ID 111353
Author
Guo, Ming-Yu Nihon University
Narita, Takanori Nihon University
Qi, Bing Nihon University
Satoh, Keitaro Nihon University
Katsumata-Kato, Osamu Nihon University
Matsuki-Fukushima, Miwako Nihon University
Fujita-Yoshigaki, Junko Nihon University
Sugiya, Hiroshi Nihon University
Keywords
oxidative stress
β-receptor
diamide
amylase release
parotid acinar cells
Content Type
Journal Article
Description
In parotid acinar cells, activation of β-adrenergic receptors provokes exocytotic amylase release via the accumulation of intracellular cAMP. Cellular redox status plays a pivotal role in the regulation of various cellular functions. Cellular redox imbalance caused by the oxidation of cellular antioxidants, as a result of oxidative stress, induces significant biological damages. In this study, we examined effect of diamide, a thioloxidizing reagent, on amylase release in rat parotid acinar cells. In the presence of diamide, isoproterenol (IPR)-induced cAMP formation and amylase release were partially reduced. Diamide had no effect on amylase release induced by forskolin and mastoparan, an adenylate cyclase activator and heterotrimeric GTP binding protein activator, respectively. In the cells pretreated with diamide, the binding affinity of [3H]dihydroalprenolol to β-receptors was reduced. These results suggest that oxidative stress results in reduction of binding affinity of ligand on β-receptor and consequently reduces protein secretory function in rat parotid acinar cells.
Journal Title
The Journal of Medical Investigation
ISSN
13496867
13431420
NCID
AA11166929
AA12022913
Publisher
Faculty of Medicine Tokushima University
Volume
56
Issue
Supplement
Start Page
284
End Page
286
Sort Key
284
Published Date
2009-12
DOI (Published Version)
URL ( Publisher's Version )
FullText File
language
eng
TextVersion
Publisher