Takasu N, Komatsu M, Aizawa T, Yamada T
Department of Gerontology, Endocrinology and Metabolism, School of Medicine, Shinshu University, Nagano-ken, Japan.
Biochem Biophys Res Commun. 1988 Sep 15;155(2):569-75. doi: 10.1016/s0006-291x(88)80532-1.
This is the first report to show that pancreatic islet cells generate H2O2 and this H2O2 generation is regulated synergistically by cytoplasmic free calcium ([Ca2+]i) and protein kinase-C. Effects of calcium ionophore A23187 and 12-O-tetradecanoylphorbol 13-acetate (TPA), a tumor promoter, on H2O2 generation were studied in whole pancreatic islets obtained from male Wistar rats. We employed A23187 to elevate cytoplasmic free calcium, and TPA to activate protein kinase-C and monitored continuously their effects on H2O2 generation, measured using homovanillic acid and horseradish peroxidase. A23187 stimulates H2O2 generation. TPA, which activates protein kinase-C, augments this A23187-stimulated H2O2 generation. H2O2 generation is stimulated by an increase in [Ca2+]i and regulated synergistically by [Ca2+]i and protein kinase-C.
这是首份表明胰岛细胞能产生过氧化氢且该过氧化氢生成受细胞质游离钙（[Ca2+]i）和蛋白激酶-C协同调节的报告。在从雄性Wistar大鼠获取的完整胰岛中，研究了钙离子载体A23187和肿瘤促进剂十四酰佛波醇乙酯（TPA）对过氧化氢生成的影响。我们使用A23187升高细胞质游离钙，使用TPA激活蛋白激酶-C，并持续监测它们对用过氧香草酸和辣根过氧化物酶测定的过氧化氢生成的影响。A23187刺激过氧化氢生成。激活蛋白激酶-C的TPA增强了这种A23187刺激的过氧化氢生成。过氧化氢生成受[Ca2+]i增加的刺激，并受[Ca2+]i和蛋白激酶-C协同调节。
