The last few years have witnessed an explosion of both interest and knowledge about apoptosis, the process by which a cell actively commits suicide. The number of publications on the topic has increased from nothing in the early 1980s to more than 10,000 papers annually today. It is now well recognized that apoptosis is essential in many aspects of normal development and is required for maintaining tissue homeostasis. The idea that life requires death seems somewhat paradoxical, but cell suicide is essential for an animal to survive. For example, without selective destruction of "non-self" T cells, an animal would lack immunity. Similarly, meaningful neural connections in the brain are whittled from a mass of cells. Further, developmental cell remodeling during tissue maturation involves programmed cell death as the major mechanism for functional and structural safe transition of undifferentiated cells to more specialized counterparts. Apoptosis research, with roots in biochemistry, developmental and cell biology, genetics, and immunology, embraces this long-ignored natural law. Failure to properly regulate apoptosis can have catastrophic consequences. Cancer and many diseases (AIDS, Alzheimer's disease, Parkinson's disease, heart attack, stroke, etc. ) are thought to arise from deregulation of apoptosis. As apoptosis emerges as a key biological regulatory mechanism, it has become harder and harder to keep up with new developments in this field.

The subject for a volume on the fat-soluble vitamins needs no justification considering the importance of this group of nutrients and the rate of expan sion of our knowledge of its role in cell biology, genetics, and disease. The level of our understanding has clearly moved from knowing what fat soluble vitamins do to how they perform their functions. Hand in hand with a knowledge of their molecular mechanisms of action is the recognition that vitamins are used sparingly, and regeneration processes operate in certain cases to recycle vitamins from their metabolites. We have divided the volume into alphabetical sections beginning with vitamin A and the carotenoids through vitamins D, E, F, and K, and ending with coenzyme Q. The contributors are all acknowledged experts in their particular fields and have made significant contributions to published research results. All have worked assiduously to deliver the product of their labors on a restricted time scale and to provide the most up-to date information on their respective topics. We are truly grateful for their indulgence."

Since its discovery in 1957, Coenzyme Q has piqued the interest of scientists from a wide range of disciplines because of its bioenergetics, vitamin-like behavior, and interactions with antioxidant vitamins E and C. Coenzyme Q: Molecular Mechanisms in Health and Disease is a comprehensive treatise on this often-studied coenzyme. International experts cover the research that led to its emergence as an exciting, new dietary supplement.

The present volume summarizes the latest developments in various areas of CoQ research. New concepts on extramitochondrial functions of CoQ are discussed in two chapters, while recent discoveries in biosynthetic pathways for CoQ based on molecular genetic approaches are presented in another chapter.

Further chapters explore the role of CoQ as an antioxidant, revealing the need for additional research in this exciting area.

This book will be of extreme interest to biochemists, biophysicists, molecular and cell biologists, as well as nutritionists and biomedical health workers.

The subject for a volume on the fat-soluble vitamins needs no justification considering the importance of this group of nutrients and the rate of expan sion of our knowledge of its role in cell biology, genetics, and disease. The level of our understanding has clearly moved from knowing what fat soluble vitamins do to how they perform their functions. Hand in hand with a knowledge of their molecular mechanisms of action is the recognition that vitamins are used sparingly, and regeneration processes operate in certain cases to recycle vitamins from their metabolites. We have divided the volume into alphabetical sections beginning with vitamin A and the carotenoids through vitamins D, E, F, and K, and ending with coenzyme Q. The contributors are all acknowledged experts in their particular fields and have made significant contributions to published research results. All have worked assiduously to deliver the product of their labors on a restricted time scale and to provide the most up-to date information on their respective topics. We are truly grateful for their indulgence."

The last few years have witnessed an explosion of both interest and knowledge about apoptosis, the process by which a cell actively commits suicide. The number of publications on the topic has increased from nothing in the early 1980s to more than 10,000 papers annually today. It is now well recognized that apoptosis is essential in many aspects of normal development and is required for maintaining tissue homeostasis. The idea that life requires death seems somewhat paradoxical, but cell suicide is essential for an animal to survive. For example, without selective destruction of "non-self" T cells, an animal would lack immunity. Similarly, meaningful neural connections in the brain are whittled from a mass of cells. Further, developmental cell remodeling during tissue maturation involves programmed cell death as the major mechanism for functional and structural safe transition of undifferentiated cells to more specialized counterparts. Apoptosis research, with roots in biochemistry, developmental and cell biology, genetics, and immunology, embraces this long-ignored natural law. Failure to properly regulate apoptosis can have catastrophic consequences. Cancer and many diseases (AIDS, Alzheimer's disease, Parkinson's disease, heart attack, stroke, etc. ) are thought to arise from deregulation of apoptosis. As apoptosis emerges as a key biological regulatory mechanism, it has become harder and harder to keep up with new developments in this field.