Carbon monoxide in biology and medicine

BioEssays - Tập 26 Số 3 - Trang 270-280 - 2004
Stefan W. Ryter1, Leo E. Otterbein2
1Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, The University of Pittsburgh School of Medicine, PA, USA.
2Department of Medicine, Division of Pulmonary, Allergy and Critical Care Medicine, The University of Pittsburgh School of Medicine

Tóm tắt

Abstract

Carbon monoxide (CO), a product of organic oxidation processes, arises in vivo during cellular metabolism, most notably heme degradation. CO binds to the heme iron of most hemoproteins. Tissue hypoxia following hemoglobin saturation represents a principle cause of CO‐induced mortality in higher organisms, though cellular targets cannot be excluded. Despite extreme toxicity at high concentrations, low concentrations of CO can confer cytoprotection during ischemia/reperfusion or inflammation‐induced tissue injury. Likewise, heme oxygenase, an enzyme that produces CO, biliverdin and iron, as well as a secondary increase in ferritin synthesis, from the oxidation of heme, can confer protection in vivo and in vitro. CO has been shown to affect several intracellular signaling pathways, including guanylate cyclase, which generates guanosine 3′:5′ cyclic monophosphate and the mitogen‐activated protein kinases (MAPK). Such pathways mediate, in part, the known vasoregulatory, anti‐inflammatory, anti‐apoptotic and anti‐proliferative effects of this gas. Exogenous CO delivered at low concentrations is showing therapeutic potential as an anti‐inflammatory agent and as such can modulate numerous pathophysiological states. This review will delve into the biological significance and medical applications of this gas molecule. BioEssays 26:270–280, 2004. © 2004 Wiley Periodicals, Inc.

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Tài liệu tham khảo

10.1073/pnas.192568299

10.1016/S0749-0704(05)70056-7

10.1002/(SICI)1099-1263(199909/10)19:5<379::AID-JAT563>3.0.CO;2-8

The Merck Index, 1989, An encyclopedia of chemicals, drugs, and biologicals

Tenhunen R, 1969, Microsomal heme oxygenase, characterization of the enzyme, J Biol Chem, 244, 6388, 10.1016/S0021-9258(18)63477-5

10.1146/annurev.pharmtox.37.1.517

10.1016/S0891-5849(99)00223-3

Furchgott RF, 1991, Endothelium‐dependent and independent vasodilation involving cyclic GMP: relaxation induced by nitric oxide, carbon monoxide and light, Blood Vessels, 28, 52

10.1089/152308602753666352

10.1023/A:1015957026924

10.1183/09031936.02.00071802

10.1007/s00134-002-1269-7

10.1126/science.7678352

10.1016/S1471-4906(03)00181-9

10.1016/S0300-483X(03)00005-2

Smith RP, 1986, Casarett and Doull's Toxicology, the basic science of poisons, 223

10.1152/jappl.1990.68.3.997

10.1006/taap.1993.1242

10.1006/exnr.1997.6584

10.1073/pnas.97.3.1305

10.1016/S0891-5849(98)00092-6

10.1021/bi00184a036

10.1042/0264-6021:3580201

10.1016/S0006-291X(75)80403-7

Guengerich FP, 1975, Purified liver microsomal cytochrome P‐450. Electron‐accepting properties and oxidation‐reduction potential, J Biol Chem, 250, 7405, 10.1016/S0021-9258(19)40959-9

10.1042/bj2040479

10.1111/j.1749-6632.1970.tb49788.x

10.1074/jbc.273.2.945

10.1007/978-1-4684-5643-1_84

10.1111/j.1748-1716.1952.tb00915.x

10.1172/JCI104802

10.1021/bi00804a016

Maines MD, 1992, Heme oxygenase: Clinical Applications and Functions

10.1073/pnas.86.1.99

10.1089/15230860260220139

10.1016/S0891-5849(98)00224-X

10.1073/pnas.90.20.9285

Haddad LM, 1990, Clinical management of poisoning and drug overdose

10.1016/0034-5687(75)90070-5

10.1046/j.1432-1033.2002.03282.x

10.1201/9781420039320.ch2

10.1126/science.176.4032.295

10.1016/S0887-2333(01)00094-7

10.1139/y98-126

10.1089/15230860260220102

10.1016/0003-9861(84)90210-8

10.1378/chest.116.4.1007

10.1034/j.1399-3003.1999.13a10.x

10.1165/ajrcmb.24.3.4001

10.1136/thorax.57.9.779

10.1164/ajrccm.164.8.2011083

10.1136/thx.53.8.668

10.1183/09031936.01.00231201

10.1186/1465-9921-4-7

10.1038/nm817

10.1038/89068

10.1038/sj.bjp.0701878

10.1038/87929

10.1074/jbc.272.52.32804

10.1073/pnas.92.5.1475

Brune B, 1987, Inhibition of platelet aggregation by carbon monoxide is mediated by activation of guanylate cyclase, Mol Pharmacol, 32, 497

10.1016/0006-2952(91)90658-R

10.1016/S0896-6273(00)80103-8

10.1006/mcne.1993.1049

10.1172/JCI118334

10.1006/bbrc.1994.2811

10.1073/pnas.93.2.795

10.1152/ajpregu.1998.275.4.R1025

10.1089/152308602753666334

10.1007/s004240050398

10.1172/JCI11218

10.1161/01.RES.0000036900.76780.95

10.1186/rr190

10.1126/science.1078456

10.1074/jbc.273.24.15257

10.1038/74680

10.1074/jbc.271.40.24313

10.1152/ajplung.2000.278.2.L312

10.1074/jbc.M108317200

10.1074/jbc.M301858200

10.1177/15353702-0322805-30

10.1165/rcmb.4851

10.1089/152308603764816514

10.1152/ajpcell.1996.270.1.C107

10.1084/jem.20031003

10.1067/msy.2003.238

10.4049/jimmunol.166.6.4185

10.1038/2063

10.1053/jhep.2002.32467

10.1161/hh0202.104530