Heme as a Playmaker in the Regulation of the Nitric Oxide System

We appreciate the interest of Li Volti et al.  in our recently published article.1In their letter, Li Volti et al.  pointed out that our conclusions could have been strengthened if there had been data indicating the effect of hemin on nitric oxide. Incidentally, we did perform these experiments, but we decided not to present these data in the article because of page limitations. We appreciate these comments and are glad to present these data in this response letter. Briefly, production of nitric oxide and expression of inducible nitric oxide synthase, i.e. , the main enzyme for nitric oxide production during sepsis,2were evaluated by chemiluminescence and immunoblotting assays, as we previously reported.3The data revealed that hemin significantly attenuated inducible nitric oxide synthase expression and nitric oxide production in lipopolysaccharide-stimulated macrophages (fig. 1). In addition, the effects of hemin on inducible nitric oxide synthase expression could be attenuated by tin protoporphyrin, the potent heme oxygenase-1 inhibitor (fig. 1). Along with our previous reports,4,5these data provide strong evidence to support the crucial role of heme oxygenase 1 on regulating inducible nitric oxide synthase expression and nitric oxide production during sepsis.

*Mackay Memorial Hospital, Taipei, Taiwan. sean@ms2.mmh.org.tw