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硫柳汞诱导人内皮细胞内钙的变化。

Thimerosal induced changes of intracellular calcium in human endothelial cells.

作者信息

Gericke M, Droogmans G, Nilius B

机构信息

Max Planck Group of Molecular and Cellular Physiology, Leuven, Belgium.

出版信息

Cell Calcium. 1993 Mar;14(3):201-7. doi: 10.1016/0143-4160(93)90067-g.

DOI:10.1016/0143-4160(93)90067-g
PMID:8500136
Abstract

We have measured the effects of the -SH oxidizing agent thimerosal on the intracellular calcium concentration in single endothelial cells from human umbilical cord vein. Application of 1 microM thimerosal after a 10 s prepulse of 10 microM evoked oscillations of intracellular calcium. Concentrations higher than 10 microM induced a few oscillations which were followed by a long lasting increase in intracellular calcium between 120 and 980 nM at 10 microM thimerosal, between 250 and 1290 nM at 100 microM. The plateau level of the thimerosal induced increase in intracellular calcium depended on the extracellular calcium concentration, and was clearly decreased in calcium free solution. It was also reduced if the extracellular potassium concentration was increased to 140 mM. Nickel (5 mM) did not block the elevation of intracellular calcium. Thimerosal induced quenching of the Fura-2 fluorescence in Ca2+ free solutions containing 1 mM Mn2+. These effects indicate that thimerosal opens a pathway for Ca2+ entry from the extracellular side. The amount of calcium which could be released by histamine was drastically reduced after initiation of the thimerosal response. If refilling of Ca2+ stores was prevented by incubation of the cells in Ca2+ free solution, histamine still induced a transient, but not maintained, increase in [Ca2+]i. After application of thimerosal in Ca2+ free solutions to prevent refilling of the stores, a transient increase in [Ca2+]i could still be recorded but the histamine response on [Ca2+]i almost disappeared indicating a discharge of Ca2+ stores by thimerosal.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

我们已测量了含硫氢基(-SH)的氧化剂硫柳汞对人脐静脉单个内皮细胞内钙浓度的影响。在施加10微摩尔的预脉冲10秒后,施加1微摩尔硫柳汞会诱发细胞内钙振荡。高于10微摩尔的浓度会诱发少量振荡,随后细胞内钙会持续增加,在10微摩尔硫柳汞时,细胞内钙浓度在120至980纳摩尔之间,在100微摩尔时,在250至1290纳摩尔之间。硫柳汞诱导的细胞内钙增加的平台水平取决于细胞外钙浓度,在无钙溶液中明显降低。如果细胞外钾浓度增加到140毫摩尔,其也会降低。5毫摩尔的镍不会阻断细胞内钙的升高。硫柳汞在含有1毫摩尔锰离子的无钙溶液中会导致Fura-2荧光猝灭。这些效应表明硫柳汞打开了一条从细胞外侧进入钙离子的途径。在硫柳汞反应开始后,组胺能够释放的钙量大幅减少。如果通过将细胞置于无钙溶液中孵育来阻止钙库的重新填充,组胺仍会诱导细胞内钙离子浓度[Ca2+]i短暂升高,但无法维持。在无钙溶液中施加硫柳汞以防止钙库重新填充后,仍可记录到[Ca2+]i的短暂升高,但组胺对[Ca2+]i的反应几乎消失,这表明硫柳汞使钙库释放了钙离子。(摘要截短于250字)

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