Lipid Mediators

The Handbook of Immunopharmacology: Lipid Mediators covers a comprehensive overview of lipid mediators, from synthesis through to inhibition. The book discusses the metabolism of arachidonic acid; the measurement of fatty acids and their metabolites; and the biological properties of cyclooxygenase products. The text also describes other essential fatty acids, their metabolites and cell-cell interactions; the inhibitors of fatty acid-derived mediators; as well as the biosynthesis and catabolism of platelet-activating factor. The cellular sources of platelet-activating factor and related lipids; the biological properties of platelet-activating factor; and the effects of platelet-activating factor receptor antagonists are also considered. Immunopharmacologists, immunologists, and pharmacologists will find the book invaluable.

Contributors Series Preface Preface 1. Metabolism of Arachidonic Acid: An Overview 1. Introduction 2. Mechanisms Involved in Bioavailability of Arachidonic Acid for Eicosanoid Production 2.1 Phospholipases Az 2.2 Phospholipase C 2.3 Phospholipase D 2.4 Other Lipases 2.5 Metabolic Pools of Prostaglandin Precursors 2.6 Triglyceride and Free Acid Stores 3. Enzymic Conversion of Arachidonic Acid to Prostaglandins and Related "Prostanoids" 3.1 Prostaglandin-H Synthase 3.2 Further Transformation of Prostaglandin H2 into Biologically Active Eicosanoids 3.3 Endogenous Factors Controlling CeUular Levels of Prostaglandin-H Synthase 3.4 Metabolic Inactivation of Eicosanoids 4. Lipoxygenase Pathways 4.1 12-Lipoxygenase Products 4.2 5-Lipoxygenase Products (Including the Leukotrienes) 4.3 15-Lipoxygenase Products and their Activity 4.4 Monooxygenase Products 4.5 Other Lipoxygenase Products 5. "Crossover" Products 6. Alternative Substrates to Arachidonic Acid in the Formation of Eicosanoids 7. Mode of Action of Anti-inflammatory Drugs 7.1 Non-steroidal ("Aspirin-Type") Drugs 7.2 Steroidal Anti-inflammatory Drugs 8. Concluding Remarks 9. References 2. Measurement of Fatty Acids and Their Metabolites 1. Introduction 2. Approaches to Assays 2.1 Specificity Versus Sensitivity 2.2 Extraction 2.3 Internal and External Standards 2.4 Accuracy and Precision 3. Methodology 3.1 Bioassays 3.2 Radioimmunoassay and Related Assays 3.3 High-Performance Liquid Chromatography 3.4 Gas Chromatography 3.5 Gas Chromatography-Mass Spectrometry 3.6 High-Performance Liquid ChromatographyThermospray Mass Spectrometry 3.7 Other Mass Spectrometry Methods 4. Group Analysis 5. Concluding Remarks 6. References 3. Biological Properties of Cyclooxygenase Products 1. In the Cardiovascular System 1.1 Thromboxane A2 1.2 Prostacyclin 1.3 Prostacyclin and Thromboxane Balance 1.4 Prostacyclin and Thromboxane A2 in Disease 1.5 Antithrombotic Action of Aspirin 1.6 Conclusions 2. In Inflammation 2.1 Inflammatory Properties of Cyclooxygenase Products 2.2 Inhibition of Cyclooxygenase 2.3 Differences between Aspirin and Salicylate 2.4 Thromboxane A2 in Inflammation 3. In the Immune System 4. In the Central Nervous System 4.1 Prostaglandin D2 in Physiological Sleep 4.2 Prostaglandin E2 in Wakefulness 4.3 Conclusions 5. In Pain Perception 5.1 Prostaglandins and Hyperalgesia 5.2 Analgesia with Aspirin-Like Drugs 6. In the Gastrointestinal Tract 6.1 Gastric Antisecretory Actions 6.2 Gastric Vascular Actions 6.3 Gastric Anti-ulcer and Protective Actions 6.4 Actions of Non-steroidal Anti-inflammatory Agents 6.5 Prostanoid Actions on Intestinal Function 7. In Fever 7.1 Experimental Studies in Animals 7.2 Mechanisms of Hyperpyrexia 7.3 Conclusions 8. In the Kidney 8.1 Prostaglandin Production by the Kidney 8.2 Effects of Prostaglandins on Kidney Function 8.3 Inhibition ofCyclooxygenase in Animal Studies 8.4 Inhibition ofCyclooxygenase in Human Studies 9. In Reproduction and Parturition 9.1 Prostaglandins in Seminal Fluid 9.2 Regulation of Uterine Contractions 9.3 Luteolytic Action 10. Acknowledgements 11. References 4. Other Essential Fatty Acids, Their Metabolites and Cell-Cell Interactions 1. Introduction 2. Prostaglandin 12 Synthesis by Endothelial Cells 3.

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