Raymond C. Valentine is currently professor emeritus at the University of California, Davis and visiting scholar in the Marine Science Institute at the University of California, Santa Barbara. He was also the scientific founder of Calgene, Inc. (Davis, California), now a campus of Monsanto, Inc. The author´s scientific interests involve the use of reductionism to address problems of fundamental scientific and societal importance, such as agricultural productivity and aging. Some of his scientific accomplishments include the discovery of ferredoxin, the identification and naming of the nitrogen fixation (nif) genes, and the development of Roundup® resistance in crops. He holds BS and PhD degrees from the University of Illinois at Urbana-Champaign.
David L. Valentine is currently a professor of earth science with affiliations in ecology, evolution, and marine biology, as well as the Marine Science Institute, at the University of California, Santa Barbara. The author´s scientific interests involve the use of a systems-based approach to investigate the interaction between microbes and the earth, particularly in the subsurface and oceanic realms. He is best known for his research on the biogeochemistry of methane and other hydrocarbons, his works on archaeal metabolism and ecology, and his scientific work on the Deepwater Horizon oil spill. DLV holds BS and MS degrees from the University of California at San Diego and MS and PhD degrees from the University of California at Irvine.
More than 7 billion people inhabit the earth and all of them are subject to aging. This book is aimed at persons interested in a molecular explanation of how our cells age. Human Longevity: Omega-3 Fatty Acids, Bioenergetics, Molecular Biology, and Evolution is built on the proposition that we age as our mitochondria age. It suggests a revised version of Harman´s famous hypothesis featuring mitochondrial oxidative and energy stresses as the root causes of aging.
Human cells are protected from the ravages of aging by a battery of defensive systems including some novel mechanisms against membrane oxidation introduced in this book. This concept is consistent with recent discoveries showing that mitochondria-targeted antioxidants prevent Huntington´s disease, Parkinson´s disease, and traumatic brain disease in animal models of neurodegeneration.
This book explores a unified theory of aging based on bioenergetics. It covers a variety of topics including an introduction to the science of human aging, the Darwinian selection of membranes enabling longevity, a revised mitochondrial membrane hypothesis of aging, and various mechanisms that protect human mitochondrial membranes, thereby enabling longevity.
Introduction to the Science of Human Aging. Darwinian Selection of Membranes Enabling Longevity. Revised Mitochondrial Membrane Hypothesis of Aging. Many Mechanisms Have Evolved to Protect Human Mitochondrial Membranes, Enabling Longevity.
Human cells are protected from the ravages of aging by defensive systems including novel mechanisms against membrane oxidation introduced in this book. The book proposes a unified concept in which aging cells faced with declining energy production by mitochondria and the relatively high cost of protecting membranes against oxidation are triggered by energy stress to activate programmed cellular death. It includes case histories illustrating the duality of polyunsaturated membranes in aging and longevity. It also explains the relationship between membrane unsaturation and longevity leading to a unified concept of aging.
Inhaltsverzeichnis
INTRODUCTION TO THE SCIENCE OF HUMAN AGING Mitochondrial Hypothesis of Aging Is Undergoing Revision Oxidative Stress Defined as a Deadly Free Radical-Mediated Chain Reaction: Case History of Paraquat Membranes of Deep-Sea Bacteria as Surrogates for Mitochondrial Membranes of Humans DARWINIAN SELECTION OF MEMBRANES ENABLING LONGEVITY Protective Mechanisms for EPA Membranes in C. elegans and Their Relationship to Life Span Remarkable Longevity of Queens of Social Insects Likely Involves Dietary Manipulation to Minimize Levels of Polyunsaturates and Decrease Membrane Peroxidation Membrane Peroxidation Hypothesis Helps Explain Longevity in Birds, Rodents, and Whales Did Longevity Help Humans Become Super Humans? REVISED MITOCHONDRIAL MEMBRANE HYPOTHESIS OF AGING Mitochondrial Diseases and Aging Have Much in Common Revised Mitochondrial Hypothesis of Aging Highlights Energy Deficiency Caused by Errors of Replication (Mutations) of mtDNA Benefits of Polyunsaturated Mitochondrial Membranes Mitochondrial Membranes as a Source of Reactive Oxygen Species (ROS) Mitochondrial Membranes as Major Targets of Oxidation MANY MECHANISMS HAVE EVOLVED TO PROTECT HUMAN MITOCHONDRIAL MEMBRANES, ENABLING LONGEVITY Apoptosis Caused by Oxidatively Truncated Phospholipids Can Be Reversed by Several Mechanisms, Especially Enzymatic Detoxification Selective Targeting of HUFAs Away from Cardiolipin and Beta-Oxidation Combine to Protect Mitochondrial Membranes Against Oxidative Damage Oxygen Limitation Protects Mitochondrial Phospholipids, Especially Cardiolipin Uncoupling Proteins (UCPs) of Mitochondria Purposely Waste Energy to Prevent Membrane Damage Mitochondrial Fission Protects against Oxidative Stress by Minting a Continuous Supply of Cardiolipin and Other Polyunsaturated Phospholipids Mitophagy Eliminates Toxic Mitochondria Longevity Genes Likely Protect Membranes Aging as a Cardiolipin Disease That Can Be Treated Index