Comparative pathophysiology and toxicology of cyclooxygenases / Zaher A. Radi.

The first thorough review of cyclooxygenase inhibitors, including their toxicity mechanisms and toxicopathological risks. Cyclooxygenases (COXs) are enzymes responsible for the formation of an important class of biological mediators called prostanoids. Prostanoids such as prostaglandins mediate infl...

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Online Access: Full Text (via ProQuest)
Main Author: Radi, Zaher A.
Format: eBook
Language:English
Published: Hoboken, N.J. : Wiley, ©2012.
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100 1 |a Radi, Zaher A. 
245 1 0 |a Comparative pathophysiology and toxicology of cyclooxygenases /  |c Zaher A. Radi. 
260 |a Hoboken, N.J. :  |b Wiley,  |c ©2012. 
300 |a 1 online resource. 
336 |a text  |b txt  |2 rdacontent. 
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504 |a Includes bibliographical references and index. 
505 0 0 |t INTRODUCTION: DISCOVERY OF CYCLOOXYGENASES AND HISTORICAL PERSPECTIVE --  |t Aspirin --  |t Prostaglandins --  |t Cyclooxygenases --  |t COX-2 Selective NSAIDs --  |g 1.  |t GASTROINTESTINAL TRACT --  |t Introduction --  |t Comparative COX-1 and COX-2 Expression in the GI Tract --  |t Effects of ns-NSAIDs on the GI Tract --  |t Effects of Arylpropionic Acid ns-NSAIDs on the GI Tract --  |t Effects of Enolic Acid (Oxicam) ns-NSAIDs on the GI Tract --  |t Effects of Acetic Acid Derivative ns-NSAIDs on the GI Tract. 
505 0 0 |t Effects of Aminonicotinic Acid Derivative ns-NSAIDs on the GI TractEffects of Pyrazolone Derivative ns-NSAIDs on the GI Tract --  |t Effects of Salicylic Acid Derivative ns-NSAIDs on the GI Tract --  |t Effects of Anthranilic Acid Derivative ns-NSAIDs on the GI Tract --  |t Effects of COX-1 Inhibitors on the GI Tract --  |t Effects of COX-2 s-NSAIDs on the GI Tract --  |t Pathophysiology and Mechanisms of NSAID-Associated GI Toxicity --  |t Role of Cyclooxygenase Potency --  |t Species Differences in NSAID-Associated Susceptibility to GI Injury --  |t GI Anatomical Differences --  |t Enterohepatic Recirculation and NSAID Toxicity. 
505 0 0 |t Role of Xenobiotic GlucuronidationAging and Stress and NSAID GI Effects --  |t Disruption of GI Physiological Mucosal Defense Mechanisms --  |t GI Disequilibrium --  |t Effects on Physiological GI Mucosal Cell Renewal Mechanisms After Mucosal Injury --  |t Effects on Leukocyte Adhesion Molecules and Trafficking --  |t Effects of GI Physiological Local pH, Gut Absorption, and Fasting --  |t NSAID Topical Effect-Mediated Injury --  |t Changes in GI Motility, Microcirculation, and Enterobacteria --  |t Decreased Phosphatidylcholine Levels --  |t Impaired Drug Metabolism --  |t Role of Toll-like Receptor (TLR)-4/MyD88 and Enteric Bacteria. 
505 0 0 |t Role of Uncoupling of Mitochondrial Oxidative PhosphorylationRole of Peroxisome Proliferator-Activated Receptor g --  |t Role of Mitogen-Activated Protein Kinases --  |t NSAID GI Injury-Associated Risk Factors --  |t Conclusions --  |g 2.  |t BONE-TENDON-LIGAMENT SYSTEM --  |t Introduction --  |t Comparative Physiological and Anatomical Aspects of the Skeleton --  |t Role of Prostaglandins in Skeleton Metabolism --  |t The Process of Bone Healing and Potential Role of Prostaglandins --  |t Inflammatory Response --  |t Bone Resorption --  |t Bone Formation. 
505 0 0 |t COX-1 and COX-2 Expression in Bone, Tendon, and Ligament During Repair and in Pathological ConditionsEffects of ns-NSAIDs on Bone Healing --  |t Effects of COX-2 s-NSAIDs on Bone Healing --  |t Effects of ns-NSAIDs on Ligament and Tendon Healing --  |t Effects of COX-2 s-NSAIDs on Ligament and Tendon Healing --  |t Conclusions --  |g 3.  |t RENAL SYSTEM --  |t Introduction --  |t Comparative Physiological, Developmental, and Anatomical Aspects of the Renal System --  |t Role of Prostaglandins in the Renal System --  |t COX-1 and COX-2 Expression in the Kidney --  |t Effects of ns-NSAIDs on the Kidney. 
505 0 0 |t Effects of COX-2 s-NSAIDs on the Kidney. 
520 |a The first thorough review of cyclooxygenase inhibitors, including their toxicity mechanisms and toxicopathological risks. Cyclooxygenases (COXs) are enzymes responsible for the formation of an important class of biological mediators called prostanoids. Prostanoids such as prostaglandins mediate inflammatory and anaphylactic reactions. For those suffering from inflammation and pain, the pharmacological inhibition of COXs, with non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, can provide relief. Yet the use of NSAIDs can trigger toxicological effects as well, leading to potential health risks. Comparative Pathophysiology and Toxicology of Cyclooxygenases provides a comprehensive overview of how COX inhibitors affect various bodily systems, specifically the toxicity mechanisms triggered when the COX enzyme is inhibited. The book provides an introduction to the discovery of cyclooxygenases, their use as therapeutic agents, as well as an historical perspective. Shedding light on the differences in expression, pathophysiology, and toxicology of COX inhibitors across species, the book offers a systematic examination of the effects and pathophysiology of COX inhibitors and their mechanisms of toxicity, beginning with the GI tract. Subsequent chapters cover: The pathophysiology of COX inhibition on bone, tendon, and ligament healing, COX inhibitors and renal system pathophysiology and mechanisms of toxicity, The pathophysiologic role of COX inhibition in the ocular system, COX inhibition and the respiratory and cardiovascular systems. The book also sheds light on the latest research devoted to developing COX inhibitors with no adverse side-effects. The first book to offer a thorough comparative look at the toxicological effects of COX inhibitors throughout the body, this invaluable resource will help advance the research and development of safer and more effective COX drugs. 
588 0 |a Print version record. 
650 0 |a Cyclooxygenases  |x Pathophysiology. 
650 0 |a Cyclooxygenases  |x Toxicology. 
650 7 |a Science.  |2 fast  |0 (OCoLC)fst01108176. 
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