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Abstract
Gasotransmitters are gas molecules produced endogenously in prokaryotic and eukaryotic cells for signalling purposes. This book provides, for the first time, a comprehensive description and systematic look at all gasotransmitters, established or proposed, since their detection in 2002. The content and scope covers the production, metabolism, and signalling roles of gasotransmitters. Conceptual advances, scientific discoveries and newly developed techniques described in this book influence our understanding of fundamental molecular and cellular events in biology and medicine.
This book serves as the state-of-the-art book for undergraduate and graduate students as well as post-doctoral fellows in biomedical disciplines and toxicologists studying the toxic mechanisms of gasotransmitters in the environment. It will also be welcomed by researchers in university and research institutes, government agencies, pharmaceutical and medical instrument industry, and clinical practice.
Dr. Rui Wang is the Vice-President Research and a professor of Biology of Laurentian University in Canada. He served as Vice President of Research, Economic Development and Innovation at Lakehead University in Canada until 2015. Prior to that, Dr. Wang was a Professor of Physiology and leader of both the Cardiovascular Research Group and the Cardiovascular and Respiratory Network at the University of Saskatchewan, and an Assistant Professor at the Université de Montréal. Dr. Wang was trained in China as a medical doctor, and later received his PhD degree in 1990 from the University of Alberta. He was the first to conceptualize the gasotransmitter family in 2002. His achievements have been recognized with numerous national and international honors and awards, including election to fellow of the Canadian Academy of Health Sciences in 2010 and recipient of the Pfizer Senior Scientist Award from Canadian Society of Pharmacology and Therapeutics in 2008. Dr. Wang has published about 266 peer-reviewed papers in leading scientific journals, including Science and Cell. His publication on H2S biology and medicine has received the highest citations in this field in the world.
Table of Contents
| Section Title | Page | Action | Price |
|---|---|---|---|
| Cover | Cover | ||
| Preface | v | ||
| Contents | vii | ||
| Chapter 1 Overview of Gasotransmitters and the Related Signaling Network | 1 | ||
| 1.1 Conceptualization and Evaluation Systems for Gasotransmitters | 2 | ||
| 1.2 Gasotransmitters – Why Does the Terminology Matter? | 10 | ||
| 1.3 The Gasotransmitter Signaling Network in Eukaryotes | 11 | ||
| 1.3.1 Interaction of Gasotransmitters with Their Producers | 12 | ||
| 1.3.2 Interaction of Gasotransmitters with Their Users/Targets | 14 | ||
| 1.3.3 Interaction of Gasotransmitters with Their Sensors | 19 | ||
| 1.3.4 Interactions Between Gasotransmitters | 23 | ||
| Acknowledgements | 24 | ||
| References | 24 | ||
| Chapter 2 Production of NO – The L-arginine/NOS/NO System | 29 | ||
| 2.1 Introduction | 29 | ||
| 2.2 Biosynthesis and Sources of NO | 30 | ||
| 2.2.1 Biosynthesis of NO from L-arginine | 31 | ||
| 2.2.2 Synthesis of NO from Inorganic Nitrates | 31 | ||
| 2.2.3 Biosynthesis of NO from Homoarginine | 34 | ||
| 2.3 Regulation of NO Production | 34 | ||
| 2.3.1 Spatial Compartmentalization and Localization | 34 | ||
| 2.3.2 Modulation at the Level of Enzymatic Activity | 35 | ||
| 2.3.3 Metabolic Control of NO Production | 35 | ||
| 2.3.4 Regulation by Arginases | 36 | ||
| 2.3.5 Regulation by Arginine Transport | 36 | ||
| 2.4 Dysregulation of NO Disposition and Disease | 37 | ||
| 2.4.1 Nitric Oxide and Cardiovascular Disease | 37 | ||
| 2.4.2 Nitric Oxide and the Reproductive System | 37 | ||
| 2.4.3 Nitric Oxide and Neurodegeneration | 37 | ||
| 2.5 Concluding Remarks | 39 | ||
| Acknowledgements | 39 | ||
| References | 39 | ||
| Chapter 3 Production of H2S – The L-cysteine/CSE-CBS-MST/H2S System | 44 | ||
| 3.1 Introduction to H2S in Mammalian Cells | 44 | ||
| 3.2 Production of H2S in Mammalian Cells Involving CSE | 46 | ||
| 3.3 Production of H2S in Mammalian Cells Involving CBS | 47 | ||
| 3.4 Production of H2S in Mammalian Cells Involving MST | 48 | ||
| 3.4.1 Discovery of H2S Production by MST | 48 | ||
| 3.4.2 Mechanisms for H2S Production by MST | 49 | ||
| 3.4.3 Tissue Distribution of MST | 50 | ||
| 3.4.4 Regulation of H2S Production by MST | 51 | ||
| 3.5 Relationship between the Production of H2S and Polysulfide | 51 | ||
| 3.6 Non-enzymatic H2S Production in Mammalian Cells | 52 | ||
| 3.6.1 Release of H2S from Bound Sulfur | 52 | ||
| 3.6.2 H2S Production from Organic Polysulfides by Thiol Reactions | 52 | ||
| 3.6.3 H2S Production by Human Erythrocytes | 52 | ||
| 3.7 Exogenous H2S Donors in Mammalian Cells | 52 | ||
| 3.7.1 Naturally Occurring Donors of H2S | 52 | ||
| 3.7.2 Synthetic H2S Donors | 53 | ||
| References | 55 | ||
| Chapter 4 HO-1-derived CO Is a Regulator of Vascular Function and Metabolic Syndrome | 59 | ||
| 4.1 Introduction | 59 | ||
| 4.2 Formation of CO | 60 | ||
| 4.3 Role of Excessive Heme in Obesity: HO-1-derived CO | 61 | ||
| 4.4 Actions of CO on the Vasculature | 64 | ||
| 4.5 CO and the Regulation of Blood Pressure | 65 | ||
| 4.6 Metabolic Syndrome and Heme Metabolism | 67 | ||
| 4.7 Mitochondrial Dysfunction in Metabolic Syndrome | 71 | ||
| 4.8 Regulatory Role of HO-1 in Mitochondrial Function and Oxidative Phosphorylation | 73 | ||
| 4.9 Oxidative Stress and Mitochondrial Dysfunction | 76 | ||
| 4.10 HO-1 Gene Targeting in Obesity and Hypertension | 78 | ||
| 4.11 Bioactive Role of Biliverdin/Bilirubin | 80 | ||
| 4.12 Bioactive Role of Iron and Ferritin | 81 | ||
| 4.13 Therapeutic Potential of the EET-Heme-HO-1-derived CO/Bilirubin | 81 | ||
| 4.14 Concluding Remarks | 84 | ||
| Acknowledgements | 84 | ||
| References | 84 | ||
| Chapter 5 Production and Signaling Functions of Ammonia in Mammalian Cells | 101 | ||
| 5.1 Introduction | 101 | ||
| 5.2 Production and Metabolism of Ammonia | 102 | ||
| 5.2.1 Production of Ammonia | 103 | ||
| 5.2.2 Transport of Ammonia | 107 | ||
| 5.2.3 Removal and Conversion of Ammonia | 108 | ||
| 5.3 Physiological Roles of Ammonia as a Gasotransmitter | 110 | ||
| 5.3.1 Roles of Ammonia in the Nervous System | 110 | ||
| 5.3.2 Effects of Ammonia on the Cardiovascular System | 122 | ||
| 5.3.3 Effects of Ammonia on the Immune System | 129 | ||
| 5.3.4 Effects of Ammonia on Other Systems | 130 | ||
| 5.4 Pathophysiological Roles of Ammonia | 132 | ||
| 5.4.1 Cytotoxic Effects and Cell Swelling and Death | 132 | ||
| 5.4.2 Energy Metabolism | 134 | ||
| 5.4.3 Oxidative/Nitrosative Stress | 135 | ||
| 5.4.4 Mitochondrial Permeability Transition | 135 | ||
| 5.4.5 Impairments in Learning and Memory | 136 | ||
| 5.4.6 Alterations in Gene Expression | 136 | ||
| 5.4.7 Toxic Effects of Ammonia on Other Organs | 137 | ||
| 5.5 Perspectives | 137 | ||
| Acknowledgements | 139 | ||
| References | 139 | ||
| Chapter 6 The Interaction of NO and H2S Signaling Systems in Biology and Medicine | 145 | ||
| 6.1 Introduction | 145 | ||
| 6.2 Biosynthesis and Metabolism of H2S and NO | 146 | ||
| 6.2.1 Biosynthesis and Metabolism of H2S | 146 | ||
| 6.2.2 Biosynthesis and Metabolism of NO | 147 | ||
| 6.3 Biochemistry of H2S and NO Interactions | 147 | ||
| 6.3.1 Mutual Regulation of the Bioavailability of H2S and NO | 147 | ||
| 6.3.2 The Direct Reaction of H2S and NO Generates Bioactive Molecules | 149 | ||
| 6.4 Interactions of H2S and NO in the Cardiovascular System | 149 | ||
| 6.4.1 H2S/NO Interactions in the Regulation of Heart Contractility | 149 | ||
| 6.4.2 H2S/NO Interactions in Cardioprotection | 150 | ||
| 6.4.3 H2S/NO Interactions in the Maintenance of Vascular Tone | 151 | ||
| 6.5 Interaction of H2S and NO in Cancer | 151 | ||
| 6.6 Interactions of H2S and NO in Inflammation | 152 | ||
| 6.7 NOSH Compounds Display Therapeutic Benefits | 153 | ||
| 6.8 Concluding Remarks | 153 | ||
| References | 155 | ||
| Chapter 7 Signaling by CO: Molecular and Cellular Functions | 161 | ||
| 7.1 Introduction | 161 | ||
| 7.2 Cellular Targets of CO | 163 | ||
| 7.2.1 Cytochrome c and Cytochrome c Oxidase | 164 | ||
| 7.2.2 Guanylate Cyclase | 165 | ||
| 7.2.3 Ion Channels | 166 | ||
| 7.2.4 NADPH Oxidase | 166 | ||
| 7.2.5 Cystathionine Beta Synthase | 167 | ||
| 7.2.6 Heme-dependent Transcription Factors | 167 | ||
| 7.2.7 Other Metal-containing Proteins Targeted by CO | 168 | ||
| 7.3 CO in the Regulation of Vascular Tone | 168 | ||
| 7.4 CO in Cell Proliferation and Apoptosis | 170 | ||
| 7.5 CO as a Neurotransmitter | 171 | ||
| 7.6 CO in Redox Regulation | 173 | ||
| 7.7 CO in Inflammation | 175 | ||
| 7.7.1 Anti-inflammatory Activity of the HO-1/CO Pathway | 175 | ||
| 7.7.2 Mechanisms Underlying the Anti-inflammatory Activity of CO | 178 | ||
| 7.8 CO in the Regulation of Energetic Metabolism | 180 | ||
| 7.9 Conclusions | 182 | ||
| Acknowledgements | 183 | ||
| References | 183 | ||
| Chapter 8 Production and Signaling of Methane | 192 | ||
| 8.1 Introduction | 192 | ||
| 8.2 Physico-chemical Properties and Toxicity of CH4 | 193 | ||
| 8.3 Methanogenesis – Biotic and Abiotic Sources in the Environment | 193 | ||
| 8.3.1 Abiotic Sources of CH4 (IncludingThermogenic Degradation of Organic Matter) | 194 | ||
| 8.3.2 Microbial Methanogenesis – Formation of CH4 by Archaea | 194 | ||
| 8.3.3 Non-archaeal CH4 Formation in Eukaryotes | 195 | ||
| 8.4 Potential Pathways of CH4 Formation in Eukaryotes | 196 | ||
| 8.5 Human CH4 Production – Archaeal and Non-archaeal Sources | 199 | ||
| 8.6 Intestinal Gases and the Influence of CH4 on Gastrointestinal Motility | 202 | ||
| 8.7 Effects of CH4 on the Metabolism | 205 | ||
| 8.8 Interaction with Other Biological Gases: CO, NO, and H2S | 207 | ||
| 8.9 Bioactivity of Exogenous CH4 | 210 | ||
| 8.9.1 CH4 Effects in Sterile and Infectious Inflammation | 212 | ||
| 8.9.2 Endotoxemia | 212 | ||
| 8.9.3 Autoimmune Inflammation | 213 | ||
| 8.9.4 Experimental Colitis | 213 | ||
| 8.9.5 Ischemia–Reperfusion | 213 | ||
| 8.9.6 Neuroprotection | 217 | ||
| 8.9.7 Mitochondrial Effects | 220 | ||
| 8.10 Mechanism of Action | 223 | ||
| 8.10.1 Theory of a Membrane-associated Mechanism of Action | 223 | ||
| 8.10.2 CH4 Accumulation May IndirectlyInfluence the Intracellular Signaling Reactions that Lead to Anti-inflammatory Effects | 225 | ||
| 8.11 Conclusions | 226 | ||
| Acknowledgements | 228 | ||
| References | 228 | ||
| Chapter 9 Gasotransmitters in Plants | 235 | ||
| 9.1 Nitric Oxide in Plants | 235 | ||
| 9.1.1 Introduction to NO in Plants | 235 | ||
| 9.1.2 Production of Endogenous NO in Plants | 236 | ||
| 9.1.3 Signal Function of NO in Plants | 238 | ||
| 9.1.4 Functional Mechanism of NO in Plants | 242 | ||
| 9.1.5 Conclusions and Perspectives | 247 | ||
| 9.2 Carbon Monoxide in Plants | 248 | ||
| 9.2.1 Introduction to CO in Plants | 248 | ||
| 9.2.2 Production of Endogenous CO in Plants | 248 | ||
| 9.2.3 Physiological Functions of CO in Plants | 248 | ||
| 9.2.4 Future of CO in Plants | 250 | ||
| 9.3 Hydrogen Sulfide in Plants | 250 | ||
| 9.3.1 Introduction to H2S | 250 | ||
| 9.3.2 Generation of Endogenous H2S in Plants | 251 | ||
| 9.3.3 Physiological Functions of H2S Signals in Plants | 252 | ||
| 9.3.4 Function Mechanism of H2S in Plants | 253 | ||
| 9.4 Ammonia in Plants | 257 | ||
| 9.4.1 Introduction to NH3 in Plants | 257 | ||
| 9.4.2 Production of Endogenous NH3 in Plants | 258 | ||
| 9.4.3 Signal Function and Mechanism of NH3 in Plants | 259 | ||
| 9.5 Methane in Methanogens and Plants | 259 | ||
| 9.5.1 Introduction to CH4 | 259 | ||
| 9.5.2 Production of Endogenous CH4 in Methanogenic Archaea and Plants | 260 | ||
| 9.5.3 Signal Functions and Mechanisms of CH4 in Plants | 264 | ||
| 9.6 Ethylene in Plants | 264 | ||
| 9.6.1 Introduction to Ethylene in Plants | 264 | ||
| 9.6.2 Production of Endogenous Ethylene in Plants | 264 | ||
| 9.6.3 Signal Functions and Mechanisms of Ethylene in Plants | 265 | ||
| 9.7 Further Research Prospects | 267 | ||
| Abbreviations | 268 | ||
| References | 271 | ||
| Appendix Gasotransmitters: Growing Pains and Joys | 283 | ||
| A.1 Appraisal of the Known Gasotransmitters | 284 | ||
| A.2 Advocacy of Gasotransmitters as Favored Signaling Molecules for Eukaryotes | 286 | ||
| A.2.1 Simplicity | 286 | ||
| A.2.2 Availability | 286 | ||
| A.2.3 Volatility | 286 | ||
| A.2.4 Effectiveness | 286 | ||
| A.3 Ambiguity of the Interactions amongGasotransmitters and the Significance of Their Crosstalk | 287 | ||
| A.4 Additions to the Gasotransmitter Family | 287 | ||
| A.4.1 Ammonia (NH3) | 288 | ||
| A.4.2 Methane (CH4) | 290 | ||
| A.4.3 Hydrogen Gas (H2) | 292 | ||
| A.5 Concluding Remarks | 292 | ||
| Acknowledgements | 293 | ||
| References | 293 | ||
| Subject Index | 296 |