Oxidative Stress in Vertebrates and Invertebrates E-Book

• Herausgeber: John Wiley & Sons
• Kategorie: Wissenschaft und neue Technologien
• Sprache: Englisch

Seitenzahl: 1286

Veröffentlichungsjahr: 2011

Beschreibung

This volume presents a unique comparative treatment of the role oxidative stress plays in vertebrates and invertebrates in multiple organ systems with regards to cell death, development, aging, and human diseases, and anti-oxidant therapy. It offers comprehensive reviews of the current understanding of oxidative stress-mediated physiology and pathology as well as directions for future research. It also provides current information on the role of oxidative stress in neurodegenerative diseases, cardiovascular diseases, and various types of cancer mediated by oxidative stress.

Leseprobe

Contents

Preface

Foreword

Acknowledgments

Contributors

Part I: Oxidative Stress in Vertebrates

Chapter 1: Generation of Reactive Oxygen Species in the Brain: Signaling for Neural Cell Survival or Suicide

1.1 Introduction

1.2 Role of Reactive Oxygen Species in Neural Cells

1.3 Ros-Mediated Survival Signaling in Neural Cells

1.4 Ros-Mediated Injury in Neural Cells

1.5 Conclusion

References

Chapter 2: Free Radicals, Signal Transduction, and Human Disease

2.1 Introduction

2.2 Reduction, Oxidation, and the Thermodynamics of Free Radical Reactions

2.3 Oxidative Stress and Redox Environment of a Cell

2.4 Ros, Signal Transduction, and Human Disease

2.5 Diabetes

2.6 Neurological Disorders

2.7 Conclusion

Acknowledgements

References

Chapter 3: Oxidative Stress and its Biochemical Consequences in Mitochondrial DNA Mutation-Associated Diseases: Implications of Redox Therapy for Mitochondrial Diseases

3.1 Introduction

3.2 Mitochondrial DNA Mutation-Elicited Oxidative Stress

3.3 Mitochondrial DNA Mutation and Mitochondrial Diseases

3.4 Biochemical Consequences of MTDNA Mutation in Mitochondrial Diseases

3.5 Alteration of Antioxidant Defense System in Mitochondrial Diseases

3.6 Redox Therapy of Mitochondrial Diseases

3.7 Genetics-Based Gene Therapy for Mitochondrial Diseases

3.8 Conclusion

Acknowledgments

References

Chapter 4: Oxidative Stress in Kainic Acid Neurotoxicity: Implications for the Pathogenesis of Neurotraumatic and Neurodegenerative Diseases

4.1 Introduction

4.2 Glycerophospholipid Metabolism Alterations in Ka-Induced Neurotoxicity

4.3 Sphingolipid Metabolism Alterations in Ka-Induced Neurotoxicity

4.4 Cholesterol Metabolism Alterations in Ka-Induced Neurotoxicity

4.5 Consequences of Interactions Among Glycerophospholipid-, Sphingolipid-, and Cholesterol-Derived Lipid Mediators in Ka-Mediated Neurotoxicity

4.6 Ka-Induced Neurotoxicity and its Implication for Neurotraumatic and Neurodegenerative Diseases

4.7 Conclusion

References

Chapter 5: Survival Strategy and Disease Pathogenesis According to the Nrf2-Small Maf Heterodimer

5.1 Introduction

5.2 The KEAP1-NRF2 System in Response to Electrophiles

5.3 NRF2 in The Cnc-Small Maf Transcription Factor Network

5.4 Dysfunction of NRF2 in Pathological Conditions

5.5 Conclusion and Future Perspectives

Acknowledgments

References

Chapter 6: Caloric Restriction and Oxidative Stress

6.1 Introduction

6.2 Oxidative Stress—Basic Characteristics

6.3 Mitochondria—The Main Cell Reactive Oxygen Species Generator

6.4 Reactive Oxygen Species Generated by Foods

6.5 Oxidative Stress Modulated by Caloric Restriction and Other Factors

6.6 Biomarkers Indicating Molecular Changes in Caloric Restriction

6.7 Conclusion

Acknowledgments

References

Chapter 7: Pathogenesis of Neurodegenerative Diseases: Contribution of Oxidative Stress and Neuroinflammation

7.1 Introduction

7.2 Oxidative and Nitrosative Stress in Neurodegenerative Diseases

7.3 Inflammation and Neurodegenerative Diseases

7.4 Significance of Interplay Among Excitotoxicity, Oxidative Stress, and Neuroinflammation

7.5 Conclusion

References

Chapter 8: Neurosteroids in Oxidative Stress-Mediated Injury in Alzheimer Disease

8.1 Introduction

8.2 Evidence For a Pathological Role for Oxidative Stress in AD

8.3 Neurosteroids

8.4 Neurosteroids and Oxidative Stress

8.5 Conclusion

References

Chapter 9: Oxidative Stress in Adult Neurogenesis and in the Pathogenesis of Alzheimer Disease

9.1 Introduction

9.2 Alzheimer Disease

9.3 Adult Neurogenesis and Enhanced Neurogenesis in Alzheimer Disease

9.4 Oxidative Stress: A Risk Factor for Developing Alzheimer Disease

9.5 Conclusion

References

Chapter 10: Oxidative Stress and Parkinson Disease

10.1 Introduction

10.2 Reactive Oxygen Species and Oxidative Stress

10.3 Oxidative Stress and PD

10.4 Therapeutic Implications

10.5 Conclusion

Acknowledgments

References

Chapter 11: Oxidative Stress in Cardiovascular Diseases

11.1 Introduction

11.2 Free Radicals—Origins and Fates

11.3 Cardiovascular Diseases

11.4 Exercise and Protection against Free Radical-Mediated Cardiovascular Diseases

11.5 Antioxidant Therapies for Cardiovascular Diseases

11.6 Conclusion

References

Chapter 12: Oxidative Stress and Aging: A Comparison between Vertebrates and Invertebrates

12.1 Introduction

12.2 Theories of Aging

12.3 Free Radical/Oxidative Stress Theory of Aging

12.4 Aging in Invertebrates: Role of Oxidative Stress

12.5 Aging in Vertebrates: Role of Oxidative Stress

12.6 Conclusion

Acknowledgments

References

Chapter 13: Oxidative Stress-Mediated Signaling Pathways by Environmental Stressors

13.1 Introduction

13.2 Oxidative Stress-Mediated Signaling Pathways

13.3 Conclusion

Acknowledgments

References

Chapter 14: Selenoproteins in Cellular Redox Regulation and Signaling

14.1 Introduction

14.2 Oxidative Stress and Selenoproteins

14.3 Selenoproteins and Redox Systems

14.4 Selenoproteins in Vertebrate Signaling

14.5 The Selenoprotein Family

14.6 Conclusion and Future Perspectives

References

Chapter 15: Antioxidant Therapy and its Effectiveness in Oxidative Stress-Mediated Disorders

15.1 Introduction

15.2 Aging

15.3 Cardiovascular Disease, Risk, and Ischemia-Reperfusion Injury

15.4 ROS and Neurodegenerative Disorders

15.5 Complex Regional Pain Syndrome

15.6 Cancer

15.7 Association Between ROS and Various Diseases

15.8 Pregnancy and Preeclampsia

15.9 Asthma

15.10 Chronic Obstructive Pulmonary Disease

15.11 Diabetes Type 1 and Type 2

15.12 Liver Diseases

15.13 Pancreatitis

15.14 Rheumatoid Arthritis

15.15 Kidney Diseases

15.16 Concluding Remarks

15.17 Conflict of Interest Statement

15.18 Statement of Authorship

Acknowledgements

References

Chapter 16: The Protective Role of Grape Seed Polyphenols against Oxidative Stress in Treating Neurodegenerative Diseases

16.1 Introduction

16.2 Alzheimer Disease Neuropathology Features: Implications for Therapeutic Developments

16.3 Potential Roles of Red Wines and Wine-Derived Polyphenols in Alzheimer Disease Prevention and/or Therapy

16.4 The Tg2576 AD Mouse Model

16.5 Exploring the Potential Benefits of Moderate RED Wine Consumption in Tg2576 Mice

16.6 Moderate Consumption of a Red Cabernet Sauvignon Wine Attenuates AD-Type Neuropathology and Cognitive Deterioration in Tg2576 Mice

16.7 Exploring for Potential Beneficial AD Disease-Modifying Activity in a Red Muscadine Wine with Different Polyphenolic Compositions Compared to Cabernet Sauvignon

16.8 Moderate Consumption of Red Muscadine Wine Attenuates AD-Type Neuropathology and Cognitive Deterioration in Tg2576 Mice

16.9 Dietary Grape-Derived Bioactive Polyphenolic Components: Implications in AD Therapy and Prevention

References

Chapter 17: Pharmacological and Therapeutic Properties of Propolis (Bee Glue)

17.1 Introduction

17.2 Propolis

17.3 Human Nutrition

17.4 Therapeutic Properties

17.5 Role in Cellular Signal Transduction

17.6 Toxic Effects

17.7 Commercial Use

17.8 Food Safety

17.9 Conclusion

References

Part II: Oxidative Stress in Invertebrates

Chapter 18: Endocrine Control of Oxidative Stress in Insects

18.1 Introduction

18.2 Endogenous Sources of Oxidative Stress

18.3 Exogenous Sources of Oxidative Stress

18.4 Defenses against Oxidative Stress

18.5 Regulation of Defenses against Oxidative Stress

18.6 Insect Hormones and Their Role in the Control of Oxidative Stress

18.7 Role of Adipokinetic Hormones in Insect Oxidative Stress

18.8 Role of Other Insect Hormones in Oxidative Stress

18.9 Conclusion

Acknowledgments

References

Chapter 19: Oxidative Stress in the Airway System of the Fruit Fly Drosophila melanogaster

19.1 Introduction

19.2 Oxidative Stress Systems in Drosophila

19.3 Reactive Oxygen Species and Aging

19.4 Oxidative Stress in the Nervous System

19.5 Oxidative Stress in the Digestive System

19.6 Oxidative Stress in the Immune System

19.7 Oxidative Stress in the Airway System

19.8 Conclusion

Acknowledgments

References

Chapter 20: Molecular Mechanisms of Antioxidant Protective Processes in Honeybee Apis mellifera

20.1 Introduction

20.2 Antioxidant System of Honeybee

20.3 ROS as Costs of an Aerobic Metabolism

20.4 Ontogenesis and Life Span

20.5 Winter Generation of Honeybee

20.6 Conclusion and Perspectives

References

Chapter 21: Molecular Basis of Iron-induced Oxidative Stress in the Honeybee Brain: A Potential Model System of Olfactory Dysfunction in Neurological Diseases

21.1 Introduction

21.2 A Comparision Between General Physiology of Olfactory Processing in Honeybees and Humans

21.3 Olfactory Neuronal Network in Honeybees

21.4 ROS, Olfactory Dysfunction, and Aging

21.5 Iron Induces Oxidative Stress in the Honeybee Brain

21.6 Molecular Basis of Iron-Induced Oxidative Stress

21.7 Honeybee Model System For Olfactory Dysfunction

21.8 Conclusion and Future Perspective

Acknowledgments

References

Chapter 22: Modulation of Oxidative Stress by Keap1/Nrf2 Signaling in Drosophila: Implications for Human Diseases

22.1 Introduction

22.2 Conclusion

References

Chapter 23: Orchestration of Oxidative Stress Responses in Drosophila melanogaster: A Promoter Analysis Study of Circadian Regulatory Motifs

23.1 Introduction

23.2 Promotor Analysis

23.3 Results

23.4 Discussion

23.5 Summary and Conclusion

Acknowledgments

References

Chapter 24: The Protective Role of Sestrins Against Chronic TOR Activation and Oxidative Stress

24.1 Introduction

24.2 Sestrin—A Unique Gene Family

24.3 Regulation of Sestrin Expression by Stresses

24.4 Sestrin as a Redox Regulator

24.5 Overview of TORC1 Signaling

24.6 Chronic TORC1 Induces Stress-Associated Pathologies

24.7 Sestrin as a Suppressor of TORC1

24.8 Sestrin Deficiency Results in Age-Associated Pathologies

24.9 Conclusion and Perspectives

References

Chapter 25: Current Advances in the Studies of Oxidative Stress and Age-Related Memory Impairment in C. elegans

25.1 Introduction

25.2 Memory Impairment During Aging

25.3 Cognitive Aging in C. Elegans

25.4 What Causes AMI?

25.5 Other Factors that May Cause AMI

25.6 Improved Learning and Memory

25.7 When Does Cognitive Aging Begin?

25.8 Role of Oxidative Stress in Aging and AMI: A Theory

25.9 Conclusion and Perspective

References

Chapter 26: Oxidative Challenge and Redox Sensing in Mollusks: Effects of Natural and Anthropic Stressors

26.1 Introduction

26.2 Oxidative Stress Linked to Variations in Oxygen Availability

26.3 Pollutant-Induced Oxidative Stress

26.4 Immune System

26.5 Conclusion

Acknowledgments

References

Chapter 27: Perspective and Directions for Future Studies

27.1 Introduction

27.2 Endogenous Antioxidant Defense Mechanisms in Vertebrates and Invertebrates

27.3 Biomarkers of Oxidative Stress in Vertebrates and Invertebrates

27.4 Oxidative Stress and Aging

27.5 Conclusion

References

Index

Copyright © 2012 by Wiley-Blackwell. All rights reserved.

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Library of Congress Cataloging-in-Publication Data

Oxidative stress in vertebrates and invertebrates : molecular aspects on cell signaling / Tahira Farooqui and Akhlaq A. Farooqui, editors.

p. cm.

Includes index.

ISBN 978-1-118-00194-3 (cloth)

1. Oxidative stress–Molecular aspects. 2. Oxidative stress–Pathophysiology. 3. Vertebrates–Cytology. 4. Invertebrates–Cytology. 5. Vertebrates–Diseases–Molecular aspects. 6. Invertebrates–Diseases–Molecular aspects. 7. Cellular signal transduction. I. Farooqui, Tahira. II. Farooqui, Akhlaq A.

RB170.O955 2012

571.9′453–dc23

2011037215

“Live as if you were to die tomorrow. Learn as if you were to live forever.”

Mohandas Karamchand Gandhi

PREFACE

All oxygen-utilizing animals and organisms have to deal with reactive oxygen species (ROS), which include superoxide anions, hydroxyl, alkoxyl, and peroxyl radicals, and hydrogen peroxide. These radicals are common products of life in an aerobic environment, and they are responsible for oxygen toxicity. Proteins, lipids, and nucleic acid are targets for ROS attack, and modification of these molecules can increase the risk of chronic neurodegenerative diseases, visceral diseases, and cancer. “Oxidative Stress in Vertebrates and Invertebrates: Molecular Aspects of Cell Signaling” provides readers with a comprehensive description of the latest research on oxidative stress and antioxidant defenses in vertebrate and invertebrate systems. In biological systems, cells respond to mild oxidative stress by inducing antioxidant defenses and other protective systems. The antioxidant capacities of tissues are well matched to the rates of oxygen consumption and radical production. In vertebrate and invertebrate systems a variety of endogenous antioxidants (reduced glutathione) and antioxidant enzymes (superoxide dismutase, glutathione peroxidase, glutathione reductase, and catalase) act in a concerted manner to protect tissues against oxidative damage. The balance among oxidants and antioxidant enzyme systems, levels of antioxidants, and endogenous antioxidant mechanisms may be of major importance in the protection against oxidative stress-mediated cell injury. Under normal conditions, the rate of production of oxidants is balanced by the rate of oxidant elimination. However, an imbalance between prooxidants and antioxidants results in oxidative stress. Increase in ROS production has a substantial impact cellular metabolism and may lead to either defective cellular function and aging or chronic neurodegenerative and visceral diseases. Therefore, a better understanding of the roles of ROS-mediated signaling in normal cellular function as well as in disease is necessary for the development of therapeutic agents for oxidative stress-related chronic diseases.

Unlike other edited books that focus on oxidative stress in mammals, this unique book provides a comparative account of oxidative stress and antioxidant defenses in vertebrates and invertebrates, dealing not only with basic mechanisms and biomarkers but also with oxidative stress-mediated chronic diseases. This edited book is a valuable source of information for both basic scientists and clinicians who are interested in basic mechanism and oxidative stress-associated diseases. In this book, chapters are organized into two sections: (1) oxidative stress in vertebrates (Chapters 1–17) and (2) oxidative stress in invertebrates (Chapters 18–26), followed by a perspective (Chapter 27).

In Part I, Chapters 1 and 2 deal with the generation of ROS in the brain and their signaling associated with neural cell survival, cell suicide, and diseases. Chapters 3 and 4 discuss mitochondrial DNA mutation-induced oxidative stress underlying biochemical and pathological consequences and redox therapy in mitochondrial diseases and changes in kainic acid-induced neurotoxicity, which can be implicated in the pathogenesis of neurotraumatic and neurodegenerative diseases. Chapter 5 covers the historical aspects of the discovery of NF-E2-related factor 2 (Nrf2), recent advances in molecular aspects of its function, and updates involving Nrf2 association with various pathological conditions. Chapter 6 discusses modulation of oxidative stress by caloric restriction, suggesting that a calorie-restricted diet and the composition of diet may significantly improve ROS homeostasis both in single cells as well as in the whole body. Chapters 7–10 deal with the contribution of oxidative stress and inflammation to the pathogenesis of neurodegenerative diseases (Alzheimer disease, Parkinson disease). Chapter 11 summarizes free radical contribution to the development of cardiovascular diseases and discusses the applicability of antioxidant therapy based on data from clinical trials. Chapter 12 provides a comparison between vertebrates and invertebrates with regard to oxidative stress and aging. Chapter 13 addresses various environmental stressor-induced toxicities in experimental animals like rats and humans to elucidate the molecular mechanisms underlying oxidative stress. Chapter 14 discusses the role of selenoproteins in cellular redox regulation and signaling. Chapter 15 gives a clinical demonstration of the effectiveness of antioxidant administration in different diseases. Chapter 16 demonstrates that grape-derived bioactive polyphenolic components from wine effectively protect against the onset and progression of Alzheimer disease phenotypes, suggesting that moderate wine consumption may have preventive and/or therapeutic value in Alzheimer disease. Finally, Chapter 17 discusses pharmacological and therapeutic properties of propolis, a resinous mixture that honeybees collect from tree buds, sap flow, and other botanical sources, which is very beneficial for human health because of its richness in phenolic compounds.

In Part II, Chapter 18 reviews the endocrine control of oxidative stress in insects. Chapter 19 focuses on oxidative stress and innate immune system in airway epithelial cells of the fruit fly Drosophila melanogaster. Chapter 20 explores the molecular mechanisms of antioxidant protective processes in the honeybee Apis mellifera. Chapter 21 describes a hypothetical mechanism associated with iron-induced oxidative stress, implicating ROS production in olfactory dysfunction in the honeybee brain. Chapter 22 covers cutting-edge information on the Keap1/Nrf2 system in flies as well as its implications in combating human diseases. Chapter 23 is devoted to orchestration of oxidative stress responses in Drosophila melanogaster and promoter analysis study of circadian regulatory motifs. Chapter 24 deals with the protective role of sestrins (a unique family of proteins that is critically involved in cellular defense) against chronic target of rapamycin complex activation and oxidative stress in Drosophila. Chapter 25 explores current advances in the studies of oxidative stress and age-related memory impairment in the nematode C. elegans. Chapter 26 elegantly reviews oxidative challenge and redox sensing in mollusks by focusing on effects of natural and anthropic stressors. Finally, Chapter 27 provides readers with an in-depth perspective on current progress on our understanding of oxidative stress. It also presents readers and researchers with information that will be important for future research dealing with oxidative stress.

Biochemists, neuropharmacologists, toxicologists, and clinicians will find this book useful for understanding basic mechanisms of oxidative stress in vertebrate and invertebrate systems. It is hoped that “Oxidative Stress in Vertebrates and Invertebrates: Molecular Aspects of Cell Signaling” will further stimulate young and senior scientists to perform research on oxidative stress and oxidative stress-associated diseases.

Tahira Farooqui

Akhlaq A. Farooqui

FOREWORD

Oxidative stress is a cytotoxic process that occurs in cells when antioxidant mechanisms are overwhelmed by reactive oxygen species (ROS). This imbalance not only causes damage to important biomolecules (lipids, proteins, and nucleic acids) in cells, but also has an impact on functional activities in both vertebrates and invertebrates. This new volume entitled “Oxidative Stress in Vertebrates and Invertebrates: Molecular Aspects of Cell Signaling” brings together important information from expert researchers in the oxidative stress-mediated cell signaling area in both vertebrate and invertebrate systems. Accumulation of high levels of ROS and significant reduction in cellular redox systems are common processes associated with acute and chronic visceral and neurodegenerative diseases, including hypertension, preeclampsia, arteriosclerosis, acute renal failure, diabetes, and Alzheimer and Parkinson diseases. This well-organized book presents up-to-date and comprehensive information on oxidative stress-related signaling events in vertebrates and invertebrates. The text is clear, concise, and easily accessible. Subject matter is divided into a vertebrate section (17 chapters) and an invertebrate section (10 chapters). The editors are known for their work on oxidative stress and neurodegeneration. They have done a commendable job in putting together this volume, and have contributed 5 chapters. These editors have taken great care in selecting the topics and describing progress that has been recently made in this field. The authors of this book also tried to ensure uniformity and mode of presentation in a simple and clear manner.

Topics addressed in the vertebrate section include the generation of ROS and their roles in cell survival and suicide; ROS-induced signal transduction and human diseases; biochemical and pathological consequences and redox therapy; pathogenesis of neurotraumatic and neurodegenerative diseases; oxidative stress mediated by caloric restriction; the role of oxidative stress and neuroinflammation in Alzheimer disease and Parkinson disease; selenoproteins in cellular redox regulation and signaling; antioxidant therapy and its effectiveness in oxidative stress-mediated disorders; pharmacological and therapeutic properties of propolis; comparison of oxidative stress in aging between vertebrates and invertebrates; and finally, oxidative stress-mediated signaling pathways by environmental stressors. The invertebrate section includes oxidative stress-induced signaling in three important phyla, namely, arthropoda, annelida, and mollusca. Topics addressed in this section include effect of oxidative stress on insect endocrine control; the innate immune system in airway epithelial cells of Drosophila; age-related memory impairment in C. elegans; olfactory learning and memory in Apis mellifera; Keap1/Nrf2 signaling in Drosophila; circadian rhythm in Drosophila; molecular antioxidant protective processes in Apis mellifera; protective role of sestrins against chronic TOR; and oxidative challenge and redox sensing in mollusks.

The subject matter in this book develops logically and progresses from one topic to another with an extensive bibliography along with major primary references. These references will help readers in pursuing their areas of interest. In order to facilitate better understanding and easier reading, this book also contains a large number of figures and line diagrams of signal transduction pathways. This book fills the gap between basic science and clinical studies and provides the reader with the skills to apply basic science to clinical settings of chronic diseases associated with oxidative stress.

This book is essential reading material for a broad range of individuals, including researchers, clinicians, graduate and medical students, as well as the many health-conscious individuals who wish to know more about the emerging field of oxidative stress in vertebrate and invertebrate systems. It can be used as a supplemental text for a range of biology courses. It is anticipated that senior neuroscientists may also find some inspiration from this book to overcome problems encountered in their research on oxidative stress in vertebrate and invertebrate systems.

Grace Y. Sun

Department of Biochemistry

Department of Pathology and Anatomical Sciences, and

Department of Nutritional Sciences

University of Missouri

Columbia, MO

ACKNOWLEDGMENTS

We express our deepest appreciation in acknowledging our teachers for their excellent teaching, guidance, inspiration, and influence on our lives. We also thank all authors for sharing their expertise by contributing chapters of high standard, thus making our editorial task much easier. We are grateful for the cooperation and patience of Dr. Karen E. Chambers and Anna Ehler at John Wiley & Sons for helpful discussions and advice during compilation of this book. We are also thankful to Kris Parrish at Wiley and Shanmuga Priya at Macmillan Publishing Solutions for handling the production process in a most efficient, cooperative, and remarkable manner.

Tahira Farooqui

Akhlaq A. Farooqui

CONTRIBUTORS

Hiromi Akanuma, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan

Danielle Anderson, Aging-Osteopathic Consortium, Department of Basic Sciences, College of Osteopathic Medicine, Touro University-California, Vallejo, CA, USA

Michael E. Andrades, Postgraduate Program in Cardiology, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil

Kandangath Raghavan Anilakumar, Biochemistry & Nutrition Discipline, Defence Food Research Laboratory, Mysore, India

Amarinder Singh Bawa, Biochemistry & Nutrition Discipline, Defence Food Research Laboratory, Mysore, India

Marla J. Berry, Department of Cell and Molecular Biology, University of Hawaii, Biomedical Sciences Building, Honolulu, HI, USA

Ethan Bier, Section of Cell and Developmental Biology, University of California San Diego, La Jolla, California, USA

Dirk Bohmann, University of Rochester Medical Center, Department of Biomedical Genetics, Rochester, NY, USA

Kelly Cabana, Aging-Osteopathic Consortium, Department of Basic Sciences, College of Osteopathic Medicine, Touro University-California, Vallejo, CA, USA

Fabrice Durand, Laboratoire d’Ecotoxicologie—Milieux Aquatiques EA, Université du Havre, Le Havre Cedex, France

Anne Eckert, Neurobiology Laboratory for Brain Aging and Mental Health, Psychiatric University Clinics, University of Basel, Basel, Switzerland

Akhlaq A. Farooqui, Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio, USA

Tahira Farooqui, Department of Entomology/Center of Molecular Neurobiology, The Ohio State University, Columbus, Ohio, USA

Louisa R. Gaifullina, Institute of Biochemistry and Genetics, Ufa Science Center RAS, Ufa, Russia

Doyle Graham, Duke-NUS Graduate Medical School, Singapore

Amandine Grimm, Neurobiology Laboratory for Brain Aging and Mental Health, Psychiatric University Clinics, University of Basel, Basel, Switzerland

Tommaso Iannitti, Department of Biological and Biomedical Sciences, Glasgow Caledonian University, Glasgow, UK

Klaudia Jomova, Department of Chemistry, Faculty of Natural Sciences, Constantine The Philosopher University, Nitra, Slovakia

Farhath Khanum, Biochemistry & Nutrition Discipline, Defence Food Research Laboratory, Mysore, India

Dalibor Kodrík, Institute of Entomology, Biology Centre, Czech Academy of Sciences, České Budějovice, Czech Republic

Natraj Krishnan, Department of Zoology, Oregon State University, Corvallis, OR, USA and Department of Biochemistry, Molecular Biology, Entomology and Plant Pathology, Mississippi State University, Starkville, MS, USA

Jun Hee Lee, Department of Molecular and Integrative Physiology, University of Michigan, Ann Arbor, Michigan, USA

François Leboulenger, Laboratoire d’Ecotoxicologie—Milieux Aquatiques EA, Université du Havre, Le Havre Cedex, France

Julie Letendre, Laboratoire d’Ecotoxicologie—Milieux Aquatiques EA, Université du Havre, Le Havre Cedex, France

Kah-Leong Lim, Department of Physiology, National University of Singapore, Singapore; Duke-NUS Graduate Medical School, Singapore; Neuroscience Research Partnership, A*STAR, Singapore; and National Neuroscience Institute, Singapore

Rodrigo Lorenzi, Faculté de Médecine, Lille 2 University, Lille, France

Yi-Shing Ma, Department of Biochemistry and Molecular Biology, School of Life Sciences, National Yang-Ming University, Taipei, Taiwan

Ayikoe Guy Mensah-Nyagan, Equipe Stéroïdes, Neuromodulateurs et Neuropathologies, Université de Strasbourg, Strasbourg, France

Masanobu Morita, Department of Medical Biochemistry, Tohoku University Graduate School of Medicine, Aoba-ku, Sendai, Japan

Hozumi Motohashi, Center for Radioisotope Sciences, Tohoku University Graduate School of Medicine, Aoba-ku, Sendai, Japan

Shin Murakami, Aging-Osteopathic Consortium, Department of Basic Sciences, College of Osteopathic Medicine, Touro University-California, Vallejo, CA, USA

Xiao-Hui Ng, Department of Physiology, National University of Singapore, Singapore

Alexey G. Nikolenko, Institute of Biochemistry and Genetics, Ufa Science Center RAS, Ufa, Russia

Kanti Bhooshan Pandey, Department of Biochemistry, University of Allahabad, Allahabad, India

Beniamino Palmieri, Department of General Surgery and Surgical Specialties, Medical School and Surgical Clinic, University of Modena and Reggio Emilia, Modena, Italy

Giulio Maria Pasinetti, Department of Neurology, The Mount Sinai School of Medicine, New York, USA

M. Mahidur Rahman, University of Rochester Medical Center, Department of Biomedical Genetics, Rochester, NY, USA

Kuntol Rakshit, Department of Zoology, Oregon State University, Corvallis, OR, USA

Arjun V. Raman, Department of Cell and Molecular Biology, University of Hawaii, Biomedical Sciences Building, Honolulu, HI, USA

Syed Ibrahim Rizvi, Department of Biochemistry, University of Allahabad, Allahabad, India

Thomas Roeder, Christian Albrechts Universitaet zu Kiel, Zoophysiology II, Kiel, Germany

Elena S. Saltykova, Institute of Biochemistry and Genetics, Ufa Science Center RAS, Ufa, Russia

Jan Škrha, Laboratory for Endocrinology and Metabolism and 3rd Department of Internal Medicine, 1st Faculty of Medicine, Charles University in Prague, U Nemocnice, Prague, Czech Republic

Hideko Sone, National Institute for Environmental Studies, Tsukuba, Ibaraki, Japan

Gerasimos P. Sykiotis, University of Patras Medical School, Department of Internal Medicine, Division of Endocrinology and Metabolism, Patras, Greece

Philippe Taupin, School of Biotechnology, Dublin City University, Glasnevin, Dublin, Ireland

Marian Valko, Department of Chemistry, Faculty of Natural Sciences, Constantine The Philosopher University, Nitra, Slovakia and Faculty of Chemical and Food Technology, Slovak Technical University, Bratislava, Slovakia

Yau-Huei Wei, Department of Biochemistry and Molecular Biology, School of Life Sciences, National Yang-Ming University, Taipei, Taiwan and Department of Medicine, Mackay Medical College, New Taipei City, Taiwan

Shi-Bei Wu, Department of Biochemistry and Molecular Biology, School of Life Sciences, National Yang-Ming University, Taipei, Taiwan

Yu-Ting Wu, Department of Biochemistry and Molecular Biology, School of Life Sciences, National Yang-Ming University, Taipei, Taiwan

PART I

OXIDATIVE STRESS IN VERTEBRATES

CHAPTER 1

GENERATION OF REACTIVE OXYGEN SPECIES IN THE BRAIN: SIGNALING FOR NEURAL CELL SURVIVAL OR SUICIDE

Akhlaq A. Farooqui

Department of Molecular and Cellular Biochemistry, The Ohio State University, Columbus, Ohio, USA

1.1 INTRODUCTION

Oxidative stress is a redox-sensitive process that occurs in the cell when antioxidant mechanisms are overwhelmed by the generation of reactive oxygen species (ROS), leading to oxidation of lipids, proteins, and DNA in ways that impair cellular function [1]. Thus oxidative stress is a threshold phenomenon characterized by a major increase in the amount of oxidized cellular components. ROS include superoxide anions, hydroxyl, alkoxyl, and peroxyl radicals, and hydrogen peroxide, which are generated as by-products of oxidative metabolism, in which energy activation and electron reduction are involved. The chemical reactivity of ROS varies from the very toxic hydroxyl (•OH−) to the less reactive superoxide radical (). The initial product, results from the addition of a single electron to molecular oxygen. is rapidly dismutated by superoxide dismutase (SOD), yielding H2O2 and O2, which can be reused to generate superoxide radical. In the presence of reduced transition metals, H2O2, although less reactive than and highly diffusible, can be converted into the highly reactive hydroxyl radical The tight regulation of ROS generation and removal makes fluctuations in their levels transient, a feature that is characteristic of second messengers. ROS may also act as an intracellular “rheostat,” closely modulating the activity of a discrete set of biochemical reactions, which contribute to cell proliferation, migration, and survival [2]. ROS not only inactivate membrane proteins and DNA but also promote peroxidation of neural membrane polyunsaturated fatty acids associated with glycerophospholipids, enhance levels of ceramide, and facilitate the formation of hydroxyl/ketocholesterol levels (Fig. 1.1). These processes promote neurodegeneration through apoptosis [3–5]. The polyunsaturated fatty acids, which are located at the sn-2 position of glycerol moiety in the glycerophospholipid, are most susceptible to free radical attack at the α-methylene carbon in the alkyl chain of the fatty acid that is adjacent to the carbon-carbon double bond. Under aerobic conditions a polyunsaturated fatty acid with an unpaired electron undergoes a molecular rearrangement by reaction with O2 to generate a peroxyl radical. The peroxyl radical captures hydrogen atoms from the adjacent fatty acids to form a lipid hydroperoxide. The lipid hydroperoxides thus formed are not completely stable in vivo and, in the presence of iron, can further break down to radicals that can propagate the chain reactions started by an initial free radical attack. The major sources of ROS are the mitochondrial respiratory chain, where is generated by electron leakage from complexes I and III of the electron transport chain () [6, 7]. Microsomes and peroxisomes are also sources of ROS, primarily HO, whereas immune cells such as neutrophils and macrophages possess oxygen-dependent mechanisms to fight against invading microorganisms. Enzymes, such as xanthine/xanthine oxidase, myeloperoxidase, cytochrome 450 in cell cytoplasm, COX, LOX, nitric oxide synthase, and NADPH oxidase contribute to ROS production in plasma membranes and mitochondria (). The presence of redox-active metals, such as iron and copper, also contributes to ROS generation. In the presence of Fe and Fe, can be generated through the Fenton reaction or the Haber–Weiss reaction [7].