title: Thiol-oxidation reduces the release of amylase induced by β-adrenergic receptor activation in rat parotid acinar cells.
abstract: In parotid acinar cells, the activation of β-adrenergic receptors induces the accumulation of intracellular cAMP, and consequently provokes the exocytotic release of amylase, a digestive enzyme. The cellular redox status plays a pivotal role in regulating various cellular functions. Cellular redox imbalance caused by the oxidation of cellular antioxidants, as a result of oxidative stress, induces significant biological damage. In this study, we examined the effects of diamide, a thiol-oxidizing reagent, on amylase release by rat parotid acinar cells. In cells treated with diamide, the formation of cAMP and the release of amylase induced by the β-agonist isoproterenol (IPR) were partially reduced. The inhibitory effect of diamide on the IPR-induced release of amylase could be abrogated by reduced glutathione or dithiothreitol. Diamide had no effect on the amylase release induced by forskolin, an adenylate cyclase activator, or by mastoparan, a heterotrimeric GTPbinding protein activator. In cells treated with diamide, the binding affinity for [(3)H]DHA, but not the number of binding sites, was reduced. These results suggest that β-adrenergic receptor function is reduced by thiol-oxidation, which inhibits amylase secretion by parotid acinar cells.
authors.affiliation: Department of Physiology, Nihon University School of Dentistry at Matsudo, Chiba, Japan.
authors.forename: Ming-Yu
authors.initials: MY
authors.lastname: Guo
authors.forename: Keitaro
authors.initials: K
authors.lastname: Satoh
authors.forename: Bing
authors.initials: B
authors.lastname: Qi
authors.forename: Takanori
authors.initials: T
authors.lastname: Narita
authors.forename: Osamu
authors.initials: O
authors.lastname: Katsumata-Kato
authors.forename: Miwako
authors.initials: M
authors.lastname: Matsuki-Fukushima
authors.forename: Junko
authors.initials: J
authors.lastname: Fujita-Yoshigaki
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Sugiya
mesh_terms: D000681:Amylases / Q000378:metabolism*; D000818:Animals; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000378:metabolism; D003958:Diamide / Q000494:pharmacology*; D004229:Dithiothreitol / Q000494:pharmacology; D005978:Glutathione / Q000494:pharmacology; D066298:In Vitro Techniques; D036341:Intercellular Signaling Peptides and Proteins; D007545:Isoproterenol / Q000494:pharmacology; D008297:Male; D010084:Oxidation-Reduction; D010306:Parotid Gland / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010455:Peptides / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D011943:Receptors, Adrenergic, beta / Q000187:drug effects* / Q000378:metabolism*; D013439:Sulfhydryl Reagents / Q000494:pharmacology*; D014862:Wasp Venoms / Q000494:pharmacology
chemical_list: D036341:Intercellular Signaling Peptides and Proteins; D010455:Peptides; D011943:Receptors, Adrenergic, beta; D013439:Sulfhydryl Reagents; D014862:Wasp Venoms; D003958:Diamide; D005576:Colforsin; C037500:mastoparan; D000242:Cyclic AMP; D000681:Amylases; D005978:Glutathione; D007545:Isoproterenol; D004229:Dithiothreitol