You are seeing this message because your Web browser does not support basic Web standards. Find out more about why this message is appearing and what you can do to make your experience on this site better.


ABOUT ARCHIVES
Advanced Search

Welcome   | My Account | E-mail Alerts | Access Rights | Sign In


  Vol. 128 No. 11, November 1993 TABLE OF CONTENTS
  Archives
  •  Online Features
  Original Articles
 This Article
 •References
 •Full text PDF
 •Send to a friend
 • Save in My Folder
 •Save to citation manager
 •Permissions
 Citing Articles
 •Citation map
 •Citing articles on HighWire
 •Contact me when this article is cited
 Related Content
 •Similar articles in this journal
 Social Bookmarking
  Add to CiteULike Add to Connotea Add to Del.icio.us Add to Digg Add to Reddit Add to Technorati Add to Twitter What's this?

Eicosanoids

Critical Agents in the Physiological Process and Cellular Injury

J. Raymond Fletcher, MD, PhD

Arch Surg. 1993;128(11):1192-1196.


Abstract

Eicosanoids were discovered as "prostaglandins" in the mid-1930s. The discovery that eicosanoids were ubiquitous in mammalian cells and that nonsteroidal antiinflammatory drugs worked by inhibiting enzymes that synthesized these chemicals heralded their extensive investigation in all fields of biology. Precursor fatty acids (arachidonic acids) are stored in cell phospholipids, acted on by two enzymes (cyclooxygenase and lipooxygenase) that yield prostaglandins, thromboxane, prostacyclin, and leukotrienes. Knowledge of their biochemical processes continue to unfold, but it is now believed that eicosanoids are part of a larger group of agents termed phospholipid mediators. Eicosanoids are intimately involved with cardiovascular function as well as central and peripheral vascular disease processes and ischemia. In the gastrointestinal tract, these potent lipids not only participate in many normal functions (eg, acid secretion and motility) but also in disease states (eg, inflammatory bowel disease and peptic ulcer disease). In shocklike states of sepsis and/or endotoxemia, eicosanoids have assumed a major role in many events that occur. Recently, discoveries have demonstrated that platelet-activating and tumor necrosis factors exert their effects in part through eicosanoids. The future will demonstrate these compounds to be critical not only in intracellular (molecular) events but also in the effects they produce that are far from the source of origin.

(Arch Surg. 1993;128:1192-1196)



Author Affiliations

From the Department of Surgery, College of Medicine, University of South Alabama, Mobile.



Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati   Add to Twitter Twitter     What's this?

THIS ARTICLE HAS BEEN CITED BY OTHER ARTICLES

NF-{kappa}B-Inducing Kinase Regulates Cyclooxygenase 2 Gene Expression in Macrophages by Phosphorylation of PU.1
Azim et al.
J. Immunol. 2007;179:7868-7875.
ABSTRACT | FULL TEXT  

CCAAT/Enhancer-Binding Protein Mediates Carbon Monoxide-Induced Suppression of Cyclooxygenase-2
Suh et al.
Am. J. Respir. Cell Mol. Bio. 2006;35:220-226.
ABSTRACT | FULL TEXT  

NF-{kappa}B activation as a pathological mechanism of septic shock and inflammation
Liu and Malik
Am. J. Physiol. Lung Cell. Mol. Physiol. 2006;290:L622-L645.
ABSTRACT | FULL TEXT  

Opposing and Hierarchical Roles of Leukotrienes in Local Innate Immune versus Vascular Responses in a Model of Sepsis
Benjamim et al.
J. Immunol. 2005;174:1616-1620.
ABSTRACT | FULL TEXT  

Transcriptional Regulation of the Cyclooxygenase-2 Gene in Macrophages by PU.1
Joo et al.
J. Biol. Chem. 2004;279:6658-6665.
ABSTRACT | FULL TEXT  

11,12-Epoxyeicosatrienoic Acid Attenuates Synthesis of Prostaglandin E2 in Rat Monocytes Stimulated with Lipopolysaccharide
Kozak et al.
Exp Biol Med 2003;228:786-794.
ABSTRACT | FULL TEXT  

Diesel Exhaust Particle Extracts and Associated Polycyclic Aromatic Hydrocarbons Inhibit Cox-2-dependent Prostaglandin Synthesis in Murine Macrophages and Fibroblasts
Rudra-Ganguly et al.
J. Biol. Chem. 2002;277:39259-39265.
ABSTRACT | FULL TEXT  

DIFFERENTIAL REGULATION OF GROWTH PLATE CHONDROCYTES BY 1{alpha},25-(OH)2D3 AND 24R,25-(OH)2D3 INVOLVES CELL-MATURATION-SPECIFIC MEMBRANE-RECEPTOR-ACTIVATED PHOSPHOLIPID METABOLISM
Boyan et al.
CROBM 2002;13:143-154.
ABSTRACT | FULL TEXT  

Cardiac-Specific Overexpression of Tumor Necrosis Factor-{alpha} Causes Oxidative Stress and Contractile Dysfunction in Mouse Diaphragm
Li et al.
Circulation 2000;102:1690-1696.
ABSTRACT | FULL TEXT  

Transcriptional Activation of the Cyclooxygenase-2 Gene in Endotoxin-treated RAW 264.7 Macrophages
Wadleigh et al.
J. Biol. Chem. 2000;275:6259-6266.
ABSTRACT | FULL TEXT  

12-O-tetradecanoylphorbol-13-acetate-induced Apoptosis Is Mediated by Tumor Necrosis Factor alpha in Human Monocytic U937 Cells
Takada et al.
J. Biol. Chem. 1999;274:28286-28292.
ABSTRACT | FULL TEXT  

Arachidonic Acid Directly Mediates the Rapid Effects of 24,25-Dihydroxyvitamin D3 Via Protein Kinase C and Indirectly through Prostaglandin Production in Resting Zone Chondrocytes
Schwartz et al.
Endocrinology 1999;140:2991-3002.
ABSTRACT | FULL TEXT  

Regulation of prostaglandin biosynthesis in vivo by glutathione
Margalit et al.
Am. J. Physiol. Regul. Integr. Comp. Physiol. 1998;274:R294-R302.
ABSTRACT | FULL TEXT  

Regulation of Macrophage Cytokine Production by Prostaglandin E2. DISTINCT ROLES OF CYCLOOXYGENASE-1 AND -2
Williams and Shacter
J. Biol. Chem. 1997;272:25693-25699.
ABSTRACT | FULL TEXT  





HOME | CURRENT ISSUE | PAST ISSUES | TOPIC COLLECTIONS | CME | SUBMIT | SUBSCRIBE | HELP
CONDITIONS OF USE | PRIVACY POLICY | CONTACT US | SITE MAP
 
© 1993 American Medical Association. All Rights Reserved.