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First published on February 13, 2006; DOI: 10.1124/mol.106.023416

0026-895X/06/6905-1507-1509$20.00
Mol Pharmacol 69:1507-1509, 2006

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Perspective

No Nitric Oxide for HO-1 from Sodium Nitroprusside

Henning Schröder

Department of Pharmacology and Toxicology, School of Pharmacy, Martin Luther University, Halle, Germany

Nitric oxide (NO) and NO donors were among the first reported inducers of the tissue-protective protein heme oxygenase-1 (HO-1) with a potential for eventual use in humans. Besides other clinically established NO releasing drugs, sodium nitroprusside (SNP) has frequently been employed as an experimental tool to explore effects of NO on HO-1 and other biological targets. In this issue of Molecular Pharmacology, Kim et al. (p. 1633) demonstrate that the effects of SNP on expression of HO-1 are mainly due to free iron released from SNP in aqueous solution, whereas NO plays a negligible role, if any, as the mediator of response to SNP. Downstream effects of iron, after being dissociated from SNP, include increases in intracellular cAMP that are causally linked to subsequent phosphorylation of specific MAPK targets and enhanced HO-1 protein levels. Based on the data reported by Kim et al. (2006), the use of SNP as an experimental tool to mimic intracellular effects of NO should be avoided in the future. This work not only helps revise concepts in NO and HO-1 research but also may direct future efforts to the role of iron and reactive oxygen species in the regulation of adenylyl cyclase.

Received February 10, 2006; accepted February 13, 2006

Address correspondence to: Henning Schröder, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA 94305-5208. E-mail: henning{at}stanford.edu


Related articles in MolPharm:

Iron Released by Sodium Nitroprusside Contributes to Heme Oxygenase-1 Induction via the cAMP-Protein Kinase A-Mitogen-Activated Protein Kinase Pathway in RAW 264.7 Cells
Hye Jung Kim, Irina Tsoy, Min Kyu Park, Young Soo Lee, Jae Heun Lee, Han Geuk Seo, and Ki Churl Chang
MolPharm 2006 69: 1633-1640. [Abstract] [Full Text]  





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