Biological Oxidants: Generation and Injurious Consequences

Biological Oxidants: Generation and Injurious Consequences is a collection of papers that describes research work done concerning molecules of the intracellular and plasma membrane generating system in leukocytes; the intracellular interactions in oxidant-induced cellular injury; malignant transformation; and intracellular mechanism of oxidant formation. One paper reviews biological oxidants and the molecular basis of chronic granulomatous disease, particularly on compositions found within the plasma membrane. One such composition concerns the discovery of a flavocytochrome b as the central electron-transporting molecule in this system. Another paper examines the early injury of cells caused by external oxidants and the consequences of DNA damage. Other papers review the metabolism of vascular endothelial-derived reactive species, the calcium-modulated cellular effects of oxidants, as well as, the mechanism of inflammatory oxidant damage in tissues. This book is suitable for biochemists, microbiologists, and academicians whose works involve research of cell membranes.

Preface Chapter 1 Composition and Function of the NADPH Oxidase of Phagocytic Cells with Particular Reference to Redox Components Located within the Plasma Membrane 1 I. Introduction 1 II. Early Attempts to Identify the Oxidase System in Cells, Organelles, and Extracts III. Identification of Cytochrome b-245 and Recognition of the Oxidase asan Electron Transport IV. Biochemical Properties V. Purification and Identification of Cytochrome b-245 VI. Molecular Biology of Genes Coding for Cytochrome b-245 and Their Abnormality in Chronic Granulomatous Disease VII. Flavocytochrome Component of the Oxidase VIII. Terminology IX. Cytosolic Factors X. Model of the Oxidase Electron Transport System References Chapter 2 Early Injury of Cells by External Oxidants and the Consequences of DNA Damage I. Introduction IL Biochemical Pathways Affected by Oxidants References Chapter 3 Cytosolic Components of NADPH Oxidase: Identity,Function, and Role in Regulation of Oxidase Activity I. Introduction II. Concept of Multiple NADPH Oxidase Components III. Primary Structure and Properties of the Cytosolic Components IV. Phosphorylation of p47-phox V. Translocation of p47-phox and p67-phox VI. Cytosolic Oxidase Components Exist as Complexes in the Unstimulated Cell VII. Cytoskeletal Involvement in NADPH Oxidase VIII. GTP-Binding Proteins Involved in NADPH Oxidase IX. Other Potential NADPH Oxidase Components ReferencesChapter 4 Generation of Reactive Species by Vascular Endothelium I. Introduction II. Identification of Sources and Quantities of Reactive Oxygen Species in Endothelium III. Xanthine Oxidase in Vascular Endothelium IV. Circulating Xanthine Oxidase and Interactions with Vascular Endothelium V. Nitric Oxide in Vascular Endothelium VI. Future Directions References Chapter 5 Composition of NADPH Oxidase of Phagocytes and Other Cell Types: Role of Flavoprotein in Proton Translocation and Oxidase Activity 1. Flavin and Cytochrome b Interactions in NADPH Oxidase II. Presence of "Phagocyte-Typic" NADPH Oxidase in Other Cell Types References Chapter 6 Calcium-Modulated Cellular Effects of Oxidants I. Introduction II. Cellular Calcium Sequestration Processes III. Control of Cellular Calcium Homeostasis IV. Modulation of Calcium Homeostasis during Cell Signaling V. Disruption of Intracellular Calcium Homeostasis by Toxic Agents VI. Mechanisms of Calcium-Mediated Cell Killing VII. Summary and Concluding Remarks References Chapter 7 Mechanisms of Inflammatory Oxidant Damage in Tissues I. Introduction II. Acute Lung Injury Developing after Systemic Activation of Complement III. Acute Lung Injury Following Deposition of Immunoglobulin G Immune Complexes IV. Acute Lung Injury Following Deposition of Immunoglobulin A Immune Complexes V. Mechanism of in Vitro Injury of Endothelial Cells VI. Summary References Chapter 8 Contributions of Oxidants and Granulocytes to Ischemia-Reperfusion Injury I. Introduction II. Ischemia-Reperfusion-Induced Granulocyte Infiltration: Role of Oxidants III. Endothelial Cell Monolayer Dysfunction Induced by Anoxia-Reoxygenation IV. Inflammatory Mediators and Ischemia-Reperfusion V. Neutrophil-Mediated Injury VI. Other Models of Intestinal Inflammation References Chapter 9 Macrophage-Derived Nitric Oxide: Generation and Consequences I. Introduction II. Discovery That Macrophages Release Reactive Nitrogen Intermediates, and Their Identification III. Biosynthetic Path for Formation of Nitric Oxide from L-Arginine IV. Purification of Nitric Oxide Synthase and Its Characterization as an FAD- and FMN-Containing Flavoprotein V. Immunologic Induction of Nitric Oxide Synthase VI.

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