Chapter 18 Interactive Relations between Nitric Oxide (NO) and Carbon Monoxide (CO)

Heme Oxygenase-1/CO Pathway Is a Key Modulator in NO-Mediated Antiapoptosis and Anti-inflammation

Hun Taeg Chung, Byung Min Choi, Young-Guen Kwon, Young Myeong Kim

Research output: Chapter in Book/Report/Conference proceedingChapter

50 Citations (Scopus)

Abstract

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.

Original languageEnglish
Title of host publicationNitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling
PublisherAcademic Press Inc.
Pages329-338
Number of pages10
ISBN (Print)9780123743091
DOIs
Publication statusPublished - 2008 Jan 1

Publication series

NameMethods in Enzymology
Volume441
ISSN (Print)0076-6879

Fingerprint

Heme Oxygenase-1
Carbon Monoxide
Modulators
Nitric Oxide
Inflammation
Chemical activation
S-Nitrosothiols
Apoptosis
Heme Oxygenase (Decyclizing)
Cytoprotection
Macrophages
p38 Mitogen-Activated Protein Kinases
Bioactivity
Heme
Nitric Oxide Synthase
Synaptic Transmission
Free Radicals
Blood Vessels
Arginine
Hepatocytes

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology

Cite this

Chung, H. T., Choi, B. M., Kwon, Y-G., & Kim, Y. M. (2008). Chapter 18 Interactive Relations between Nitric Oxide (NO) and Carbon Monoxide (CO): Heme Oxygenase-1/CO Pathway Is a Key Modulator in NO-Mediated Antiapoptosis and Anti-inflammation. In Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling (pp. 329-338). (Methods in Enzymology; Vol. 441). Academic Press Inc.. https://doi.org/10.1016/S0076-6879(08)01218-4
Chung, Hun Taeg ; Choi, Byung Min ; Kwon, Young-Guen ; Kim, Young Myeong. / Chapter 18 Interactive Relations between Nitric Oxide (NO) and Carbon Monoxide (CO) : Heme Oxygenase-1/CO Pathway Is a Key Modulator in NO-Mediated Antiapoptosis and Anti-inflammation. Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling. Academic Press Inc., 2008. pp. 329-338 (Methods in Enzymology).
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abstract = "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.",
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Chung, HT, Choi, BM, Kwon, Y-G & Kim, YM 2008, Chapter 18 Interactive Relations between Nitric Oxide (NO) and Carbon Monoxide (CO): Heme Oxygenase-1/CO Pathway Is a Key Modulator in NO-Mediated Antiapoptosis and Anti-inflammation. in Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling. Methods in Enzymology, vol. 441, Academic Press Inc., pp. 329-338. https://doi.org/10.1016/S0076-6879(08)01218-4

Chapter 18 Interactive Relations between Nitric Oxide (NO) and Carbon Monoxide (CO) : Heme Oxygenase-1/CO Pathway Is a Key Modulator in NO-Mediated Antiapoptosis and Anti-inflammation. / Chung, Hun Taeg; Choi, Byung Min; Kwon, Young-Guen; Kim, Young Myeong.

Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling. Academic Press Inc., 2008. p. 329-338 (Methods in Enzymology; Vol. 441).

Research output: Chapter in Book/Report/Conference proceedingChapter

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N2 - 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.

AB - 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.

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DO - 10.1016/S0076-6879(08)01218-4

M3 - Chapter

SN - 9780123743091

T3 - Methods in Enzymology

SP - 329

EP - 338

BT - Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling

PB - Academic Press Inc.

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Chung HT, Choi BM, Kwon Y-G, Kim YM. Chapter 18 Interactive Relations between Nitric Oxide (NO) and Carbon Monoxide (CO): Heme Oxygenase-1/CO Pathway Is a Key Modulator in NO-Mediated Antiapoptosis and Anti-inflammation. In Nitric Oxide, Part G Oxidative and Nitrosative Stress in Redox Regulation of Cell Signaling. Academic Press Inc. 2008. p. 329-338. (Methods in Enzymology). https://doi.org/10.1016/S0076-6879(08)01218-4