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This book illustrates the importance and significance of oxidative stress in the pathophysiology of various human diseases. The book initially introduces the phenomenon of oxidative stress, basic chemical characteristics of the species involved and summarizes the cellular oxidant and anti-oxidant system and the cellular effects and metabolism of the oxidative stress. In addition, it reviews the current understanding of the potential impact of oxidative stress on telomere shortening, aging, and age-related diseases. It also examines the role of oxidative stress in chronic diseases, including cancer, diabetes, cardiovascular diseases, and neurodegenerative disorders. Further, the book presents novel technologies for the detection of oxidative stress biomarkers using nanostructure biosensors, as well as in vitro and in vivo models to monitor oxidative stress. Lastly, the book addresses the drug delivery carriers that can help in combating oxidative stress.
Due to that at present, the majority of diseases are associated with alterations in oxidative stress and inflammatory processes, and in that Nrf-2 is a modulator of these processes; knowing how this transcriptional factor functions and is regulated opens a therapeutic window to diverse diseases. Therefore, the efforts of various investigation groups are centered on finding activators and/or inhibitors of Nrf-2 to prevent or control diverse diseases, for example, cancer, where it would be important to regulate Nrf-2 in order for it to activate apoptosis pathways in cancerogenous cells, or in neurodegenerative diseases where cell death is predominant, it would be important for Nrf-2 to activate antiapoptotic pathways.
Oxidative Stress and Antioxidant Protection: The Science of Free Radical Biology and Disease Oxidative Stress and Antioxidant Protection begins with a historical perspective of pioneers in oxidative stress with an introductory section that explains the basic principles related to oxidative stress in biochemistry and molecular biology, demonstrating both pathways and biomarkers. This section also covers diagnostic imaging and differential diagnostics. The following section covers psychological, physiologic, pharmacologic and pathologic correlates. This section addresses inheritance, gender, nutrition, obesity, family history, behavior modification, natural herbal-botanical products, and supplementation in the treatment of disease. Clinical trials are also summarized for major medical disorders and efficacy of treatment, with particular focus on inflammation, immune response, recycling, disease progression, outcomes and interventions. Each of the chapters describes what biomarker(s) and physiological functions may be relevant to a concept of specific disease and potential alternative therapy. The chapters cover medical terminology, developmental change, effects of aging, senescence, lifespan, and wound healing, and also illustrates cross-over exposure to other fields. The final chapter covers how and when to interpret appropriate data used in entry level biostatistics and epidemiology. Authored and edited by leaders in the field, Oxidative Stress and Antioxidant Protection will be an invaluable resource for students and researchers studying cell biology, molecular biology, and biochemistry, as well professionals in various health science fields.
Oxidative stress is the result of an imbalance in pro-oxidant/antioxidant homeostasis that leads to the generation of toxic reactive oxygen species. Brain cells are continuously exposed to reactive oxygen species generated by oxidative metabolism, and in certain pathological conditions defense mechanisms against oxygen radicals may be weakened and/or overwhelmed. DNA is a potential target for oxidative damage, and genomic damage can contribute to neuropathogenesis. It is important therefore to identify tools for the quantitative analysis of DNA damage in models on neurological disorders. This book presents detailed information on various neurodegenerative disorders and their connection with oxidative stress. This information will provide clinicians with directions to treat these disorders with appropriate therapy and is also of vital importance for the drug industries for the design of new drugs for treatment of degenerative disorders. * Contains the latest information on the subject of neurodegenerative disorders* Reflects on various factors involved in degeneration and gives suggestions for how to tackle these problems
Oxidative Stress and Biomaterials provides readers with the latest information on biomaterials and the oxidative stress that can pose an especially troubling challenge to their biocompatibility, especially given the fact that, at the cellular level, the tissue environment is a harsh landscape of precipitating proteins, infiltrating leukocytes, released oxidants, and fluctuations of pH which, even with the slightest shift in stasis, can induce a perpetual state of chronic inflammation. No material is 100% non-inflammatory, non-toxic, non-teratogenic, non-carcinogenic, non-thrombogenic, and non-immunogenic in all biological settings and situations. In this embattled terrain, the most we can hope for from the biomaterials we design is a type of “meso-compatibility, a material which can remain functional and benign for as long as required without succumbing to this cellular onslaught and inducing a local inflammatory reaction. Explores the challenges of designing and using biomaterials in order to minimize oxidative stress, reducing patterns of chronic inflammation and cell death Brings together the two fields of biomaterials and the biology of oxidative stress Provides approaches for the design of biomaterials with improved biocompatibility
The imbalance between the production of reactive oxygen species (ROS) and antioxidant defenses determines a state known as oxidative stress. Higher levels of pro-oxidants compared to antioxidant defenses may generate oxidative damage, which, in turn, may lead to modifications in cellular proteins, lipids, and DNA, reducing functional capacity and increasing the risk of diseases. Nevertheless, the clearance of harmful reactive chemical species is achieved by the antioxidant defense systems. These protection systems are referred to as the first and second lines of defense and comprise the classic antioxidants, enzymatic and nonenzymatic defenses, including glutathione. This book presents and discusses the advancement of research on health and diseases and their underlying mechanisms, exploring mainly aspects related to the glutathione antioxidant system.
Recognition that aging is not the accumulation of disease, but rather comprises fundamental biological processes that are amenable to experimental study, is the basis for the recent growth of experimental biogerontology. As increasingly sophisticated studies provide greater understanding of what occurs in the aging brain and how these changes occur
This first volume of the comprehensive, two-volume work on oxidative stress in lung disease introduces the molecular mechanisms, and the role of oxidants in the progression of different lung diseases. The lungs of humans and animals are under constant threat from oxidants from either endogenous (e.g. in situ metabolic reactions) or exogenous sources (e.g. air pollutants). Further, oxidative stress causes the oxidation of proteins, DNA and lipids, which in turn generates secondary metabolic products. The book consists of sections, each focusing on different aspects of oxidant-mediated lung diseases. As such it is a unique reference resource for postgraduate students, biomedical researchers and also for the clinicians who are interested in studying and understanding oxidant-mediated lung diseases. The second volume will incorporate other aspects of oxidant-mediated lung diseases, including prevention and therapeutics.
In the past few years there has been the increased recognition that the effects of oxidative stress are not limited to the damage of cellular constituents. There is now evidence that reactive oxygen species (ROS) can alter cell function by acting upon the intermediates, or second messengers, in signal transductions. Such effects on signaling mechanisms probably account for the role of oxidative stress in inflammation, aging, and cancer. This volume brings together internationally recognized researchers in both the major areas covered by the book, oxidative stress and signal transduction. The work is organized in three sections. The first deals with the immediate cellular responses to oxidative stress and the production of second messengers. The second details the connection between second messengers and the gene. The third part looks more closely at the level of the gene.
One of the major biomedical triumphs of the post-World War II era was the defmitive demonstration that hypercholesterolemia is a key causative factor in atherosclerosis; that hypercholesterolemia can be effectively treated; and that treatment significantly reduces not only coronary disease mortality but also all cause mortality. Treatment to lower plasma levels of cholesterol - primarily low density lipoprotein (LDL) cholesterol - is now accepted as best medical practice and both physicians and patients are being educated to take aggressive measures to lower LDL. We can confidently look forward to important decreases in the toll of coronary artery disease over the coming decades. However, there is still uncertainty as to the exact mechanisms by which elevated plasma cholesterol and LDL levels initiate and favor the progression of lesions. There is general consensus that one of the earliest responses to hypercholesterolemia is the adhesion of monocytes to aortic endothelial cells followed by their penetration into the subendothelial space, where they differentiate into macrophages. These cells, and also medial smooth muscle cells that have migrated into the subendothelial space, then become loaded with mUltiple, large droplets of cholesterol esters . . . the hallmark of the earliest visible atherosclerotic lesion, the so-called fatty streak. This lesion is the precursor of the more advanced lesions, both in animal models and in humans. Thus the centrality of hypercholesterolemia cannot be overstated. Still, the atherogenic process is complex and evolves over a long period of time.