caused by 10 pM CCK-8S, but inhibited the amylase release induced by CCK-8S at concentrations higher than 100 pM. An ROS scavenger, Mn(III)tetrakis(4-benzoic acid)porphyrin chloride, increased amylase release caused by CCK-8S at concentrations higher than 100 pM, although lower concentrations of CCK-8S-induced amylase release was not affected. To examine whether the effect of on CCK-8S-induced amylase release was exerted via modulation of intracellular signaling, we measured the changes in intracellular concentration in fura-2 loaded acinar cells. Although did not induce any increase in by itself, it increased the frequency and amplitude of oscillations caused by 10 pM CCK-8S. However, had little effect on 1 nM CCK-8S-induced increase in . ROS scavenger, 1 mM N-acetylcysteine, did not affect changes induced by 10 pM or 1 nM CCK-8S. Therefore, it was concluded that enhanced low concentration of CCK-8S-induced amylase release probably by increasing oscillations while it inhibited high concentration of CCK-8S-induced amylase release.
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KEYWORD
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cholecystokinin, amylase release, pancreatic acinar cells, H202
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