钙螯合对大鼠腮腺细胞中环磷酸腺苷介导的胞吐作用的抑制是由于细胞内三磷酸腺苷水平降低所致。

The inhibition of cyclic AMP-mediated exocytosis from rat parotid cells by calcium chelation is due to depression of cellular ATP.

作者信息

Hincke M T

机构信息

Department of Anatomy, Faculty of Health Sciences, University of Ottawa, Canada.

出版信息

Biochim Biophys Acta. 1988 Nov 17;967(2):204-10. doi: 10.1016/0304-4165(88)90010-4.

DOI:10.1016/0304-4165(88)90010-4

PMID:2461228

Abstract

The role of second messenger calcium in cAMP-mediated exocytosis from parotid cell aggregates has been assessed following extracellular (ethylene glycol bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA] and intracellular (quin2) calcium chelation. Only in the former case was inhibition (60-70%) of isoproterenol- and N6,O2-dibutyryl cAMP-stimulated amylase release observed. This inhibition was accompanied by a 70% decrease in cellular ATP levels. Depression of ATP levels with mitochondrial inhibitors was also correlated with inhibition of amylase secretion. Overall, our results suggest that depletion of cellular Ca2+ with EGTA leads to an inhibition of mitochondrial function and that these experimental conditions are therefore inappropriate for the evaluation of the role of cytosolic Ca2+ transients during stimulus-secretion coupling.

摘要

在细胞外（乙二醇双（β-氨基乙醚）-N，N，N'，N'-四乙酸（EGTA））和细胞内（喹啉2）钙螯合后，已评估了第二信使钙在腮腺细胞聚集体中cAMP介导的胞吐作用中的作用。仅在前一种情况下，观察到异丙肾上腺素和N6，O2-二丁酰cAMP刺激的淀粉酶释放受到抑制（60-70%）。这种抑制伴随着细胞ATP水平下降70%。用线粒体抑制剂降低ATP水平也与淀粉酶分泌的抑制相关。总体而言，我们的结果表明，用EGTA耗尽细胞Ca2+会导致线粒体功能受到抑制，因此这些实验条件不适用于评估刺激-分泌偶联过程中胞质Ca2+瞬变的作用。