A secondary metabolite, 4,5-dibromopyrrole-2-carboxylic acid, from marine sponges of the genus Agelas alters cellular calcium signals

A secondary metabolite, 4,5-dibromopyrrole-2-carboxylic acid, from marine sponges of the genus Agelas alters cellular calcium signals
复制标题

DOI:
10.1016/j.etap.2004.12.003
复制
发表时间:
2005-05-01
影响因子:
4.3
通讯作者:
Schütt, C
Schütt, C
中科院分区:
环境科学与生态学3区
文献类型:
--
作者:
Bickmeyer, U;Assmann, M;Schütt, C

文献摘要

被引文献

相似文献

研究了Agelas属海绵的次级代谢产物4,5-二溴吡咯-2-羧酸对PC 12细胞中细胞钙稳态的影响。4,5-二溴吡咯-2-羧酸如果单独应用而没有细胞去极化,则不改变细胞内钙水平。在使用高钾溶液的细胞膜去极化期间,使用Fura II作为钙指示剂揭示了细胞内钙升高的剂量依赖性降低。在一系列实验中,在高于30 μ M的浓度下观察到显著降低,但在单个实验中,300 nM的浓度仍然是可逆有效的。在相同浓度范围内,4,5-二溴吡咯-2-羧酸显著延迟去极化诱导的钙升高。去极化诱发的钙升高的剂量依赖性减少和延迟可能是由于通过电压操作的钙通道的钙进入减少。4,5-二溴吡咯-2-羧酸对鱼类的拒食潜力的一种细胞作用模式可能是与暴露细胞的细胞钙稳态相互作用。(c)2005 Elsevier B. V.保留所有权利。
A secondary metabolite from sponges of the genus Agelas, 4,5-dibromopyrrole-2-carboxylic acid, which is well known as feeding deterrent, was investigated for effects on the cellular calcium homeostasis in PC12 cells. 4,5-Dibromopyrrole-2-carboxylic acid did not change intracellular calcium levels if applied alone without cell depolarization. During depolarization of the cellular membrane using high potassium solution, a dose dependent reduction of intracellular calcium elevation was revealed utilizing Fura II as calcium indicator. Significant reduction was seen at concentrations higher than 30 mu M in a series of experiments, but in single experiments a concentration of 300 nM was still reversible effective. In the same concentration range, the onset of depolarization induced calcium elevations was significantly delayed by 4,5-dibromopyrrole-2-carboxylic acid. Dose dependent reduction and delay of depolarization evoked calcium elevations are probably due to a reduction of calcium entry via voltage operated calcium channels. One cellular mode of action of the feeding deterrent potential of 4,5-dibromopyrrole-2-carboxylic acid to fishes may be an interaction with the cellular calcium homeostasis of exposed cells. (c) 2005 Elsevier B.V. All rights reserved.