Nitric oxide (NO) and carbon monoxide (CO) are synthesized from l-arginine and heme by the catalytic reaction of NO synthase (NOS) and heme oxygenase (HO). NO, a highly reactive free radical, plays an important role in the regulation of vascular and immune function, antiapoptosis, and neurotransmission by producing cGMP, nitrosyl iron complexes, and S-nitrosothiols. CO, a more stable molecule, exerts similar biological activities to those of NO by cGMP production, p38 mitogen-activated protein kinase activation, and nuclear factor-κB activation. NO induces the suppression of apoptosis and inflammation in hepatocytes and macrophages by an elevation in HO-1 and CO production, and these effects were not observed in mice lacking HO-1 as well as in cells treated with a HO-1 inhibitor. These evidences indicate that the HO-1/CO pathway is a key player in NO-mediated cytoprotection and anti-inflammation. This chapter reviews new advances in the interactive relations between iNOS/NO and HO-1/CO pathways in the regulation of apoptosis and inflammation.
|Title of host publication||Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling|
|Publisher||Academic Press Inc.|
|Number of pages||10|
|Publication status||Published - 2008|
|Name||Methods in Enzymology|
Bibliographical noteFunding Information:
This work was supported by the Vascular System Research Center Grant from the Korea Science and Engineering Foundation.
All Science Journal Classification (ASJC) codes
- Molecular Biology