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To produce energy, aerobic organisms transform oxygen molecules into water. This reductive mechanism yields toxic radical intermediates, collectively known as reactive oxygen species (ROS). Paradoxically, these physiological processes entail the production of potentially damaging species. Evolution has turned this apparent disadvantage into an opportunity for transmitting information. As a result, redox signaling within the cell is an efficient exquisitely organized process. A key element for its regulation is the physical separation of sources and targets into different cell compartments. Peroxiporins, H2O2 transporting proteins spanning biological membranes, distribute the signal from emitters to receptors. Thus, these channels are strategically situated in the thin line between life and death, guaranteeing adequate but safe signaling. Key Features: - Provides a brief history of the discovery and characterization of peroxiporins - Reviews key findings on hydrogen peroxide transport across biological membranes - Discusses the cartography of redox signaling in crowded cells - Includes lavish illustrations and comprehensive images to facilitate teaching - Highlights recent findings, outstanding controversies and open questions
Much of the biology of oxidative stress and oxidative signalling centres on the generation and handling of hydrogen peroxide. The overall aim for this book would be to provide an insightful and useful forum to assist with the understanding of the relevance of hydrogen peroxide generation and how this is managed in human biology. The target audience would be those who currently have an interest in the generation of ROS, but who do not have expertise in chemistry, as well as those experts in the chemistry of oxidative stress, but without detailed understanding of the biologically relevant setting. We would aim to bridge the gap in understanding between chemistry and biology.
Oxidative Stress: Eustress and Distress presents current knowledge on oxidative stress within the framework of redox biology and translational medicine. It describes eustress and distress in molecular terms and with novel imaging and chemogenetic approaches in four sections: - A conceptual framework for studying oxidative stress. - Processes and oxidative stress responses. Signaling in major enzyme systems (oxidative eustress), and damaging modification of biomolecules (oxidative distress). - The exposome addresses lifelong exposure and impact on health, nutrient sensing, exercise and environmental pollution. - Health and disease processes, including ischemia-reperfusion injury, developmental and psychological disorders, hepatic encephalopathy, skeletal muscle disorders, pulmonary disease, gut disease, organ fibrosis, and cancer. Oxidative Stress: Eustress and Distress is an informative resource useful for active researchers and students in biochemistry, molecular biology, medicinal chemistry, pharmaceutical science, nutrition, exercise physiology, analytical chemistry, cell biology, pharmacology, clinical medicine, and environmental science. - Characterizes oxidative stress within the framework of redox biology, redox signaling, and medicine - Empowers researchers and students to quantify specific reactants noninvasively, identify redox biomarkers, and advance translational studies - Features contributions from international leaders in oxidative stress and redox biology research
These proceedings of the 2018 XIII International Symposium on Spermatology focus on comparative biology, and encourages discussion and the exchange of ideas. The aim of this Symposium was to provide a unique opportunity and bring together scientists from a wide spectrum of research fields – human, domestic animals and other mammals, vertebrates, insects, and plants. The underlying focus is on the function of the spermatozoon – a common feature for sexual reproduction, but extremely varied. By exploring the variability, a better understanding of male reproductive functions can develop. These proceedings address the mechanisms of physiology and pathophysiology, rather than diagnosis and treatment. The symposium featured keynote lectures by invited speakers, followed by presentations on specific aspects of the general topic of the session. Experimental studies are given priority over clinical studies of patient populations. The proceedings comprise both keynote speakers' texts and selected free communications. Posters were considered for publication in the proceedings, and the volume includes exhibited materials on the work of prominent spermatologists, highlighting their important past achievements in the field.
Glutathione (GSH) has been described for a long time just as a defensive reagent against the action of toxic xenobiotics (drugs, pollutants, carcinogens), both directly and as a cofactor for GSH transferases. As a prototype antioxidant, it has been involved in cell protection from the noxious effect of excess oxidant stress, both directly and as a cofactor of glutathione peroxidases. In addition, it has long been known that GSH is capable of forming disulfide bonds with cysteine residues of proteins, and the relevance of this mechanism ("S-glutathionylation") in regulation of protein function has been well documented in a number of research fields. Rather paradoxically, it has also been highlighted that GSH—and notably its catabolites, as originated by metabolism by gamma-glutamyltransferase—can promote oxidative processes, by participating in metal ion-mediated reactions eventually leading to formation of reactive oxygen species and free radicals. Also, a fundamental role of GSH has been recognized in the storage and transport of nitric oxide (NO), in the form of S-nitrosoglutathione (GSNO). The significance of GSH as a major factor in regulation of cell life, proliferation, and death, can be regarded as the integrated result of all these roles, as well as of more which are emerging in diverse fields of biology and pathophysiology. Against this background, modulation of GSH levels and GSH-related enzyme activities represents a fertile field for experimental pharmacology in numerous and diverse perspectives of animal, plant and microbiologic research. This research topic includes 14 articles, i.e. 4 Opinion Articles, 6 Reviews, and 4 Original Research Articles. The contributions by several distinguished research groups, each from his own standpoint of competence and expertise, provide a comprehensive and updated view over the diverse roles, the changing faces of GSH and GSH-related enzymes in cell’s health, disease and death.
Molecular Biology of Plants presents the formal scientific presentations delivered on the symposium on plant molecular biology, held at the University of Minnesota in 1976. The topics in this book are organized around the central dogma of molecular biology. Section I describes the organization and replication of DNA in plant chromosomes, including chloroplast genomes; Section II discusses molecular aspects of transcription and translation, ribosomal RNA gene systems and hormonal control of protein synthesis. Section III examines plant viruses and bacterial agents, in particular the crown gall system, viroids, and the replication of plant RNA viruses. Each of these specific topics contributes to an integrated knowledge of plant molecular biology. The book will be of interest to geneticists, cell biologists, plant breeders, plant physiologists, plant pathologists, and biochemists.
Ascorbic acid (AsA), vitamin C, is one of the most abundant water-soluble antioxidant in plants and animals. In plants AsA serves as a major redox buffer and regulates various physiological processes controlling growth, development, and stress tolerance. Recent studies on AsA homeostasis have broadened our understanding of these physiological events. At the mechanistic level, AsA has been shown to participate in numerous metabolic and cell signaling processes, and the dynamic relationship between AsA and reactive oxygen species (ROS) has been well documented. Being a major component of the ascorbate-glutathione (AsA-GSH) cycle, AsA helps to modulate oxidative stress in plants by controlling ROS detoxification alone and in co-operation with glutathione. In contrast to the single pathway responsible for AsA biosynthesis in animals, plants utilize multiple pathways to synthesize AsA, perhaps reflecting the importance of this molecule to plant health. Any fluctuations, increases or decreases, in cellular AsA levels can have profound effects on plant growth and development, as AsA is associated with the regulation of the cell cycle, redox signaling, enzyme function and defense gene expression. Although there has been significant progress made investigating the multiple roles AsA plays in stress tolerance, many aspects of AsA-mediated physiological responses require additional research if AsA metabolism is to be manipulated to enhance stress-tolerance. This book summarizes the roles of AsA that are directly or indirectly involved in the metabolic processes and physiological functions of plants. Key topics include AsA biosynthesis and metabolism, compartmentation and transport, AsA-mediated ROS detoxification, as well as AsA signaling functions in plant growth, development and responses to environmental stresses. The main objective of this volume is therefore to supply comprehensive and up-to-date information for students, scholars and scientists interested in or currently engaged in AsA research.
In the two decades since the last comprehensive work on plant peroxisomes appeared, the scientific approaches employed in the study of plant biology have changed beyond all recognition. The accelerating pace of plant research in the post-genomic era is leading us to appreciate that peroxisomes have many important roles in plant cells, including reserve mobilisation, nitrogen assimilation, defence against stress, and metabolism of plant hormones, which are vital for productivity and normal plant development. Many plant scientists are finding, and will no doubt continue to find, that their own area of research is connected in some way to peroxisomes. Written by the leading experts in the field, this book surveys peroxisomal metabolic pathways, protein targeting and biogenesis of the organelle and prospects for the manipulation of peroxisomal function for biotechnological purposes. It aims to draw together the current state of the art as a convenient starting point for anyone, student or researcher, who wishes to know about plant peroxisomes.
Get Insight on the Function of Supercomplexes in Biological SystemsRedox Proteins in Supercomplexes and Signalosomes is one of the first books to explore the key role played by redox proteins and their interaction network in a wide range of essential cellular processes in all domains of life. The book explains how the mitochondrial respiratory chai
This volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson’s disease. Moreover, it comprehensively reviews the current search for therapies, and proposes how molecules are involved in specific functions as attractive therapeutic targets. It is expected to facilitate critical thought and discussion about the fundamental aspects of neurodegeneration in Parkinson’s disease and foster the development of therapeutic strategies among researchers and graduate students. Theories of idiopathic Parkinson’s etiology support roles for chronic inflammation and exposure to heavy metals or pesticides. Interestingly, as this project proposes, a case can be made that abnormalities in mitochondrial morphology and function are at the core of each of these theories. In fact, the most common approach to the generation of animal and cell-culture models of idiopathic Parkinson’s disease involves exposure to mitochondrial toxins. Even more compelling is the fact that most familial patients harbor genetic mutations that cause disruptions in normal mitochondrial morphology and function. While there remains to be no effective treatment for Parkinson’s disease, efforts to postpone, prevent and “cure” onset mitochondrial aberrations and neurodegeneration associated with Parkinson’s disease in various models are encouraging. While only about ten percent of Parkinson’s patients inherit disease-causing mutations, discovering common mechanisms by which familial forms of Parkinson’s disease manifest will likely shed light on the pathophysiology of the more common idiopathic form and provide insight to the general process of neurodegeneration, thus revealing therapeutic targets that will become more and more accessible as technology improves.