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About the Authors:
Wayne Chadwick
Affiliation: Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Yu Zhou
Affiliation: Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Sung-Soo Park
Affiliation: Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Liyun Wang
Affiliation: Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Nicholas Mitchell
Affiliation: Department of Biology, Saint Bonaventure University, Saint Bonaventure, New York, United States of America
Matthew D. Stone
Affiliation: Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Kevin G. Becker
Affiliation: Gene Expression and Genomics Unit, Research Resources Branch, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Bronwen Martin
Affiliation: Metabolism Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Stuart Maudsley
* E-mail: [email protected]
Affiliation: Receptor Pharmacology Unit, National Institute on Aging, National Institutes of Health, Baltimore, Maryland, United States of America
Introduction
Cellular adaptations to environmental changes are likely to be highly complex and involve many of the basic cellular functions. It is crucial for cellular/organismal homeostasis during lifespan that molecular systems can adapt and retain functionality despite long-term variation of environment. Aging is a complex multifactorial process, unique in its exact etiology to each individual. There are however several key factors common amongst current hypotheses of aging, one of them being accumulated oxidative stresses. The Harman free radical/oxidative stress theory of aging underpins one of the most popular concepts regarding the biochemical/molecular factors in aging [1]. Harman proposed that physiological iron and other metals would cause reactive oxygen species (ROS) to form in cells as a by-product of normal redox reactions. ROS are a by-product of a variety of pathways in aerobic metabolism. The mitochondrial electron transport chain accounts for the majority of the total oxygen metabolized by the cell, and the by-products produced by the electron transport chain (e.g., superoxide anion radicals, hydrogen peroxide, and hydroxyl radicals) are potential sources of oxidative damage to the mitochondrion itself and other cellular compartments. Endogenous ROS-scavenging...