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Methods in Toxicology, Volume 2: Mitochondrial Dysfunction provides a source of methods, techniques, and experimental approaches for studying the role of abnormal mitochondrial function in cell injury. The book discusses the methods for the preparation and basic functional assessment of mitochondria from liver, kidney, muscle, and brain; the methods for assessing mitochondrial dysfunction in vivo and in intact organs; and the structural aspects of mitochondrial dysfunction are addressed. The text also describes chemical detoxification and metabolism as well as specific metabolic reactions that are especially important targets or indicators of damage. The methods for measurement of alterations in fatty acid and phospholipid metabolism and for the analysis and manipulation of oxidative injury and antioxidant systems are also considered. The book further tackles additional methods on mitochondrial energetics and transport processes; approaches for assessing impaired function of mitochondria; and genetic and developmental aspects of mitochondrial disease and toxicology. The text also looks into mitochondrial DNA synthesis, covalent binding to mitochondrial DNA, DNA repair, and mitochondrial dysfunction in the context of developing individuals and cellular differentiation. Microbiologists, toxicologists, biochemists, and molecular pharmacologists will find the book invaluable.
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.
This book is a printed edition of the Special Issue "Mitochondrial Dysfunction in Ageing and Diseases" that was published in IJMS
Mitochondria are far more than the “powerhouse” of the cell as they have classically been described. In fact, mitochondria biological activities have progressively expanded to include not only various bioenergetic processes but also important biosynthetic pathways, calcium homeostasis and thermogenesis, cell death by apoptosis, several different signal transduction pathways mainly related to redox control of gene expression and so on. This functional and structural complexity may undergo important derangements so to justify the definition of ‘mitochondrial medicine’, which should include all the clinical consequences of congenital or acquired mitochondrial dysfunctions. There are actually a growing number of studies which assign a significant pathogenic role to damaged mitochondria in different diseases: ischemia/reperfusion injury, neurodegenerative diseases, cancer with its dramatic sequelae (i.e, metastasis), metabolic syndrome, hyperlipidemias, just to mention a few of the most important pathologies. In this context, a further aspect that should not be disregarded is the interaction of pharmacological agents with mitochondria, not only in regard of the toxicological aspects but, above all, of the potential therapeutic applications. In fact, it is interesting to note that, while the properties of different so-called “mitoxicants” are well-known, the subtle linkages between drugs and mitochondria is still in need of a real pharmacological and therapeutic control at the clinical level. This lack of consideration can often lead to an underestimation of unwanted toxic effects but also of desirable therapeutic activities. A reevaluation of the potential clinical role of mitochondria could give a new light on some yet obscure aspects of human pathophysiology.
In recent years, several scientific papers have highlighted the role of the thyroid system in cardioprotection, and several clinical studies – including multicenter studies – have identified the role of thyroid hormones (TH) in the development and progression of cardiovascular disease, making an update of TH and heart relationship both necessary and timely. This second edition of Thyroid and Heart failure provides a careful and updated review of the experimental, clinical and epidemiological results in the field of TH and heart failure, with a particular focus on the translational - bench to bedside - significance of the obtained results. It discusses topics such as the molecular, structural, functional, cellular and histological cardiac changes; the reversibility of these changes with TH replacement therapy; the systemic effects – kidney, hormonal pathways systems, brain, muscle, etc – of altered TH metabolism in HF, as well as the clinical and prognostic implications. The section devoted to the potential therapeutic treatments has been expanded. Thanks to its translational approach to this highly complex subject, the book will be of interest to a broad readership, including cardiologists, endocrinologists and internists.
With information for patients and practitioners on optimizing mitochondrial function for greater health and longevity Why do we age? Why does cancer develop? What's the connection between heart failure and Alzheimer's disease, or infertility and hearing loss? Can we extend lifespan, and if so, how? What is the Exercise Paradox? Why do antioxidant supplements sometimes do more harm than good? Many will be amazed to learn that all these questions, and many more, can be answered by a single point of discussion: mitochondria and bioenergetics. In Mitochondria and the Future of Medicine, Naturopathic Doctor Lee Know tells the epic story of mitochondria, the widely misunderstood and often-overlooked powerhouses of our cells. The legendary saga began over two billion years ago, when one bacterium entered another without being digested, which would evolve to create the first mitochondrion. Since then, for life to exist beyond single-celled bacteria, it's the mitochondria that have been responsible for this life-giving energy. By understanding how our mitochondria work, in fact, it is possible to add years to our lives, and life to our years. Current research, however, has revealed a dark side: many seemingly disconnected degenerative diseases have tangled roots in dysfunctional mitochondria. However, modern research has also endowed us with the knowledge on how to optimize its function, which is of critical importance to our health and longevity. Lee Know offers cutting-edge information on supplementation and lifestyle changes for mitochondrial optimization, such as CoQ10, D-Ribose, cannabinoids, and ketogenic dietary therapy, and how to implement their use successfully. Mitochondria and the Future of Medicine is an invaluable resource for practitioners interested in mitochondrial medicine and the true roots of chronic illness and disease, as well as anyone interested in optimizing their health.
Developed as a one-stop reference source for drug safety and toxicology professionals, this book explains why mitochondrial failure is a crucial step in drug toxicity and how it can be avoided. • Covers both basic science and applied technology / methods • Allows readers to understand the basis of mitochondrial function, the preclinical assessments used, and what they reveal about drug effects • Contains both in vitro and in vivo methods for analysis, including practical screening approaches for drug discovery and development • Adds coverage about mitochondrial toxicity underlying organ injury, clinical reports on drug classes, and discussion of environmental toxicants affecting mitochondria
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.
Mitochondria in Obesity and Type 2 Diabetes: Comprehensive Review on Mitochondrial Functioning and Involvement in Metabolic Diseases synthesizes discoveries from laboratories around the world, enhancing our understanding of the involvement of mitochondria in the etiology of diseases, such as obesity and type 2 diabetes. Chapters illustrate and provide an overview of key concepts on topics such as the role of mitochondria in adipose tissue, cancer, cardiovascular comorbidities, skeletal muscle, the liver, kidney, and more. This book is a must-have reference for students and educational teams in biology, physiology and medicine, and researchers.
Mitochondria have traditionally been associated with metabolic functions; however recent research has uncovered a central role for these organelles in cell signaling, cell survival, and cell death. Mitochondrial dysfunction is a factor in a myriad of pathophysiological conditions, including age-related neurodegenerative disorders, cancer, metabolic