Application of Heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury

Atsunori Nakao, David J. Kaczorowski, Ryujiro Sugimoto, Timothy R. Billiar, Kenneth R. McCurry

Research output: Contribution to journalReview article

69 Citations (Scopus)

Abstract

Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.

Original languageEnglish
Pages (from-to)78-88
Number of pages11
JournalJournal of Clinical Biochemistry and Nutrition
Volume42
Issue number2
DOIs
Publication statusPublished - Mar 2008
Externally publishedYes

Fingerprint

heme oxygenase (biliverdin-producing)
Biliverdine
Heme Oxygenase (Decyclizing)
Heme Oxygenase-1
carbon monoxide
Carbon Monoxide
ischemia
Reperfusion Injury
heme
oxygenases
Oxidative stress
Heme
Surgery
Reactive Oxygen Species
Anti-Inflammatory Agents
mesenteric arteries
Iron
Mesenteric Arteries
Cytokines
Degradation

Keywords

  • Biliverdin
  • Carbon monoxide
  • Heme oxygenase
  • Intestinal ischemia reperfusion injury
  • Reactive oxygen species

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Food Science

Cite this

Application of Heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury. / Nakao, Atsunori; Kaczorowski, David J.; Sugimoto, Ryujiro; Billiar, Timothy R.; McCurry, Kenneth R.

In: Journal of Clinical Biochemistry and Nutrition, Vol. 42, No. 2, 03.2008, p. 78-88.

Research output: Contribution to journalReview article

Nakao, Atsunori ; Kaczorowski, David J. ; Sugimoto, Ryujiro ; Billiar, Timothy R. ; McCurry, Kenneth R. / Application of Heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury. In: Journal of Clinical Biochemistry and Nutrition. 2008 ; Vol. 42, No. 2. pp. 78-88.
@article{459c0439e5464e6596a515999b7cf0ec,
title = "Application of Heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury",
abstract = "Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.",
keywords = "Biliverdin, Carbon monoxide, Heme oxygenase, Intestinal ischemia reperfusion injury, Reactive oxygen species",
author = "Atsunori Nakao and Kaczorowski, {David J.} and Ryujiro Sugimoto and Billiar, {Timothy R.} and McCurry, {Kenneth R.}",
year = "2008",
month = "3",
doi = "10.3164/jcbn.2008013",
language = "English",
volume = "42",
pages = "78--88",
journal = "Journal of Clinical Biochemistry and Nutrition",
issn = "0912-0009",
publisher = "The Society for Free Radical Research Japan",
number = "2",

}

TY - JOUR

T1 - Application of Heme oxygenase-1, carbon monoxide and biliverdin for the prevention of intestinal ischemia/reperfusion injury

AU - Nakao, Atsunori

AU - Kaczorowski, David J.

AU - Sugimoto, Ryujiro

AU - Billiar, Timothy R.

AU - McCurry, Kenneth R.

PY - 2008/3

Y1 - 2008/3

N2 - Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.

AB - Intestinal ischemia/reperfusion (I/R) injury occurs frequently in a variety of clinical settings, including mesenteric artery occlusion, abdominal aneurism surgery, trauma, shock, and small intestinal transplantation, and is associated with substantial morbidity and mortality. Although the exact mechanisms involved in the pathogenesis of intestinal I/R injury have not been fully elucidated, it is generally believed that polymorphonuclear neutrophils, pro-inflammatory cytokines, and mediators generated in the setting of oxidative stress, such as reactive oxygen species (ROS), play important roles. Heme oxygenase (HO) is the rate-limiting enzyme that catalyzes the degradation of heme into equimolar quantities of biliverdin and carbon monoxide (CO), while the central iron is released. An inducible form of HO (HO-1), biliverdin, and CO, have been shown to possess generalized endogenous anti-inflammatory activities and provide protection against intestinal I/R injury. Further, recent observations have demonstrated that exogenous HO-1 expression, as well as exogenously administered CO and biliverdin, have potent cytoprotective effects on intestinal I/R injury as well. Here, we summarize the currently available data regarding the role of the HO system in the prevention intestinal I/R injury.

KW - Biliverdin

KW - Carbon monoxide

KW - Heme oxygenase

KW - Intestinal ischemia reperfusion injury

KW - Reactive oxygen species

UR - http://www.scopus.com/inward/record.url?scp=45749111532&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=45749111532&partnerID=8YFLogxK

U2 - 10.3164/jcbn.2008013

DO - 10.3164/jcbn.2008013

M3 - Review article

VL - 42

SP - 78

EP - 88

JO - Journal of Clinical Biochemistry and Nutrition

JF - Journal of Clinical Biochemistry and Nutrition

SN - 0912-0009

IS - 2

ER -