This timely volume describes the contributions of free radicals and reactive oxygen species to disease processes in a variety of tissues. Topics include the roles of lipid peroxide-modified lipoproteins in atherosclerosis, peroxidation products in retinopathy, reactive oxygen species and neutrophils in mycardial ischemia-reflow injury, iron and reactive oxygen species in hemoglobin-mediated CNS damage and in asbestos-mediated lung injury. Critical reviews examine the evidence for radical species in ethanol-induced liver injury and in muscular dystrophy. The wealth of new information presented makes this book valuable for teaching and an important reference volume for researchers exploring problems in human disease.
PROPOSED FREE RADICAL MECHANISMS OF TISSUE INJURY (Charles V. Smith). Requirements for Free Radical-Mediated Injury. Evidence for Free Radicals. Types of Free Radical Reactions. Measurement of Lipid Peroxidation. HEMOGLOBIN-INDUCED OXIDANT DAMAGE TO THE CENTRAL NERVOUS SYSTEM (Sayed M.H. Sadradeh and John W. Eaton). Introduction. Does Hemoglobin Promote CNS Damage? Does Hemoglobin Contribute to the Oxidation of CNS Components? Specific Mechanisms of Hemoglobin-Mediated CNS Damage. Conclusions. RADICALS AND OXIDANTS IN ETHANOL-INDUCED LIVER INJURY (Bernhard H. Lauterburg and Brigitte de Quay). Metabolism of Ethanol. Pathogenesis of Alcoholic Liver Injury. Role of Radicals and Oxidants in Ethanol-Induced Cell Injury. Potential Sources of Radicals and Oxidants. LIPID PEROXIDE-DEPENDENT MODIFICATIONS OF LIPOPROTEINS IN ATHEROSCLEROSIS (Margaret E. Haberland and Charles V. Smith). Introduction. Role of Lipid Peroxidation in Formation of Macrophage-Derived Foam Cells. Cytotoxicity of Oxidized Low-Density Lipoprotein. Role of Lipid Peroxidation in Triggering Early Cellular Events. Lipoproteins in the Atherosclerotic Lesion: Interfacial Rather than Solution Chemistry. Conclusions. REACTIVE OXYGEN SPECIES, NEUTROPHIL AND ENDOTHELIAL ADHERENCE MOLECULES, AND LIPID-DERIVED INFLAMMATORY MEDIATORS IN MYOCARDIAL ISCHEMIA-REFLOW INJURY (Addison A. Taylor and Scott B. Shappell). Pathophysiology of Myocardial Ischemia and Reperfusion. Role of Reactive Oxygen Species (ROS) in Myocardial Ischemia-Reperfusion Injury. Evidence for Formation of Reactive Oxygen Species During Myocardial Ischemia-Reperfusion. Role of Neutrophils in Myocardial Ischemia-Reperfusion Injury. Summary and Future Directions. BIOACTIVATION OF XENOBIOTICS BY THE RESPIRATORY BURST OF HUMAN GRANULOCYTES (Michael D. Corbett and Bernadette R. Corbett). Introduction. Effect of the Respiratory Burst on Xenobiotics. Respiratory Burst-Induced Binding of Arylamines to Nucleic Acids. Significance of Respiratory Burst-Induced Bioactivation of Xenobiotics. ROLE OF IRON AND REACTIVE OXYGEN SPECIES IN ASBESTOS-INDUCED LUNG INJURY (Susan Shull, Muniraj Monohar, Joanne P. Marsh, Yvonne M.W. Janssen, and Brooke T. Mossman). Asbestos and Lung Injury. Involvement of Reactive Oxygen Species (ROS) in Asbestos-Mediated Lung Cell Injury. Protection of Asbestos-Mediated Lung Cell Injury by Iron Chelators. Regulation of Antioxidant Enzymes by Reactive Oxygen Species (ROS). THE VASCULAR ENDOTHELIUM IN OXIDANT-INDUCED LUNG INJURY (Stephen J. Elliot and WIlliam P. Schilling). Pulmonary Oxidant Injury. Oxidant Stress and the Vascular Endothelium. Calcium Signaling in Vascular Endothelial Cells. Oxidant Stress and Calcium Signaling. Inhibition of Glutathione Reductase. Conclusion. OXYGEN-INDUCED RETINOPATHY IN THE RAT: A PROPOSED ROLE FOR PEROXIDATION REACTIONS IN THE PATHOGENESIS (John S. Penn). The Retina and Peroxidation. Retinopathy of Prematurity (ROP). Pathogenesis of ROP. Oxygen-Induced ROP in the Rat. Recent Studies of ROP in Rats. FREE RADICALS IN MUSCULAR DYSTROPHY (James P. Kehrer and Michael E. Murphy). Overview. Duchenne Muscular Dystrophy (DMD). Animal Models. Hypothesis Regarding the Cause of DMD. Conclusions. PROTECTION AGAINST FREE RADICAL MEDIATED TISSUE INJURY (Mary Treinen Moslen). Types of Evidence Implicating Free Radicals in Tissue Injury. Molecular and Functional Alterations Due to Free Radicals or ROS. Systems that Protect Against Free Radicals or ROS. Complementary and Auxiliary Protection Systems. Deficiency, Induction and Activation of Protection Systems. Conclusions.