Record Display for the EPA National Library Catalog

RECORD NUMBER: 24 OF 72

OLS Field Name OLS Field Data
Main Title Human longevity : omega-3 fatty acids, bioenergetics, molecular biology, and evolution /
Type EBOOK
Author Valentine, R. C.
Other Authors
Author Title of a Work
Valentine, David L.,
Publisher Taylor & Francis,
Year Published 2015
Call Number QP86.V35 2015
ISBN 9781466594876 (e-book : PDF); 9781466594869 (hardback)
Subjects Aging--Genetic aspects. ; Mitochondria. ; Oxidative stress. ; Omega-3 fatty acids--Health aspects.
Internet Access
Description Access URL
https://www.taylorfrancis.com/books/9781466594876
Collation 1 online resource : text file, PDF
Notes
Includes bibliographical references and index.
Due to license restrictions, this resource is available to EPA employees and authorized contractors only
Contents Notes
section 1. Introduction to the science of human aging -- section 2. Darwinian selection of membranes enabling longevity -- section 3. Revised mitochondrial membrane hypothesis of aging -- section 4. 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. "-- "This book is built on the proposition that we age as our mitochondria age. We suggest a revised version of Harman's famous hypothesis featuring mitochondrial oxidative and energy stresses as the root causes of aging. It is well known that cellular death or apoptosis is triggered by energy stress or oxidative stress. There is convincing data showing that as mitochondria age mitochondrial DNA (mtDNA) accumulates mutations decreasing energy output. Protecting highly unsaturated mitochondrial membranes against oxidative stress also consumes an extraordinary amount of energy"--