The book starts with the editors' preface summarizing the contributions of each of the following thirteen articles dealing with chemical and pharmacological aspects of the molecular modulators of the oxidative stress in regard to various therapeutic approaches in cardiovascular and neurodegenerative diseases, cancer, and diabetes. The seven articles present data from original research studies enlightening the roles and mechanisms of action of small molecular weight compounds (natural and synthetic; ascorbic acid/vitamin C, deferoxamine, N-acetylcysteine, MitoVitE, α-tocopherol, trolox, and ezetimibe) or proteins (SIRT3) in modulation of oxidative stress. In the six review papers, the authors present and discuss the possible therapeutic potential of novel approaches and compounds that are promising and deserve further investigation, in modulation of oxidative stress.

Current Advances for Development of Functional Foods Modulating Inflammation and Oxidative Stress presents the nutritional and technological aspects related to the development of functional foods with anti-inflammatory and antioxidant effects. Specifically, analytical approaches for the characterization of anti-inflammatory and antioxidant properties of healthy foods and functional constituents, as well as technological strategies for the extraction of compounds and fractions from raw materials to produce anti-inflammatory and antioxidant ingredients are addressed. In addition, the molecular mechanisms by which foods and their components can modulate inflammation and their oxidative stress effects on disease prevention are explored. Finally, clinical research addressing nutritional needs in pathological subjects with inflammatory diseases are considered. - Covers methods of analysis and extraction of anti-inflammatory and antioxidant compounds - Offers an overview of the main anti-inflammatory and antioxidant compounds in foods - Provides a guide on the mechanisms of action and health benefits of anti-inflammatory and antioxidant dietary bioactives

This book bridges the gap between fundamental and translational research in the area of heart disease. It describes a multidisciplinary approach, and demonstrates biochemical mechanisms associated with dysregulation of redox signaling, which leads heart disease. Presenting recent studies on improved forms of ROS scavenging enzymes; specific inhibitors for different ROS generating enzymes; and oxidant induced signaling pathways and their antagonists that allow subtle modulation of redox signaling, it also discusses the spatial and temporal aspects of oxidative stress in the cardiovascular system, which are of vital importance in developing better strategies for treating heart disease. Each chapter offers researchers valuable insights into identifying targets for drug development for different types of heart disease.

The use of antioxidants in sports is controversial due to existing evidence that they both support and hinder athletic performance. Antioxidants in Sport Nutrition covers antioxidant use in the athlete ́s basic nutrition and discusses the controversies surrounding the usefulness of antioxidant supplementation. The book also stresses how antioxidants may affect immunity, health, and exercise performance. The book contains scientifically based chapters explaining the basic mechanisms of exercise-induced oxidative damage. Also covered are methodological approaches to assess the effectiveness of antioxidant treatment. Biomarkers are discussed as a method to estimate the bioefficacy of dietary/supplemental antioxidants in sports. This book is useful for sport nutrition scientists, physicians, exercise physiologists, product developers, sport practitioners, coaches, top athletes, and recreational athletes. In it, they will find objective information and practical guidance.

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

A consequence of rapid progress in the science of nutrigenomics and nutrigenetics is the substantial accumulation of data covering nutrienal modulation of gene expression at the cellular and subcellular levels. Current research is increasingly focused on the role of nutrition and diet in modifying oxidative damage in the progression of disease. Die

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.