Iron ions derived from the nitric oxide donor sodium nitroprusside inhibit mineralization
- 作者：Leonie F.A. Huitema ; P. René ; van Weeren ; Ab Barneveld ; Chris H.A. van de Lest ; J. Bernd Helms and Arie B. Vaandrager
- 关键词：Mineralization ; Calcification ; Sodium nitroprusside ; Inorganic phosphate ; Iron ion
- 刊名：European Journal of Pharmacology
- 出版年：2006
- 期刊代码：24_00142999
- 类别：neu
- 出版时间：7 August 2006
- 卷：542
- 期：1-3
- 页码：48-53
- 文件大小：214 K
摘要
Sodium nitroprusside (SNP) is a nitric oxide (NO) donor drug, which is therapeutically used as a vasodilating drug in heart transplantations. In our previous study it was found that SNP at a concentration of 100 μM inhibited mineralization in a cell culture system, indicating that the beneficial effects of this drug may also include inhibition of vascular calcification. The aim of this study was to investigate which bioactive compounds generated from SNP inhibit mineralization. ATDC5 cells were grown for 14 days and mineralization was induced by addition of 5 mM phosphate for 24 h. Mineralization was determined by staining precipitated calcium with an alizarin red stain. It was found that the NO donors S-nitrosogluthatione and S-nitroso-N-acetylpenicillamine were not able to inhibit mineralization and NO scavengers could not antagonize the inhibiting effect of SNP on mineralization. The iron chelator deferoxamine (200 μM) antagonized the inhibiting effect on mineralization mediated by SNP and ammonium iron sulfate inhibited mineralization in a dose-dependent manner (10–100 μM). Furthermore, iron ions (30 μM) were detected to be released from SNP in the cell culture. These data show that the iron moiety of sodium nitroprusside, rather than nitric oxide inhibits mineralization.