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 intended as an in-depth account of knowledge and problems in the field of oxygen-related damage in biological systems. The topics range from an assessment of molecular events in in vitro model systems to complex problems in clinical medicine. Organized into two parts with a total of 18 chapters, this book begins with an introduction to oxidative stress, elucidating specific topics on reactive oxygen species, detoxification system, and nature of oxidative damage. The first part focuses on models used with cells and tissues in the study of oxidative stress, whereas the second part describes the processes elicited by oxidative stress.

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

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.

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 book aims to provide a comprehensive review of the most up-to-date knowledge of the sources and molecular mechanisms of oxidative stress, and its role in disease and cancer. It also focuses on the novel agents and methods that can be employed to prevent oxidative stress and associated diseases.The authors first review the most recent data on the basic mechanisms of oxidative stress. The second section discusses oxidative stress leading to several diseases and cancers, and in the third section, the strategies employed in the prevention and treatment of oxidative stress-related diseases are discussed.

This book offers a systematic review of the cutting-edge knowledge in stress medicine. Cellular redox imbalance, resulting from overproduction of reactive oxide species (ROS), leads to oxidative stress and subsequent occurrence and development of many diseases, such as cancer, diabetes, pain, etc. In addition, ROS can induce post-translational modification of proteins and play roles through redox signaling pathways. In this book, the authors attempt to re-define the key concepts in oxidative stress, such as oxidative eustress and oxidative distress, revisit the pivotal signaling of oxidative stress in human diseases, and discuss the debate in current anti-oxidant strategies, such as natural products and drug repurposing. This book serves as a reference to graduate students and researchers in this growing field.